A review on the effect of green tea extract against obesity

Abstract

Obesity is a public health crisis that has reached epidemic proportions worldwide, demanding urgent attention. To combat obesity, people endeavor to follow a healthy diet and regularly engage in physical activities. However, maintaining a healthy diet and physical activity is challenging, highlighting the need for novel effective therapies. This review aims to evaluate the therapeutic efficacy and safety of a well-researched functional food ingredient, green tea extract, for combating obesity. To assess the effectiveness of green tea extract, the review systematically examines various obesity indicators. It focuses on markers for body fat reduction in rodent models and humans, including weight, BMI, body fat percentage, and waist circumference. Furthermore, it explores the potential for suppressing and preventing obesity-related metabolic disorders. By thoroughly examining the effectiveness and mechanism of green tea extract, the study seeks to understand the potential of green tea extract as a nutraceutical/functional food for obesity management and prevention.

Introduction

Obesity has emerged as a serious public health issue worldwide. The World Health Organization (WHO) utilizes the body mass index (BMI) as a standardized metric for defining obesity (Phelps et al., 2024). This index is calculated by dividing an individual’s body weight (kg) by the square of their height (m²). According to WHO guidelines, a BMI threshold of 30 or higher categorizes an individual as obese. Furthermore, the WHO has issued warnings about the increased risk of chronic diseases associated with obesity, including cardiovascular diseases, diabetes, arthritis, and certain forms of cancer. These declarations underscore the critical public health implications of obesity and the necessity for effective management and preventative strategies (Phelps et al., 2024). Despite individual efforts to control their diet and engage in regular exercise, it is often challenging to sustain such healthy lifestyle habits. Consequently, the food industry has been making significant efforts to develop ingredients for functional foods that can prevent and manage obesity. There is ongoing research in the improvement and prevention of obesity using naturally derived functional food ingredients, with a variety of functional food development studies based on these findings. In this review paper, a comprehensive evaluation and investigation will be conducted on the efficacy and safety of green tea extract (GTE), a functional food ingredient actively researched for its potential to manage and prevent obesity. Specifically, it will be focus on the fat reducing effects of GTE and its influence on metabolic indicators of obesity. The objective of this review is to assess the efficacy and safety of GTE, and resultingly offer strategies for easier obesity management using GTE as a functional food ingredient.

In recent years, the prevalence of obesity has emerged as a paramount global health concern, as highlighted by a comprehensive report issued by WHO. This report draws on data from a wide-ranging global survey conducted, tracking trends from 1990 to 2022. Notably, the findings indicate that the prevalence of obesity among women worldwide has more than doubled over this period, escalating from 8.8% to 18.5%. This significant increase translates to approximately 540 million obese women globally. In parallel, the rate of obesity among men has also experienced a considerable rise, from 4.8% in 1990 to 14% in 2022, corresponding to around 374 million obese men worldwide. Additionally, focused research pertaining to the population of the United States further corroborates this global trend. The study reveals that within the U.S., the obesity rate escalated from 19.8% in 2000 to 27.2% in 2010, indicating a persistent upward trend. These statistics collectively highlight that the surge in obesity rates is not an isolated phenomenon but a pervasive issue affecting diverse demographics across the globe. The substantial escalation in obesity rates calls for immediate international collaboration to mitigate the associated health risks and necessitates the formulation of comprehensive health policies, intervention strategies, and preventive measures aimed at curbing the obesity epidemic. These initiatives are crucial not only for stemming the increase in obesity but also for alleviating the burden of associated chronic conditions, such as diabetes, cardiovascular diseases, and certain types of cancer, which are exacerbated by excess weight.

Causes and health risks of obesity

Obesity is a multifaceted condition stemming from a complex interplay between biological factors, adverse environmental conditions, lifestyle habits, and socioeconomic factors. This confluence significantly heightens the risk of developing severe health complications, including type 2 diabetes, cardiovascular diseases, liver diseases, and various cancers. These health challenges not only compromise an individual’s well-being but also augment societal burdens, thereby necessitating concerted efforts to mitigate these risks.

The genesis of obesity is a multifactorial, a combination of biological factors, negative environmental factors, lifestyle habits, and socioeconomic factors (Martinez, 2000; Wright and Aronne, 2012) (Fig. 1). Obesity arises from an interplay of these various elements, including their complex interactions (Wright and Aronne, 2012). Biological factors, both monogenic and polygenic, are prominently mediated by pivotal genes such as the MC4R, POMC, and LEPR genes, and further modulated by epigenetic alterations, notably DNA methylation. These genetic elements exert significant influence over the regulatory mechanisms of body weight through essential signaling pathways (Loos and Yeo, 2022). Negative environmental factors, including exposure to chemical pollutants and the structural and accessibility aspects of residential settings, transportation systems, and public infrastructures, significantly impact physical activity levels and escalate obesity risks. These factors detrimentally affect metabolic health and the accessibility to physical activities and nutritious diets, especially in regions marred by socioeconomic disadvantages (Herrera and Lindgren, 2010). Pertaining to lifestyle habits, dietary practices, physical activity levels, stress and sleep deprivation emerge as direct contributors to energy imbalance and subsequent weight gain. The exacerbation of these factors by stress and inadequate sleep further amplifies obesity risk (Farooqi and O’Rahilly, 2006). The nutrient quality, characterized by diets deficient in proteins yet abundant in fats and carbohydrates, compounded by dietary reporting inaccuracies and a predilection for high fat food, critically influences the obesity prevalence (Nicolaidis, 2019). From a socioeconomic viewpoint, the disparity in the availability and accessibility to healthful foods and healthcare resources underscores the influence of socioeconomic status on obesity risk, perpetuating health outcome disparities (Albuquerque et al., 2017). In summation, the emergence of obesity is attributed to the dynamic interaction among biological determinants, adverse environmental exposures, lifestyle choices, and socioeconomic conditions. An in-depth comprehension of these contributing factors is crucial for the development of comprehensive intervention and treatment strategies aimed at the effective prevention and management of obesity.

Fig. 1.

Various factors of obesity. The factors contributing to obesity are categorized into four groups: biological factors, environmental factors, lifestyle habits, and socioeconomic factors. These factors interact and can potentially lead to the development of obesity

Obesity extends beyond mere aesthetic concerns, presenting significant risks for severe health complications and the onset of chronic conditions. The morbidities associated with obesity include, but are not limited to, Type 2 diabetes, cardiovascular disorders, hepatic diseases, and a spectrum of cancers (Fig. 2). Obesity markedly increases the risk of developing Type 2 diabetes through mechanisms such as enhanced insulin resistance, induction of chronic inflammation, and increased secretion of hormones and inflammatory mediators within adipose tissues (Boles et al., 2017; Mokdad et al., 2003; Scherer and Hill, 2016; Smyth and Heron, 2006). These mechanisms disrupt insulin action, lead to hyperglycemia, and provoke vascular micro-inflammation, thus accelerating the onset of diabetes and elevating the risks associated with cardiovascular diseases (Boles et al., 2017; Scherer and Hill, 2016). Moreover, obesity induces substantial alterations in the structure and function of the cardiovascular system, increasing the risks of myocardial infarction, hypertension, and diabetes. It instigates metabolic abnormalities and inflammation, thereby escalating the risks of cardiovascular diseases, and may lead to arrhythmias, such as atrial fibrillation (Mandviwala et al., 2016). The magnitude, distribution, and persistence of obesity critically influence cardiovascular events (Scherer and Hill, 2016). Furthermore, obesity contributes to steatosis by increasing fatty acids in adipocytes, exacerbating oxidative stress, and promoting the secretion of pro-inflammatory cytokines, which in turn promotes liver fibrosis. It is also closely linked with insulin resistance, amplifying the risks of liver diseases (Marchesini et al., 2008; Moore, 2010; Samuel and Shulman, 2018). Additionally, obesity impacts cancer risk through hormonal and metabolic dysregulations that affect various tumors. It facilitates the genesis of site-specific tumors due to complications in organs affected by obesity and drives systemic inflammation, which worsens the prognosis of cancer (De Pergola and Silvestris, 2013; Ortega et al., 2016; Wolin et al., 2010). Obesity plays a pivotal role in the pathogenesis of a myriad of diseases, serving as a critical factor in the onset of such chronic conditions. This association contributes to a decline in the quality of life and overall health of individuals, rendering obesity a grave societal concern. Consequently, sustained management and preventive measures against obesity are imperative.

