Effects of Dietary Supplementation with Coriander Seed Powder on Serum Lipid Profile, Glycemic Indices, and Oxidative Stress Biomarkers in Patients with Type 2 Diabetes Mellitus: A Randomized, Double-Blind, Placebo-Controlled Trial

Abstract

This study aimed to investigate the effects of coriander seed supplementation on serum lipid profiles, glycemic indices, and oxidative stress biomarkers in patients with type 2 diabetes mellitus (T2DM). In total, 40 such patients aged 30－60 years were allocated into two groups receiving either coriander seed powder (1,000 mg/d, n=20) or placebo (1,000 mg/d, n=20) for 6 weeks. Serum lipid profile: total cholesterol (TC), high-density lipoprotein cholesterol, low-density lipoprotein cholesterol (LDL-C), and triglycerides (TGs); anthropometric measurements; dietary intake; and biochemical parameters including fasting blood serum (FBS), serum insulin, homeostatic model assessment for insulin resistance (HOMA-IR), and malondialdehyde (MDA); and total antioxidant capacity (TAC) were assessed before and after supplementation. Coriander seed powder markedly reduced the FBS (156.15±23.19 to 130.30±21.15 mg/dL), serum insulin (17.72±0.47 to 17.12±0.76 µU/mL), HOMA-IR (6.82±0.95 to 5.52±0.99), TC (183.85±55.68 to 145.20±31.36 mg/dL), TG (152.50±37.59 to 130.40±27.96 mg/dL), LDL-C (127.35±23.45 to 111.40±25.71 mg/dL), and MDA (1.65±0.15 to 1.49±0.15 nmol/mL). However, the serum TAC significantly increased (1.93±0.12 to 1.97±0.09 mmol/L) (P<0.05). Anthropometric measurements did not differ remarkably between groups. Post-dose significant inter-group differences in FBS, serum insulin, HOMA-IR, TC, TG, LDL-C, MDA, and TAC levels were identified after adjusting for baseline values (P<0.05). This study demonstrated that coriander seed supplementation positively improved glycemic indices, lipid profile, and oxidative stress status in patients with T2DM, suggesting its potential as a useful complementary treatment for managing this condition.

INTRODUCTION

Diabetes mellitus (DM) is a global health challenge (Hossain et al., 2024), with type 2 diabetes mellitus (T2DM) representing a metabolic disorder characterized by hyperglycemia, insulin resistance, and impaired insulin secretion (Lima et al., 2022). In 2021, ∼537 million people were living with diabetes, a figure expected to rise to 643 million by 2030 and 783 million by 2045 (IDF, 2015). Global trends in T2DM-related complications and mortality, highlighting the rising rates in low- and middle-income countries due to factors like obesity and poor lifestyle (Ali et al., 2022). The worldwide T2DM burden has risen dramatically since 1990, with all-age deaths increasing by 203.9% (from 0.238 to 0.7237 million) and disability-adjusted life years (DALYs) surging by 276.7% (from 10.4 to 39.3 million). Projections indicate a continued upward trend, with deaths expected to reach 1.2967 million and DALYs to reach 85.5 million by 2045 (Huang et al., 2025).

The pathogenesis of DM involves multiple interconnected factors, including chronic hyperglycemia, dyslipidemia (Dagnew et al., 2021; Maldonado et al., 2025), and marked disturbances in the oxidant-antioxidant homeostasis (Iacobini et al., 2021; Singh et al., 2024). Excessive production of free radicals (Pérez-Matute et al., 2009; Chandimali et al., 2025) and an impaired antioxidant defense system (Rais et al., 2024) are among the main factors contributing to the etiology of diabetes and could potentially modulate the related complications. Oxidative stress (OS) is a prominent risk factor associated with T2DM pathogenesis (Singh et al., 2022). Oxidative damage occurs due to the production of free radicals beyond the antioxidant capacities of cells with OS, partly affecting the formation of lipid peroxidation products such as malondialdehyde (MDA) (Rains and Jain, 2011). MDA can potentially lead to a risk of insulin resistance and subsequent development of cardiovascular disease (CVD) (Rains and Jain, 2011). Moreover, OS and insulin resistance are associated with elevated concentrations of inflammation-related biomarkers (Andreadi et al., 2022). Therefore, controlling OS might influence hyperlipidemia to better manage T2DM-related complications (Caturano et al., 2025).