Fig. 2.

Various diseases that can be caused by obesity. Mechanism by which obesity can contribute to diseases such as diabetes, cardiovascular disorders, hepatic diseases, and cancers

Evaluation criteria for obesity

This review systematically evaluates various indicators employed to represent and measure the extent of obesity. Specifically, it places emphasis on markers used to assess body fat reduction in both rodent models and humans, providing a comprehensive assessment of weight, body mass index (BMI), body fat percentage, and waist circumference. Furthermore, it aims to suggest ways to suppress obesity and prevent obesity-related metabolic disorders by using indicators that assess obesity-related metabolism. To support these assertions, the study evaluates concentrations of fat-related substances in the blood and adipokines secreted from adipose tissues in both rodent models and humans. Additionally, it assesses blood glucose levels and insulin resistance, which are closely associated with diabetes.

Body weight

Body weight is universally acknowledged as a fundamental and essential indicator for the assessment of obesity. It reacts swiftly to the accumulation of adipose tissue, thereby rendering changes in body weight, a valuable measure for evaluating the extent of obesity. Individuals adhering to calorie-restricted diets for weight reduction often report significant decreases in body weight, which are crucial for effective weight management and reduction of obesity-related risk factors. Consequently, weight management plays a pivotal role in treating obesity, underscoring the importance of ongoing weight monitoring and regulation. This approach is critical in mitigating the health complications associated with obesity, highlighting the necessity for continuous monitoring and weight adjustment within comprehensive obesity management programs (Jovanovski et al., 2021).

Body mass index

BMI, calculated by dividing an individual’s weight in kilograms by the square of their height in meters, serves as a critical metric for assessing the relationship between obesity and chronic energy deficiency. This index is internationally recognized for classifying obesity and predicting associated health risks. The standard classification for BMI defines: under 18.5 as underweight, between 18.5 and 24.9 as normal weight, between 25.0 and 29.9 as overweight. Moreover, a BMI between 30.0 and 34.9 qualifies as Obesity Class I, between 35.0 and 39.9 as Obesity Class II, and 40.0 or higher as Obesity Class III. These categories are essential for guiding public health policies and formulating individual health management strategies (Weisell, 2003).

Body fat percentage

The body fat percentage is an essential metric that denotes the proportion of total body fat in relation to the overall body mass, thereby serving as a significant indicator for assessing individual health status. For adult males, it is typically recommended to maintain a body fat percentage within the range of 10–20%, while for females, a range of 18–28% is considered optimal. These guidelines are predicated on evaluating body composition and understanding the influence of adipose tissue on overall health. This parameter transcends mere body weight measurements by providing a more accurate reflection of the composition of fat and lean tissues within the body, enabling a more precise assessment of health. Consequently, body fat percentage is not only critical for effective weight management but also plays a pivotal role in health management (Mamrot and Hanć, 2019).

Waist circumference

Waist circumference, defined as the measurement around the waist, is recognized as a critical indicator for assessing the extent of abdominal obesity. This metric is instrumental in evaluating an individual’s health status and assessing the risk associated with metabolic disorders. It specifically reflects the quantity of fat concentrated in the abdominal area, thereby providing a more accurate diagnosis of health risk factors that may not be apparent through body weight or BMI alone (Burns et al., 2018).

Lipid profile

In the context of obesity research, the metrics of total cholesterol (TC), triglycerides (TG), low density lipoprotein cholesterol (LDL), and high density lipoprotein cholesterol (HDL) serve as essential indicators. TC is used to assess overall cholesterol levels in the body, significantly correlated with obesity. It plays an indispensable role in enhancing the predictive capabilities of surrogate markers for central adiposity, underscoring the necessity of incorporating plasma lipid concentrations in the analysis of obesity-related studies. Similarly, TG levels, indicative of plasma triglycerides, are closely associated with obesity and improve the predictive accuracy of central adiposity surrogate markers by taking lipid profiles into account. Furthermore, LDL and HDL, representing low density and high density lipoprotein cholesterol respectively, are critically linked to obesity. LDL is crucial in refining the predictive accuracy of surrogate markers for central adiposity and obesity, emphasizing the importance of evaluating plasma lipid concentrations. HDL, attributed with positive health effects, complements this predictive refinement, illustrating the intricate link between lipid profiles and obesity. In the context of lipid profiles, it is generally recognized that a healthier profile entails lower levels of TC, TG, and LDL, along with higher levels of HDL (Barazzoni et al., 2019).

Insulin resistance & blood glucose

Blood glucose denotes the concentration of glucose within the bloodstream, whereas insulin resistance describes a condition in which cellular responsiveness to insulin is diminished, leading to inefficient glucose metabolism. The interrelation between insulin resistance and blood glucose level is of paramount importance as it can precipitate a myriad of metabolic disorders, including obesity, diabetes mellitus, hypertension, dyslipidemia, and cardiovascular diseases. Insulin resistance adversely impacts the functionality of pancreatic beta cells, integral for the regulation of blood glucose, potentially serving as a harbinger of diabetes onset. Moreover, insulin resistance is associated with hepatic insulin resistance, which may augment TG synthesis in the liver, thus elevating plasma TG levels. Such a condition can further exacerbate glucose intolerance, complicating the management of glucose control in diabetes or prediabetes scenarios (Ferrannini et al., 2007). Obesity exerts a negative influence on glucose regulation and is intricately linked with glucose imbalance, dyslipidemia, hypertension, and enhanced insulin resistance. The excessive accumulation of adipose tissue can attenuate insulin efficacy, thereby impeding glucose regulation and fostering insulin resistance. This underscores obesity’s pivotal role in elevating diabetes risk (Ferrannini et al., 2007). Homeostatic model assessment for insulin resistance (HOMA-IR) serves as a critical metric in assessing insulin resistance was employed as a benchmark for insulin resistance within this review. Utilizing fasting blood glucose and insulin concentrations, HOMA-IR estimates insulin resistance, with higher values indicating increased insulin resistance. The formula for HOMA-IR calculation is (fasting blood glucose × fasting insulin) a designated constant, with lower scores meaning enhanced insulin sensitivity. Furthermore, this review scrutinized various research findings utilizing the Quantitative Insulin Sensitivity Check Index (QUICKI) index as a metric to gauge insulin resistance. The QUICKI index serves as a valuable tool for measuring insulin sensitivity, offering insights into the association between insulin resistance and metabolic disturbances (Chen et al., 2003).

Adipokine

Adipokines, which are bioactive cytokines/molecules secreted by adipose tissue, play pivotal roles in a myriad of physiological processes and have been implicated in the pathogenesis of obesity-related metabolic syndrome and cardiovascular diseases. Leptin, predominantly secreted by adipose tissue, correlates with the mass of adipose tissue and is integral to appetite regulation, neuroendocrine functions, reproduction, angiogenesis, and blood pressure modulation. Notably, circulating levels of leptin are found to be elevated in obese individuals, reflecting an increased adipose tissue mass that secretes higher quantities of leptin (Frühbeck et al., 2018). Furthermore, adiponectin, another critical adipokine, engages in diverse physiological activities and occupies a central role in the metabolic syndrome associated with obesity. Observations indicate that both the expression of adiponectin within adipose tissue and serum adiponectin levels are diminished in individuals with obesity, leading to the emergence of dysfunctional adipose tissue. This dysfunction is characterized by persistent inflammation, maladaptive extracellular matrix remodeling, and compromised angiogenesis, which are hallmark features associated with obesity (Frühbeck et al., 2018). Moreover, the adiponectin/leptin ratio, a comparative measure of these adipokines, may be inversely-related to the risk of arteriosclerosis in obese adolescents, suggesting that the balance between adiponectin and leptin serves as a significant marker for evaluating the risk of metabolic and cardiovascular disorders linked to obesity (Frühbeck et al., 2018). This delineation underscores the critical importance of adipokines in mediating the complex interplay between obesity and its associated health implications.