Oral hypoglycemic agents could be associated with various side effects; hence, adherence to these treatments is low. Therefore, much attention has been paid recently to natural herbal remedies (IDF, 2021). Herbal remedies can improve glycemic responses (Rajeshwari and Andallu, 2011). Coriander (Coriandrum sativum L.) is one of the most important herbs with healing properties (Mohammed et al., 2017). It has been widely used as a culinary spice and medicinal herb in various traditional systems, including Mediterranean, Middle Eastern, and South Asian folk medicine, particularly for managing metabolic disorders such as diabetes and dyslipidemia. Its long-standing ethnobotanical significance and cultural acceptance make it an ideal candidate for culturally sensitive dietary interventions in populations where it is a staple food (Jabeen et al., 2009; Laribi et al., 2015; Sobhani et al., 2022; Shahrajabian and Sun, 2023).

Coriander seeds are rich in bioactive compounds with strong antioxidant properties, including flavonoids, polyphenols, carotenoids, steroids, tannins, limonene, linalool, α-pinene, β-caryophyllene, and γ-terpene (Paarakh, 2009), of which polyphenols and linalool (coriandol) are primary (Hosseinzadeh et al., 2014). Polyphenols can inhibit OS by suppressing free radicals and coriandol levels by enhancing the efficiency of the antioxidant defense system (Hosseinzadeh et al., 2014). Recent animal model studies indicated the beneficial effects of coriander seeds on glycemic indices (Aissaoui et al., 2011), lipid profile (Dhanapakiam et al., 2008; Aissaoui et al., 2011; Joshi et al., 2012; Hosseinzadeh et al., 2014), and OS (Deepa and Anuradha, 2011; Joshi et al., 2012; Msaada et al., 2017). Only one clinical trial on the influence of coriander seeds on T2DM has been conducted (Parsaeyan, 2012). Thus, the number of studies regarding the impacts of coriander seeds on DM in humans is limited. In particular, no data exist to reveal the ameliorating effects of these seeds on OS in T2DM patients. Thus, this clinical trial was planned to study the effects of coriander seed powder supplementation on serum glycemic indices, lipid profile, and OS parameters in T2DM patients.

MATERIALS AND METHODS

Subjects

This randomized, double-blind, placebo-controlled trial was conducted at the Diabetes Clinic of Sina Hospital, managed by the Tabriz University of Medical Sciences, Tabriz, Iran. The inclusion criteria were: males and females, aged 30－60 years, having T2DM for >3 years, and willing to participate. The exclusion criteria were: smokers; pregnant or breastfeeding females; those with thyroid, liver, digestive, kidney, or immune system dysfunctions; CVD; uncontrolled T2DM; and/or insulin-dependent diabetes patients using non-steroidal anti-inflammatory drugs, hormone therapy, and antioxidant supplements during the last three months before the study.

The study protocol was approved by the Ethics Committee of the Tabriz University of Medical Sciences (No. IR.TBZMED.REC.1398.677) and registered on the Iranian Registry of Clinical Trials website (IRCT20190224042821N2). Before recruitment, all subjects were fully informed about the study, and written consent was obtained from each. The sample size was calculated based on the fasting blood serum (FBS) results following a protocol reported by Parsaeyan (2012). Considering a confidence level of 95% and power of 80%, calculations required the inclusion of 18 subjects in each group; but accounting for the likelihood of dropout (20%), 22 subjects were recruited in each group (total sample size: 44).

Study design and measurements

Diabetic patients referred to the Sina Diabetes Clinic, with a medical record at this center, and eligible for inclusion were informed about the study. Individuals willing to participate were divided into case and placebo groups based on the numbers inserted on their case (couple and individual). Of the 44 patients who met the inclusion criteria, four patients were lost due to dissatisfaction during follow-up (Fig. 1). Finally, 20 controls and 20 cases in each group who completed the interventions were included to conduct the statistical analysis. First, coriander seeds were washed, air-dried at room temperature (25°C), and then ground into a fine powder using a Model SL-2023 electric mill (Silver Crest) with a mesh size of 0.5 mm to ensure particle uniformity, which was packed in 500 mg gelatin capsules. To prepare the placebo, cornstarch was filled into 500 mg capsules using a capsule filler under aseptic conditions and sterilized with 70% ethanol to prevent secondary contamination. The capsules were quality checked and cleaned with sterile cotton.