Green tea extract

Green tea extract (GTE) is derived from tea plant leaves and encompasses not only polyphenols and alkaloids but also a diverse array of amino acids, vitamins, and minerals. The principal active constituents are polyphenols, which belong to an extensive group of plant derived compounds, including subgroups such as flavonoids, phenolic acids, and lignans. Notably, the catechin components, namely epicatechin (EC), epicatechin gallate (ECG), epigallocatechin (EGC), and epigallocatechin gallate (EGCG), are closely associated with the weight loss effects of GTE and have thus attracted significant attention (Braicu et al., 2013; Senanayake, 2013). In addition to catechins, the flavonoid profile of GTE includes quercetin, kaempferol, myricetin, and their glycosides (Senanayake, 2013). Among the alkaloid constituents in green tea, caffeine acts as an antioxidant and stimulates the central nervous system, reducing fatigue, enhancing metabolism, facilitating the breakdown of fatty acids, and aiding their conversion into energy (Westerterp-Plantenga, 2010). The primary amino acids in GTE include theanine, arginine, glutamic acid, tryptophan, and glycine. Furthermore, it contains vitamins such as vitamin C, riboflavin, and thiamine, along with minerals like manganese, potassium, calcium, iron, and zinc, rendering it a functional material with multiple health benefits. In selecting an extraction method for GTE, factors such as the desired type of components, extraction efficiency, cost, and safety must be considered. Hot water extraction, one of the most prevalent extraction methods, utilizes high temperatures to extract catechins from tea components. The ultrasonic extraction method, which uses ultrasonic energy to disrupt the cell walls of tea leaves, offers speed and efficiency but requires specialized equipment and may also risk denaturing some components. Enzymatic extraction, although minimizing the denaturation of components, necessitates expensive enzymes and involves a complex process. Additionally, research continues on with methods such as supercritical CO₂ extraction and the use of various organic solvents including ethanol, methanol, and acetone (Jun et al., 2011; Pasrija and Anandharamakrishnan, 2015; Senanayake, 2013). This review comprehensively assessed the weight loss effects of GTE, focusing particularly on its impact on obesity-related metabolic indicators, to evaluate its functionality and stability.

Effects of green tea extract on obesity in mouse models

This study investigated the impact of GTE on obesity using a mouse model. Initially, weight changes were assessed to confirm reductions in body fat in the mouse model, and adipose tissue weight was also evaluated. Furthermore, metabolic indicators associated with obesity were analyzed to review improvements and preventive effects against obesity-related metabolic abnormalities and associated conditions. To comprehensively evaluate obesity-related metabolism in the mouse model, lipid profiles (TC, TG, LDL, HDL), blood glucose levels, insulin resistance, and adipokines (leptin and adiponectin) were evaluated. Ultimately, this study aims to indicate potential efficacy of GTE in humans through a comprehensive evaluation of body fat reduction and obesity-related metabolic indicators in the mouse model.

Body weight

To investigate the fat reducing effects of GTE in mouse models, studies addressing changes in body weight and adipose tissue weight following GTE administration were reviewed. These studies, which varied in conditions such as the types of mice, dosages, and durations, consistently demonstrated either weight reduction or inhibition of weight gain when GTE or its polyphenols, including EGCG, were administered (Table 1). In all reviewed studies, mice that consumed GTE exhibited consistent weight loss or inhibited weight gain compared to those that received a placebo. Specifically, in a study where 5 week old male C57BL/6J mice were given a diet containing 2% GTE for 6 weeks, the GTE group showed approximately 25% weight loss and a 40% reduction in adipose tissue weight compared to the placebo group (Bruno et al., 2008). Another study with the same type of mice on a diet with 1% GTE for 6 weeks found that weight gain was inhibited in the GTE group compared to the placebo group. After 6 weeks, the GTE group had about 18% lower body weight, and their adipose tissue weight was approximately 21% lower than that of the placebo group (Park et al., 2011). Moreover, in a study where 4-week-old male C57BL/6J mice were given a diet with 0.5% EGCG for 8 weeks, the average body weight of the EGCG group decreased from 38.5 g to 35.2 g, while the placebo group’s weight increased from 38.9 g to 44.2 g. After 8 weeks, the EGCG group’s body weight was about 20% lower than that of the placebo group. Additionally, the adipose tissue weight of the EGCG group was about 24% lower than that of the placebo group (Lee et al., 2009). These findings collectively demonstrate a consistent pattern of weight reduction and inhibition of weight gain, suggesting that GTE has a positive effect on weight control in mouse models.

Table 1.

Effects of green tea extract on body weight in mouse models

Variable	Administration	Dose / Duration / Diet	Effect	References
Body weight	GTE	2% in diet / 6 weeks / modified AIN-93G	↓	(Bruno et al., 2008)
	GTE	0.01% in water / 12 weeks / high-fat diet	↓	(Cho et al., 2020b)
	GTE	200 mg/kg / 12 weeks / high-fat diet	↓	(Cho et al., 2020a)
	GTE	0.5% in diet / 11 months / high-fat diet	↓	(Murase et al., 2002)
	GTE	1% in diet / 6 weeks / modified AIN-93G	↓	(Park et al., 2011)
	GTE	300 mg/kg / 4 weeks / high-fat diet	↓	(Minatti et al., 2012)
	GTP	240 mg/kg / 4 weeks / high-fat & sucrose diet	↓	(Henning et al., 2018)
	GTP	0.5% in water / 4 months / high-fat diet	↓	(Lu et al., 2012)
	GTP	0.025% in diet / 16 weeks /high-fat & sucrose diet	↓	(Heber et al., 2014)
	EGCG	0.32% in diet / 17 weeks / high-fat diet	↓	(Chen et al., 2011)
	EGCG	0.5% in diet / 8 weeks / high-fat diet	↓	(Lee et al., 2009)
	EGCG	3.2 g/kg / 12 weeks / high-fat diet	↓	(Bose et al., 2008)
Adipose tissue weight	GTE	2% in diet / 6 weeks / modified AIN-93G	↓	(Bruno et al., 2008)
	GTE	200 mg/kg / 12 weeks / high-fat diet	↓	(Cho et al., 2020a)
	GTE	0.5% in diet / 11 months / high-fat diet	↓	(Murase et al., 2002)
	GTE	1% in diet / 6 weeks / modified AIN-93G	↓	(Park et al., 2011)
	GTP	24 mg/kg / 4 weeks / high-fat & sucrose diet	↓	(Henning et al., 2018)
	GTP	0.025% in diet / 16 weeks / high-fat & sucrose diet	↓	(Heber et al., 2014)
	EGCG	0.32% in diet / 17 weeks / high-fat diet	↓	(Chen et al., 2011)
	EGCG	0.5% in diet / 8 weeks / high-fat diet	↓	(Lee et al., 2009)
	EGCG	3.2 g/kg / 12 weeks / high-fat diet	↓	(Bose et al., 2008)

This table depicts the changes in body weight and adipose tissue weight among various mouse models following administration of GTE, GTP, and EGCG, which are components of GTE

In this study, comparisons were made between the GTE group and the placebo group

*^aGTP, green tea polyphenols

(↓ Decrease or inhibit the increase)

Lipid profile

To assess the impact of GTE on lipid profiles in obesity-related metabolism, a thorough review was conducted, utilizing TC, TG, LDL, and HDL across various studies. These investigations encompassed diverse strains of mice, employing varied dosages and durations. The majority of these findings revealed a consistent trend towards decreased TC, TG, and LDL levels, alongside an elevation in HDL levels (Table 2). Specifically, in a study targeting 12 week old female CD-1 mice administered with a 0.01% dosage of GTE in drinking water, HDL levels in the GTE treated group were observed to be 62 mg/dL, approximately 214% higher than the 29mg/dL observed in the placebo group (Cho et al., 2020b). In another investigation involving 7-week-old male C57BL/6J mice administered with a 0.5% dosage of GTE, reductions in TC and TG levels were noted. Following the study’s conclusion, TC in the GTE treated group was 85.3 mg/dL, approximately 48% lower than the 164.1 mg/dL in the placebo group, while TG was 21.6 mg/dL, around 14% lower than the 25.2 mg/dL in the placebo group (Murase et al., 2002). Additionally, in an 8-week study involving 4-week-old male C57BL/6J mice administered with a 0.5% dosage of EGCG in their diet, decreases in TC, TG, and LDL levels were observed. TC in the EGCG treated group was 2.88 mmol/L, roughly 30% lower than the 4.13 mmol/L in the placebo group. TG was 0.69 mmol/L, approximately 35% lower than the 1.06 mmol/L in the placebo group and LDL was 0.71 mmol/L, about 54% lower than the 1.55mmol/L in the placebo group (Lee et al., 2009). Moreover, in another study involving 12 week old male C57BL/6N mice administered with a dosage of 200 mg/kg/day of GTE, reductions in TC, TG, and LDL were observed, while HDL exhibited a minor increase, although statistically insignificant (Cho et al., 2020a). While some experiments yielded statistically insignificant results regarding lipid profiles after GTE administration, the majority of studies showed decreases in TC, TG, and LDL levels, indicating an improvement in adverse lipid profiles. Furthermore, the overall increase in HDL levels suggests a positive impact on lipid profile. In summary, considering these lipid profile outcomes, the administration of GTE is assessed to ameliorate unfavorable lipid profiles and enhance favorable lipid profiles, offering promise for beneficial effects on human lipid profiles.

Table 2.

Effects of green tea extract on obesity-related metabolic indicators in mouse models

Administration	Dose / Duration / Diet	Effects	References
GTE	0.01% in water / 12 weeks / high-fat diet	Lipid profile (TC -, TG -, HDL↑) / blood glucose↓	(Cho et al., 2020b)
GTE	200 mg/kg / 12 weeks / high-fat diet	Lipid profile (TC↓, TG↓, LDL↓, HCL -) / blood glucose↓ / insulin resistance↓ / adipokine (leptin↓, adiponectin↑)	(Cho et al., 2020a)
GTE	0.5% in diet / 11 months / high-fat diet	Lipid profile (TC↓, TG↓) / blood glucose↓ / adipokine (leptin↓)	(Murase et al., 2002)
GTP	0.025% in diet / 16 weeks / high-fat & sucrose diet	Adipokine (leptin↓)	(Heber et al., 2014)
EGCG	0.32% in diet / 17 weeks / high-fat diet	Blood glucose↓ / insulin resistance↓	(Chen et al., 2011)
EGCG	0.5% in diet / 8 weeks / high-fat diet	Lipid profile (TC↓, TG↓, LDL↓, HDL↑) / adipokine (leptin↓)	(Lee et al., 2009)
EGCG	3.2 g/kg / 12 weeks / high-fat diet	Blood glucose↓ / insulin resistance↓	(Bose et al., 2008)

This table illustrates the changes in lipid profiles (TC, TG, LDL, HDL), blood glucose, insulin resistance (HOMA-IR), and adiponectin (leptin adiponectin) among various mouse models following the administration of GTE, GTP, and EGCG, which are components of GTE

In this study, comparisons were made between the GTE group and the placebo group

^*aGTP, green tea polyphenols

(- Not significant, ↓ Decrease, ↑Increase)

Insulin resistance & blood glucose

Focusing on insulin resistance and blood glucose changes among metabolic indicators associated with obesity, the effects of GTE on insulin resistance evaluated by HOMA-IR and the consequent alterations in blood glucose levels were investigated through various studies. A synthesis of multiple research outcomes consistently revealed a pattern of GTE administration. Specifically, reductions in insulin resistance and blood glucose levels were consistently observed, with no exceptions noted (Table 2). Analyzing numerical data from most graphically represented studies, for instance, in a study administering 0.5% GTE dosage to 7 week old male C57BL/6J mice, the blood glucose level in the GTE group was 187.2 mg/dL, approximately 23% lower than the 244.6 mg/dL observed in the placebo group (Murase et al., 2002). Additionally, in a study where 0.32% EGCG dosage was administered to male C57BL/6J mice aged 5–6 weeks for 17 weeks, reductions in insulin resistance and blood glucose levels were noted. Particularly, the insulin resistance measured by HOMA-IR in the EGCG treated group was 29.1, about 33% lower than the 43.6 observed in the placebo group (Chen et al., 2011). Furthermore, another study administering 3.2 g/kg dosage of EGCG to male C57BL/6J mice aged 5–6 weeks for 12 weeks showed reductions in insulin resistance and blood glucose levels (Bose et al., 2008). Collectively, these findings indicate a positive effect of GTE administration in reducing insulin resistance and regulating blood glucose levels in mouse models. Therefore, these results suggest potential positive effects on insulin resistance and blood glucose regulation in humans as well.

Adipokine

The effects of GTE on leptin and adiponectin, hormones primarily secreted by adipose tissue and associated with obesity, were examined in a mouse model. Multiple research findings consistently indicated a decrease in leptin levels. For instance, in a study administering 0.5% GTE to 7 week old male C57BL/6J mice, the leptin concentration in the GTE group was 5.1 ng/mL, approximately 91% lower than the 54.7 ng/mL observed in the placebo group (Murase et al., 2002). Similarly, another study administering 0.5% GTE to 4 week old male C57BL/6J mice for 8 weeks showed that the leptin concentration in the GTE group was 12.3 ng/mL, approximately 46% lower than the 22.8 ng/mL observed in the placebo group (Lee et al., 2009). Regarding adiponectin, analysis of graphs from a study where 200 mg/kg/day of GTE was administered to 4-week-old male C57BL/6N mice for 12 weeks revealed that the adiponectin concentration in the GTE group was approximately 2.8 ng/mL, compared to approximately 2.4 ng/mL in the placebo group. The adiponectin concentration in the GTE group was about 17% higher than the placebo group (Cho et al., 2020a). These findings collectively suggest that the decrease in leptin secretion, attributed to the reduction in adipose tissue resulting from GTE intake, may play a role in regulating appetite and promoting energy expenditure. Additionally, the observed increase in adiponectin levels is anticipated to positively influence metabolism and blood glucose regulation. These research outcomes imply potential positive effects on leptin and adiponectin levels in humans as well.

Effects of green tea extract on obesity in humans

After observing the positive effects of GTE on body fat reduction and obesity-related metabolism in mouse models, our study extended its focus to evaluate its impact on human subjects. Assessing the potential of GTE to reduce body fat in humans involved four key indicators: body weight, BMI, body fat percentage, and waist circumference. Additionally, the influence of GTE on obesity-related metabolic indicators was analyzed, including lipid profiles (TC, TG, LDL, HDL), blood glucose levels, insulin resistance, and adipokines (leptin and adiponectin). Through this comprehensive analysis, the aim was to determine the potential of GTE in improving and preventing obesity-related metabolic abnormalities and associated conditions in humans.

Body weight

To evaluate the potential impact of GTE on reducing body fat, the study initially scrutinized the results of investigations focusing on changes in body weight. These studies encompassed various demographics and were conducted under different conditions regarding GTE dosage and the duration of experiments. Overall, when GTE or its constituent EGCG was administered, either weight loss or inhibition of weight gain was generally observed (Table 3). However, in studies involving 100 obese women aged 16–60 years receiving 1200 mg/day of GTE for 12 weeks and 42 postmenopausal women receiving 300 mg/day of EGCG for the same duration, no significant changes in body weight were noted (Hill et al., 2007; Hsu et al., 2008). Similarly, in a study involving 42 women aged 25–40 years diagnosed with polycystic ovary syndrome and receiving 540 mg/day of GTE for 3 months, while the placebo group experienced significant weight gain, a slight decrease in body weight was observed in the GTE group (Chan et al., 2006). Except for these studies, all other research outcomes indicated significant weight loss. Particularly noteworthy was a study involving 18 men aged 40–60 years and 42 postmenopausal women receiving 100 mg/day of GTE for 12 weeks, where the GTE group exhibited a 7% decrease in body weight after 12 weeks, while the placebo group maintained their weight (Auvichayapat et al., 2008). Furthermore, in a study involving 38 Japanese men aged 24–46 years receiving 202.9mg/day of GTE for 12 weeks, the GTE group showed a decrease of 2.4 kg in body weight compared to a 1.3 kg decrease in the placebo group, indicating that the GTE group experienced approximately 85% more weight loss than the placebo group (Nagao et al., 2005). Additionally, in a study involving 128 individuals aged 21–65 years with a TC level greater than or equal to 5.2 mmol/L and a BMI ranging from 25 to 40 kg/m², those who received 625mg/day of GTE for 12 weeks experienced a decrease in body weight of 2.2 kg, compared to a decrease of 1 kg in the placebo group. This suggests that the GTE group achieved approximately 120% more weight loss than the placebo group (Maki et al., 2009). These findings collectively demonstrate a consistent pattern, suggesting that GTE has a positive effect on weight loss and weight gain inhibition in humans.