Fig. 1.

Study flow diagram.

The researchers were blinded to the intervention or placebo group allocation; the coriander seed powder and placebo capsules appeared similar. Therefore, neither the participants nor the researchers were aware of the therapeutic assignments (double-blinded). To control for the potential confounding effects of diabetes medications on glycemic and lipid parameters, the patients were asked not to alter the type, dosage, and frequency of their medication (metformin or glibenclamide) and their physical activity routine during the study period. They were asked to take the capsules twice daily, 30 min before lunch and dinner, for 6 weeks. The adherence to capsule intake guidelines was assessed via telephonic interview once a week. At the end of the study (6th week), patients were re-examined. Furthermore, the baselines of diabetic medication use in the two groups were compared to confirm successful randomization and ensure that no significant differences existed at the study outset (Table 1).

Table 1.

General characteristics, medications, and physical activity levels of the study participants

Variable	Placebo group (n=20)	Coriander seed group (n=20)	P-value1)
Age (years)	47.60±8.70	50.00±7.48	0.329
Diabetes duration (years)	3.38±2.29	3.64±1.57	0.432
Sex			0.752
Male	9 (45.0)	10 (50.0)
Female	11 (55.0)	10 (50.0)
Education			>0.999
Primary	6 (30.0)	5 (25.0)
Under diploma	4 (20.0)	3 (15.0)
Diploma	9 (45.0)	10 (50.0)
Higher education	1 (5.0)	2 (10.0)
Physical activity level			0.255
Low	13 (65.0)	14 (70.0)
Moderate	7 (35.0)	6 (30.0)
High	0 (0.0)	0 (0.0)
Glibenclamide (5 mg)			0.749
Not used	11 (55.0)	12 (60.0)
Using≥1/d	9 (45.0)	8 (40.0)
Metformin (500 mg)			0.519
1 tablet/d	13 (65.0)	11 (55.0)
2－3 tablet/d	7 (35.0)	9 (45.0)

Values are presented as mean±standard deviation or number (%).

P<0.05 was considered significant.

¹⁾P-values indicate comparison between groups (chi-squared test, independent sample t-test, or Mann-Whitney U-test, as appropriate).

Anthropometric assessments

At the beginning of the trial, patient demographic characteristics were noted, and they were asked to complete the International Physical Activity Questionnaire (IPAQ) to assess their physical activity levels (Moghaddam et al., 2012). Based on its standard guidelines, the short-form IPAQ evaluates weekly metabolic equivalent (MET-min/week) across four domains: vigorous, moderate, walking, and sitting. Participants were categorized into low (<600 MET-min/week), moderate (600－3,000 MET-min/week), or high (>3,000 MET-min/week) activity groups. Furthermore, anthropometric measurements were performed at both the beginning and end of the trial. They included weight, height, and waist-hip circumference (WC-HC), which were ascertained using the calibrated Seca scale, stadiometer, and non-stretch tape instruments. The body mass index (BMI) was classified per the World Health Organization criteria: underweight <18.5, normal 18.5－ 24.9, overweight 25－29.9, and obese ≥30; abdominal obesity was defined as WC ≥102 cm for males or ≥88 cm for females. The body weight (BW) was measured to the nearest 0.5 kg using a Seca scale, with patients being barefoot and wearing light clothing. The height was also determined with a mounted tape, with the participant’s arms hanging freely by the sides, and recorded to the nearest 0.5 cm. BMI was calculated by dividing the weight (kg) by the square of the height (m). WC was obtained employing an inelastic tape measure to the nearest 1 mm. The length of the midpoint between the last rib and the iliac crest was recorded as the WC. HC was measured at the widest point of the hip. The waist-hip ratio (WHR) was calculated.

Nutritional assessments

Information regarding dietary intake was gathered for 3 days (including 2 working days and 1 weekend) a week before and at the end of supplementation using a 24-hour recall method. Total energy and the intake of macronutrients and antioxidant vitamins were determined with the Nutritionist IV software program (First Databank Inc., Hearst Corp.). The dietary intake of vitamins C and E was assessed, as they are considered key representative vitamins with antioxidant activity due to their established role in OS and a feasible, accurate estimation method employing the available food composition databases. Dietary antioxidant intake was quantified based on an analysis of the 3-day food records (two food diaries+one 24-hour recall) using the Nutritionist IV software. The USDA/Iranian food composition databases for antioxidant-rich foods (citrus, pomegranate, spinach, and nuts) served as the reference.