Table 3.

Effects of green tea extract on reduction of body fat in humans

Administration	Dose / Duration / Participants	Effects	References
GTE	420 mg/day / 3 months / avg. body mass index = 29.6 ± 2.6 kg/m2 in adult M (n = 23) & F (n = 53)	Body weight↓, body mass index↓, body fat percentage↓, waist circumference↓	(Westerterp-Plantenga et al., 2005)
GTE	500 mg/day / 8 weeks / overweight women aged 38.36 ± 3.16y (n = 30)	Body weight ↓, body mass index ↓, body fat percentage ↓, waist circumference -	(Bagheri et al., 2020)
GTE	1200 mg/day / 12 weeks / obese women aged 16–60 y, body mass index ≥ 27 kg/m2 (n = 100)	Body weight -, body mass index –, body fat percentage -, waist circumference -	(Hsu et al., 2008)
GTE	100 mg/day / 12 weeks / avg. body mass index ≥ 25 kg/m2 in M aged 40-60y (n = 18) & postmenopausal F ≥ 1y (n = 42)	Body weight ↓, body mass index ↓, body fat percentage ↓, waist circumference ↓	(Auvichayapat et al., 2008)
GTE	540 mg/day / 3 months / women aged 25-40y, body mass index ≤ 28 kg/m2, diagnosed with PCOS (n = 42)	Body weight ↓, body mass index ↓, body fat percentage ↓, waist circumference ↓	(Chan et al., 2006)
GTE	625 mg/day / 12 weeks / abdominal obesity M and W aged 21-65y, TC ≥ 5.2 mmol/L, body mass index = 25–40 kg/m2 (n = 128)	Body weight ↓, body mass index ↓, body fat percentage ↓, waist circumference ↓	(Maki et al., 2009)
GTE	870 mg/day / 8 weeks / avg. body mass index = 37 kg/m2 in adult M (n = 5) & F (n = 17)	Body weight ↓, body mass index ↓, body fat percentage -, waist circumference -	(Basu et al., 2010)
GTE	202.9 mg/day / 12 weeks / overweight Japanese M (n = 38) aged 24-46y	Body weight ↓, body mass index ↓, body fat percentage ↓, waist circumference ↓	(Nagao et al., 2005)
GTE	655.1 mg/day / 12 weeks / healthy Japanese adults, 25-55y, body mass index 24–30 kg/m2 (n = 270)	Body weight ↓, body mass index ↓, body fat percentage ↓, waist circumference ↓	(Nagao et al., 2007)
GTE	665.9 mg/day / 12 weeks / healthy Japanese adults, body mass index 22.5–30 kg/m2 aged 20-65y, M (n = 98) & F (n = 97)	Body weight ↓, body mass index ↓, waist circumference ↓	(Kajimoto et al., 2005)
EGCG	300 mg/day / 12 weeks / post-menopausal W (n = 42), FSH ≥ 25 IU/L, aged 45–70y, body mass index = 25–39.9 kg/m2	Body weight -, body mass index—body fat percentage -, waist circumference -	(Hill et al., 2007)
EGCG	856.8 mg/day / 12 weeks / Taiwanese W, body mass index ≥ 27 kg/m2, aged 20-60y (n = 92)	Body weight ↓, body mass index ↓, waist circumference -	(Erba et al., 2005)

This table depicts the results regarding the changes in body weight, BMI, body fat percentage, and waist circumference among various cohorts following the administration of GTE and EGCG, components of GTE

In this study, comparisons were made between the GTE group and the placebo group

* (—Not significant, ↓ Decrease)

Body mass index

To assess the potential impact of GTE on body fat reduction in humans, the second indicator we investigated was BMI. Reviewed studies involving various study populations showed a general decrease in BMI when GTE or EGCG was administered (Table 3). However, significant BMI changes were not observed in studies where 1200 mg/day of GTE was administered to 100 obese women aged 16–60 years or where 300 mg/day of EGCG was administered to 42 postmenopausal women for 12 weeks (Hill et al., 2007; Hsu et al., 2008). Furthermore, in a study involving 42 women aged 25–40 years diagnosed with polycystic ovary syndrome and receiving 540 mg/day of GTE for 3 months, while the placebo group showed a significant increase in BMI, a slight decrease in BMI was observed in the GTE group (Chan et al., 2006). Except for these, all other study results indicated a clear decrease in BMI. Particularly, in a study where 100mg/day of GTE was administered for 12 weeks to 18 men aged 40–60 years and 42 postmenopausal women, the BMI of the GTE group decreased by approximately 7%, while the placebo group maintained their BMI (Auvichayapat et al., 2008). Additionally, in a study involving 270 healthy Japanese adults aged 25–55 years with a BMI of 24–30 kg/m², consuming 655.1mg/day of GTE for 12 weeks resulted in a BMI decrease of 0.7 kg/m² in the GTE group compared to a decrease of 0.1 kg/m² in the placebo group. This indicates that the BMI reduction in the GTE group was approximately six times greater than that in the placebo group (Nagao et al., 2007). Furthermore, in another study involving 98 men and 97 women aged 20–65 years with a BMI of 22.5–30 kg/m², consuming 665.9 mg/day of GTE for 12 weeks resulted in a decrease in BMI from 25.7 kg/m² to 25.5 kg/m² in the GTE group, while the placebo group showed an increase from 25.7 kg/m² to 25.9 kg/m². Overall, these results demonstrate a generally consistent pattern, suggesting that GTE has a positive effect on reducing BMI in humans.

Body fat percentage

Additionally, to assess the potential impact of GTE on fat reduction in humans, the third set of research findings regarding changes in body fat percentage was examined. In the reviewed studies involving diverse study populations, a general decrease in body fat percentage was observed when GTE or EGCG was administered (Table 3). However, in a study where 870 mg/day of GTE was administered to 5 adult males and 17 females with an average BMI of 37 kg/m² for 8 weeks, a decrease in body fat percentage was observed but did not reach statistical significance. Except for two studies that showed similar results, all other study results demonstrated a clear decrease in body fat percentage (Basu et al., 2010; Hill et al., 2007; Hsu et al., 2008). Specifically, in a study targeting 42 individuals with an average BMI of 25 kg/m² or higher in males aged 40–60 years and postmenopausal females for 12 weeks with a dosage of 100 mg/day of GTE, the body fat percentage in the GTE group decreased to 32.25% after the 12-week treatment period, while the placebo group maintained a body fat percentage of 36.92%. This indicates that the GTE group had approximately a 13% lower body fat percentage compared to the placebo group (Auvichayapat et al., 2008). Moreover, in a study involving 128 individuals aged 21–65 years with abdominal obesity, a TC level of 5.2 mmol/L or higher, and a BMI of 25–40 kg/m², those who received 625 mg/day of GTE for 12 weeks experienced a decrease in body fat percentage by 5.2 kg, while the placebo group showed a decrease of 3.5 kg. This suggests that the body fat percentage in the GTE group decreased by 49% more compared to the placebo group (Maki et al., 2009). Overall, these results demonstrate a generally consistent pattern regarding human body fat percentage, indicating a positive effect of GTE on reducing body fat percentage in humans.

Waist circumference

Finally, to evaluate the potential impact of GTE on fat reduction in humans, changes in waist circumference were investigated. Across various studies involving diverse populations, a consistent trend of decreased waist circumference was observed with the administration of GTE or EGCG (Table 3). However, in an 8 week study administering 870 mg/day of GTE to adult males and females with a total of 5 males and 17 females, and a 12 week study administering 856.8 mg/day of EGCG to Taiwanese women aged 20–60 years with a BMI greater than or equal to 27 kg/m², reductions in waist circumference were noted but did not reach statistical significance (Basu et al., 2010; Erba et al., 2005). Except for these two studies, significant reductions in waist circumference were observed across all other study results (Hill et al., 2007; Hsu et al., 2008). Specifically, in a study administering 665.9 mg/day of GTE to 98 males and 97 females aged 20–65 years with a BMI of 22.5–30 kg/m², the group receiving EGCG experienced a 2.7 cm reduction in waist circumference compared to a 2.15 cm reduction in the placebo group, indicating approximately 26% lower waist circumference in the EGCG group (Kajimoto et al., 2005). Furthermore, in a study administering 870 mg/day of GTE to adult males and females with a total of 5 males and 17 females with an average BMI of 37 kg/m², the GTE group exhibited a significant decrease in waist circumference compared to the placebo group. Additionally, within the same study, the total abdominal fat area decreased by 7.7 kg in the GTE group compared to 0.3 kg in the placebo group, indicating approximately 26 times greater reduction in the GTE group. Moreover, subcutaneous fat area decreased by 6.2 kg in the GTE group while increasing by 0.8 kg in the placebo group, and intra-abdominal fat area decreased by 8.87 kg in the GTE group compared to 1.4 kg in the placebo group (Maki et al., 2009). In these various research findings, consistent reductions in weight, BMI, fat percentage, and waist circumference are observed, along with decreases in total abdominal, subcutaneous, and intra-abdominal fat area. Overall, this indicates a positive effect of GTE on weight, BMI, fat percentage, and waist circumference reduction in humans, suggesting its potential for reducing body fat.

Lipid profile

A comprehensive examination was conducted to assess the influence of GTE on the lipid profile concerning obesity-related parameters, utilizing TC, TG, LDL, and HDL. Various cohorts, dosages, and study durations were incorporated into the review. The findings generally demonstrated decreases in TC, TG, and LDL levels, accompanied by a modest elevation in HDL levels (Table 4). Regarding TC, while some studies showed non-significant trends in either direction within the reviewed literature, the prevailing pattern in the majority of studies indicated a consistent decrease in TC levels. For example, in a study targeting adult males and females with an average BMI of 37 kg/m² over an 8 week period, administering 870 mg/day of GTE resulted in a 11.4 mg/dL lower TC compared to the placebo group (Basu et al., 2010). Another study focusing on healthy women aged 20–45 years with a BMI of 27.5–28.9 kg/m² over 12 weeks demonstrated a reduction of 11.467 mg/dL in TC for the GTE group compared to a decrease of 1.545 mg/dL in the placebo group, suggesting a nearly sevenfold greater reduction in TC for the GTE group (Ferreira et al., 2017). Additionally, in a study targeting Taiwanese women aged 20–60 years with a BMI greater than or equal to 27 kg/m² over 12 weeks, administering 856.8 mg/day of EGCG resulted in a decrease of 14.9 mg/dL in TC for the EGCG group, while TC increased by 4.4 mg/dL for the placebo group (Chen et al., 2016). Regarding TG, an increasing trend was observed in one study, while a minor decrease was observed in some other studies. Excluding the former, a consistent decrease in TG levels was observed in other reviewed studies. For instance, in a study targeting obese women with a body mass index greater than or equal to 27 kg/m² over 12 weeks, administering 1200 mg/day of GTE resulted in a decrease of 32.6 mg/dL in TG for the GTE group compared to a decrease of 8.6 mg/dL in the placebo group, suggesting an approximately fourfold greater reduction in TG for the GTE group (Hsu et al., 2008). In a study involving 25 patients aged 45–65 years with type 2 diabetes, who were administered a dosage of 400 mg/day of GTE for 12 weeks, the TG levels in the GTE group decreased by 78.7 mg/dL, while those in the placebo group increased by 24.4 mg/dL (Quezada-Fernández et al., 2019). In another study comprising 128 individuals aged 21–65 years with abdominal obesity, TC levels equal to or greater than 5.2 mmol/L, and a BMI ranging from 25 to 40 kg/m², who received a dosage of 625 mg/day of GTE for 12 weeks, the TG decreased by 11.2% compared to baseline in the GTE group, while increasing by 1.9% compared to baseline in the placebo group (Maki et al., 2009). With respect to LDL, a consistent downward trend was observed across the reviewed studies. Particularly noteworthy is a study focusing on obese women with a BMI greater than or equal to 27 kg/m² over a 12-week period. In this study, administering 1200 mg/day of GTE resulted in a decrease of 16.1 mg/dL in LDL for the GTE group compared to a decrease of 5.6 mg/dL in the placebo group, indicating approximately 3 times greater reduction in LDL for the GTE group (Hsu et al., 2008). In another study involving 5 men and 17 women with an average BMI of 37 kg/m² over an 8 week period, who were administered 870 mg/day of GTE, the group receiving GTE exhibited a reduction in LDL levels by 14.7 mg/dL compared to the placebo group (Basu et al., 2010). In a separate investigation comprising 25 patients aged 45–65 years with type 2 diabetes over a 12 week duration, who received a daily dose of 400mg of GTE, the LDL levels decreased by 11 mg/dL in the GTE group, while increasing by 16.3mg/dL in the placebo group (Quezada-Fernández et al., 2019). Furthermore, in a study involving 92 Taiwanese women aged 20–60 years with a BMI greater than or equal to 27 kg/m² over a 12 week period, who were administered 856.8 mg/day of EGCG, the GTE group exhibited a decrease of 12.6 mg/dL in LDL levels, whereas the placebo group showed an increase of 2.3mg/dL (Chen et al., 2016). Concerning HDL, some studies showed an increasing trend. Over a period of 12 weeks, a study targeting 100 obese women aged 16–60 years with a BMI greater than or equal to 27 kg/m² administered 1200 mg/day of GTE. Another study, conducted over a 42-day duration, involved 24 healthy women with an average BMI of 19.1 kg/m² and an average age of 26 years, who received 320 mg/day of GTE. Additionally, a study targeting postmenopausal women aged 45–60 years administered 800 mg/day of GTE over a 4-week period. All three studies reported an increase in HDL levels (Erba et al., 2005; Hsu et al., 2008; Tadayon et al., 2018). However, inconsistent non-significant results were observed in other reviewed studies, indicating the necessity for further investigation into the positive effects of GTE administration on human HDL. The review suggests that, overall, GTE administration tends to reduce human TC, TG, and LDL levels, with only a few insignificant exceptions. However, further investigation is warranted to address the inconsistent findings regarding HDL. These results imply that improving TC, TG, and LDL levels through GTE administration could potentially decrease the risk of cardiovascular diseases associated with obesity and enhance vascular health.

Table 4.

Effects of green tea extract on obesity-related metabolic indicators in humans

Administration	Dose / Duration / Participants	Effects	References
GTE	1200 mg/day / 12 weeks / obese women aged 16–60 y, body mass index ≥ 27 kg/m2 (n = 100)	Lipid profile (TC -, TG↓, LDL↓, HDL↓) / blood glucose↓ / insulin resistance↓ / adipokine (leptin↓, adiponectin↑)	(Hsu et al., 2008)
GTE	100 mg/day / 12 weeks / avg. body mass index ≥ 25 kg/m2 in M aged 40-60y (n = 18) & postmenopausal F ≥ 1y (n = 42)	Adipokine (leptin↓)	(Auvichayapat et al., 2008)
GTE	625 mg/day / 12 weeks / abdominal obesity M and W aged 21-65y, TC ≥ 5.2 mmol/L, body mass index = 25–40 kg/m2 (n = 128)	Lipid profile (TC↓, TG↓, LDL↓, HDL -)	(Maki et al., 2009)
GTE	870 mg/day / 8 weeks / avg. body mass index = 37 kg/m2 in adult M (n = 5) & F (n = 17)	Lipid profile (TC -, TG↑, LDL↓, HDL -) / blood glucose↓ / insulin resistance↑	(Basu et al., 2010)
GTE	202.9 mg/day / 12 weeks / overweight Japanese M (n = 38) aged 24-46y	Lipid profile (TC↓, TG↓, LDL↓, HDL -) / blood glucose↓ / adipokine (leptin -)	(Nagao et al., 2005)
GTE	655.1 mg/day / 12 weeks / healthy Japanese adults, 25-55y, body mass index 24–30 kg/m2 (n = 270)	Lipid profile (TC↓, TG -, LDL↓, HDL -)	(Nagao et al., 2007)
GTE	665.9 mg/day / 12 weeks / healthy Japanese adults, body mass index 22.5–30 kg/m2 aged 20-65y, M (n = 98) & F (n = 97)	Lipid profile (TC↓, TG↓, LDL↓, HDL -)	(Kajimoto et al., 2005)
GTE	400 mg/day / 12weeks / patients with type 2 diabetes, aged 45-65y (n = 25)	Lipid profile (TC↓, TG↓, LDL↓, HDL -) / blood glucose↓	(Quezada-Fernández et al., 2019)
GTE	320 mg/day / 42 days / avg. body mass index = 19.1 kg/m2, avg. aged 26y healthy W (n = 24)	Lipid profile (TC↓, TG -, LDL↓, HDL↑)	(Erba et al., 2005)
GTE	1000 mg/day / 12 weeks / body mass index = 27.5–28.9 kg/m2, HOMA-IR ≥ 3.6, aged 20-45y, healthy W (n = 120)	Lipid profile(TC -, TG -, LDL↓, HDL -) / insulin resistance↓	(Ferreira et al., 2017)
GTE	800 mg/day / 4 weeks / postmenopausal W aged 45-60y	Lipid profile (TC -, TG↓, LDL↓, HDL↑)	(Tadayon et al., 2018)
EGCG	300 mg/day / 12 weeks / post-menopausal W (n = 42), FSH ≥ 25 IU/L, aged 45–70y, body mass index = 25–39.9 kg/m2	Blood glucose↓ / adipokine (leptin↑, adiponectin -)	(Hill et al., 2007)
EGCG	856.8 mg/day / 12weeks / Taiwanese W, body mass index ≥ 27 kg/m2, aged 20-60y (n = 92)	Lipid profile (TC -, TG -, LDL↓, HDL -) / insulin resistance↓, adipokine (leptin -, adiponectin -)	(Chen et al., 2016)

This table depicts the alterations in lipid profiles (TC, TG, LDL, HDL), blood glucose levels, insulin resistance (HOMA-IR), and adiponectin (leptin adiponectin) among different cohorts after the administration of GTE and EGCG, both components of GTE

In this study, a comparison was conducted between the GTE group and the placebo group

^* (—Not significant, ↓ Decrease, ↑ Increase)

Insulin resistance & Blood glucose

The influence of GTE on insulin resistance and consequent changes in blood glucose levels, evaluated through HOMA-IR, a metabolic indicator associated with obesity, has been examined across multiple studies (Table 4). Among the reviewed studies, only one trial administering 870 mg/day of GTE to a cohort consisting of 5 adult males and 17 females with an average BMI of 37 kg/m² over an 8-week duration reported a slight increase in insulin resistance. Conversely, all other scrutinized studies indicated a decrease in insulin resistance (Basu et al., 2010). For instance, a study encompassing 100 obese women aged 16–60 years with a BMI equal to or exceeding 27 kg/m² over a 12 week period revealed that the group receiving 1200 mg/day of GTE experienced a reduction of 0.64 in HOMA-IR, while the placebo group exhibited an increase of 0.1 in HOMA-IR (Hsu et al., 2008). Regarding blood glucose levels, a consistent downward trajectory was observed across all reviewed studies. In the aforementioned 12 week trial involving obese women aged 16–60 years with a BMI equal to or exceeding 27 kg/m², the GTE administered group displayed blood glucose levels approximately three-fold lower than the placebo group (Hsu et al., 2008). Similarly, in another trial comprising 25 patients with type 2 diabetes aged 45–65 years over a 12 week period and receiving 400 mg/day of GTE, the GTE group manifested a reduction of 30.5 mg/dL in blood glucose levels, compared to a decrease of 4.5 mg/dL in the placebo group, underscoring a nearly sevenfold difference in blood glucose levels between the two groups (Ferreira et al., 2017). In summation, these collective findings suggest that the administration of GTE yields a favorable effect on diminishing insulin resistance and regulating blood glucose levels. Moreover, the amelioration in insulin resistance and blood glucose levels consequent to GTE administration implies a potential mitigation of diabetes-related complications, such as cardiovascular diseases, hypertension, and an overall enhancement of health.

Adipokine

Research has explored the impact of GTE supplementation on leptin and adiponectin, hormones primarily secreted by adipose tissue and closely linked to obesity, in human subjects (Table 4). Concerning leptin, a study administering 300 mg/day of EGCG to 42 post-menopausal women aged 45–70 years with BMI ranging from 25 to 39.9 kg/m² over a 12 week period revealed a slight increase, although overall, a downward trend was observed with numerous non-significant outcomes (Quezada-Fernández et al., 2019). Significant findings from the studies revealed a decrease in leptin levels. One study included 100 obese women aged 16–60 years with a BMI of 27 kg/m² or higher who were administered 1200 mg/day of GTE over a period of 12 weeks. Another study involved 18 men aged 40–60 years with an average BMI of 25 kg/m² or higher, along with 42 postmenopausal women, who received 100 mg/day of GTE over the same duration (Auvichayapat et al., 2008; Hsu et al., 2008). As for adiponectin, while an increasing trend was observed in the reviewed studies, several non-significant results were also noted. Significant elevation in adiponectin levels was noted in studies involving 100 obese women aged 16–60 years with BMI of 27 kg/m² or higher receiving 1200 mg/day of GTE over 12 weeks, as well as in the study involving 18 men aged 40–60 years with an average BMI of 25 kg/m² or higher and 42 postmenopausal women receiving 100 mg/day of GTE over the same duration (Hsu et al., 2008). In summary, studies on the effects of GTE intake on leptin and adiponectin in humans have shown diverse outcomes, indicating a need for further investigation and review due to the limited reported data. Additionally, it is deemed imperative to conduct additional research to clearly establish the potential positive effects and health benefits, such as appetite regulation, body fat regulation, energy expenditure promotion, insulin sensitivity enhancement, and metabolic activity stimulation, induced by the improvement of leptin and adiponectin.

Mechanism of fat reduction by green tea extract

GTE contributes to reducing body fat and managing obesity through multiple mechanisms. The various compounds in GTE, particularly polyphenols and catechins such as EGCG, regulate the activity of key transcription factors involved in adipocyte differentiation, such as CCAAT/enhancer binding protein (C/EBP) and peroxisome proliferator activated receptor γ (PPARγ), as well as genes and enzymes involved in fatty acid and lipid synthesis (Yang et al., 2016; Im et al., 2022). Specifically, GTE affects the protein kinase B (AKT) pathway, a critical protein in regulating cell survival, growth, and metabolism, and the glycogen synthase kinase-3β (GSK-3β) pathway, an important regulatory protein in cell cycle, signaling, differentiation, insulin signaling, and metabolic processes, during the cell growth and preparation (G1 phase) and DNA synthesis and replication (S phase) of the cell cycle. These pathways help inhibit the expression of C/EBP and PPAR γ, thereby reducing fat accumulation (Pan et al., 2016). The involvement of GTE in the activity of transcription factors, genes, and enzymes-related to adipocyte differentiation regulates the cell cycle, affecting the size and number of adipocytes, lipid metabolism within the cells, and the stages of lipid production. This inhibition of differentiation from pre-adipocytes to mature adipocytes reduces the creation of new fat cells (Wolfram et al., 2006; Yang et al., 2016; Im et al., 2022). Additionally, GTE inhibits digestive enzymes that break down fats and proteins in the intestine, thus decreasing the absorption of lipids and proteins, which leads to reduced calorie intake and contributes to body fat reduction (Pan et al., 2016; Yang et al., 2016). Furthermore, GTE influences AMP-activated protein kinase (AMPK), a major protein in regulating cellular energy metabolism in the liver, muscles, and adipose tissue. AMPK is activated through phosphorylation of Thr172, and it plays a role in reducing fat synthesis by inhibiting fatty acid production and decreasing fat accumulation (Yang et al., 2016). AMPK also detects low energy states, promoting the breakdown of fatty acids and glucose to activate energy production processes, enhancing mitochondrial function, and increasing oxidative energy production, which in turn stimulates fat breakdown (Yang et al., 2016; Im et al., 2022). Additionally, studies have shown that thermal processing of GTE can increase the concentration of catechins, which can lower visceral fat, TG levels in the liver and serum, and reduce the activity of enzymes involved in fatty acid synthesis (Yang et al., 2016). These findings suggest that GTE, through its regulation of key transcription factors (C/EBP, PPAR γ), genes, and enzyme activities, inhibits the formation and growth of adipocytes. It also activates AMPK, regulating lipid metabolism and enhancing mitochondrial function within adipocytes, thereby promoting metabolic processes and contributing to weight loss and the alleviation of metabolic syndrome.

Side effects of green tea extract

This review comprehensively analyzed various research findings to assess the diverse side effects resulting from GTE administration (Table 5). Notably, the majority of studies investigating the effects of GTE on humans did not report significant adverse effects. Specifically, studies administering 100 mg/day of GTE to 18 men aged 40–60 years and 42 postmenopausal women, as well as studies administering 202.9 mg/day of GTE to 38 overweight Japanese men and 665.9 mg/day of GTE to 98 men and 97 women with a BMI of 22.5–30 kg/m², reported GTE administration as safe (Kajimoto et al., 2005; Nagao et al., 2005; Auvichayapat et al., 2008). Moreover, in a study administering 200 mg/day of GTE to 100 obese women, mild abdominal pain was reported in some participants, while gas formation, heartburn, and insomnia were reported in a study administering 390 mg/day of EGCG to women with a BMI of 18.5–30 over 6 months. Additionally, headaches, fatigue, mild diarrhea, and insomnia were reported in a study administering 201.4 mg/day of EGCG to lung cancer patients over 3 years, and mild increases in blood pressure were observed in a study administering EGCG to 14 healthy men at doses ranging from 270 to 1200 mg/day over 24 h (Bérubé-Parent et al., 2005; Biro et al., 2021; Hsu et al., 2008; Zhao et al., 2019). However, these side effects were reported to be mild and promptly improved upon discontinuation of administration. Noteworthy adverse events reported in some studies include liver dysfunction and acute liver failure in a study administering 720 mg/day of GTE to a previously healthy 44-year-old woman over 6 months, indicating potential liver toxicity and side effects associated with GTE administration. Another study administering 400 mg/day of EGCG to a 16-year-old Hispanic boy for 2 months suggested the risk of hepatotoxicity. Nevertheless, considering the reported hepatotoxicity and liver failure, it is anticipated that further research will be necessary to explore hepatorenal side effects. Therefore, it is advisable to remain cautious regarding these aspects when consuming GTE, highlighting the importance of additional investigations. Overall, considering the generally mild nature of side effects associated with GTE, most individuals can safely consume GTE. However, it is crucial to adhere to recommended dosages, understand individual physiological responses, consider health profiles and concurrent medication regimens, and promptly seek guidance from healthcare professionals if adverse reactions are detected when consuming GTE.

Table 5.

Side effects of green tea extract

Administration	Dose / Duration / Participants	Side effects	References
GTE	720 mg/kg / 6 months / a previously healthy 44y white W	Liver dysfunction and acute liver failure	(Molinari et al., 2006)
GTE	1200 mg/kg / 12 weeks / obese W aged 16-60y, body mass index ≥ 27 kg/m2 (n = 100)	Mild diarrhea and abdominal pain	(Hsu et al., 2008)
GTE	100 mg/day / 12weeks / avg. body mass index ≥ 25 kg/m2 in M aged 40-60y (n = 18) & postmenopausal F ≥ 1y (n = 42)	safe	(Nagao et al., 2005; Auvichayapat et al., 2008)
GTE	202.9 mg/day / 12 weeks / overweight Japanese M (n = 38) aged 24-46y	safe	(Nagao et al., 2005)
GTE	665.9 mg/day / 12 weeks / healthy Japanese adults, body mass index 22.5–30 kg/m2 aged 20-65y, M (n = 98) & F (n = 97)	safe	(Kajimoto et al., 2005)
EGCG	390 mg/day / 6 months / body mass index = 18.5–30 W, aged = 33-49y (n = 25)	Gas(n = 3), heartburn(n = 5), insomnia(n = 2)	(Biro et al., 2021)
EGCG	400 mg/day / 2 months / a 16y Hispanic boy	Hepatotoxicity	(Patel et al., 2013)
EGCG	201.4 mg/day / 3 years / lung cancer patient (n = 83)	Headaches, fatigue, mild diarrhea, and insomnia	(Zhao et al., 2019)
EGCG	270–1200 mg/day / 24 h / body mass index = 20–27, aged = 20-50y, healthy M (n = 14)	Mild increase in blood pressure	(Bérubé-Parent et al., 2005)

This table displays the side effects observed in various participants following the administration of GTE and its component EGCG

Discussion and conclusion

Summary

Obesity presents a significant challenge to global public health, accompanied by numerous health risks. This review evaluates the efficacy and safety of GTE in obesity management, specifically focusing on its effects on body fat reduction in both mouse models and human studies. In mouse models, GTE has demonstrated promising anti-obesity effects. GTE administration tends to decrease or inhibit weight gain, improve lipid profiles by reducing TC, TG and LDL levels, and increase HDL levels. Additionally, GTE positively influences insulin resistance, aids in blood glucose regulation, and beneficially modulates obesity-related hormones such as leptin and adiponectin. Human studies have also evaluated the anti-obesity effects of GTE, showing similar trends. Indicators-related to body fat reduction, such as weight, BMI, body fat percentage, and waist circumference, generally exhibit a tendency to decrease. Furthermore, evaluations of obesity-related markers after GTE administration show significant reductions in TC, TG and LDL levels, although some studies do not reach statistical significance. In contrast, HDL levels typically increase but often do not show statistically significant differences. GTE appears to positively affect insulin resistance in humans, aiding in better blood glucose control. However, the results regarding adipokines are mixed; while leptin shows some positive effects, adiponectin does not consistently yield significant results. In terms of safety, GTE typically demonstrates a favorable safety profile. However, some studies have identified isolated cases of mild symptoms alleviating upon discontinuation of GTE and potential risks of hepatotoxicity.

Limitations

GTE administration in both animal models and human subjects suggests potential for reducing body fat and managing obesity. However, certain human studies have yielded mixed results concerning lipid profiles and adipokines. After GTE administration, evaluations of obesity-related markers have indicated significant decreases in TC, TG, and LDL levels in some studies; however, statistical significance has been inconsistent. Conversely, while HDL levels have shown an increasing trend, they have not consistently achieved statistical significance. Furthermore, leptin has exhibited some positive effects among adipokines, whereas adiponectin has not consistently shown significant results across several studies. The varied outcomes observed in humans following GTE administration underscore the intricate interplay of physiological factors, genetic factors, and environmental influences affecting weight reduction and obesity management. This underscores the necessity for additional research in this field.

Challenges and opportunities

To maximize the efficacy of green tea extract (GTE) in managing obesity and reducing body fat more safely, additional research and support are crucial. Firstly, investigating the physiological mechanisms underlying its effects on obesity management and fat reduction is necessary. Clinical studies comparing the effects of GTE across diverse populations, along with a thorough analysis of potential side effects and risks related to previously reported hepatic toxicity, are essential. Furthermore, extensive research is needed on the sustainability of the effects of obesity management and fat reduction over prolonged use. This includes examining how GTE can contribute to maintaining these positive changes and ensuring safety. Exploring how GTE can be utilized as a supplement to exercise programs in strategies for obesity management and fat reduction also requires further investigation. Lastly, attention should be given to developing personalized approaches that consider individual genetic, physiological, and lifestyle characteristics, as well as environmental factors. Proposing tailored strategies for obesity management, including GTE, and exploring the possibility of holistic treatment approaches that encompass physical, mental, emotional, and social aspects is also recommended.

Declarations

Conflict of interest

On behalf of all authors, the corresponding author states that there is no conflict of interest.