Laboratory assessments

At the beginning and at the end of the trial period, 5 mL of blood was sampled from each patient after an overnight (12 h) fast. All serum samples were stored at −70°C until use. FBS, serum total cholesterol (TC), triglycerides (TGs), and high-density lipoprotein cholesterol (HDL-C) were measured using the standard enzymatic colorimetric method on a BS-200 Full Auto Chemistry Analyzer (Mindray) and the Pars-Azmoon Diagnostic Kits (Shokouh Pars Azmoon Co.). The formula devised by Friedewald et al. (1972) was used to ascertain the low-density lipoprotein cholesterol (LDL-C) levels. Serum insulin concentration was determined with an ELISA kit (DiaMetra Srl, Bioassay Technology Laboratory). The homeostatic model assessment for insulin resistance (HOMA-IR), based on the formula: HOMA-IR=fasting insulin (µU/mL)×fasting glucose (mg/dL)/405 (Antuna-Puente et al., 2008), was applied to measure insulin resistance. The serum MDA concentration was determined via the thiobarbituric acid reactive substances method (Bilici et al., 2001). Total antioxidant capacity (TAC) was measured utilizing the spectrophotometry method with a Randox kit (Randox Laboratories, Ltd.).

Statistical analysis

Data were analyzed by the SPSS software version 21.0 (IBM Corp.). The Kolmogorov-Smirnov test was used to check the data normality. Quantitative and qualitative data were reported as the mean±standard deviation and frequency (%), respectively. The differences between variables before and after treatment were compared by a paired t-test. Inter-group comparisons were made employing either a chi-squared, independent sample t-test, or Mann-Whitney U-test, as appropriate. Analysis of covariance (ANCOVA) was used to identify any inter-group differences at the end of the study, after adjusting for baseline values. An ANCOVA was also performed on all outcome measures, after adjusting for baseline values to control the effects of potential confounders and the use of diabetic medications (coded as a binary or categorical variable based on type and dosage) to isolate the influences of coriander seed supplementation from those of the concomitant pharmacotherapy. A P<0.05 was considered statistically significant.

RESULTS

Finally, 40 T2DM patients (20 per group) completed this double-blind trial without any adverse events. The baseline characteristics of age (47.60±8.70 years vs. 50.00±7.48 years, P=0.329), sex distribution (45% vs. 50% male, P=0.752), diabetes duration (3.38±2.29 years vs. 3.64±1.57 years, P=0.432), or medication use (e.g., 65% vs. 55% with metformin, P=0.519) did not differ significantly between groups, confirming successful randomization (Table 1). Table 2 presents the anthropometric measurements that were made throughout the study. After 6 weeks of intervention, no marked changes were observed in the BW, BMI, WC, or WHR in either group (P>0.05). For example, weight changes were 0.02±0.54 kg in the placebo and −0.27±0.89 kg in the coriander groups (P=0.532). According to Table 3, daily intake of energy, macronutrients (carbohydrates, proteins, and fats), as well as vitamins C and E, stabilized in both groups throughout the study (all P>0.05). For instance, vitamin E intake in the placebo group changed from 3.85±1.81 mg/d at baseline to 3.50±2.10 mg/d at the endpoint (P=0.685), while in the coriander group it altered from 3.60±1.94 to 3.80±2.20 mg/d (P=0.786).

Table 2.

Anthropometric measurements of the subjects at baseline and after 6 weeks of coriander seed powder supplementation

Variable	Placebo group (n=20)	Coriander seed group (n=20)	P-value
Weight (kg)
Baseline	74.05±12.18	73.51±12.35	0.8881)
After 6 weeks	74.05±12.59	73.26±12.56	0.6362)
MD (95% CI)	0.02 (—0.52, 0.56)	—0.27 (—1.16, 0.61)
P-value3)	0.920	0.532
BMI (kg/m2)
Baseline	31.25±5.07	30.88±5.17	0.7971)
After 6 weeks	31.26±5.24	30.76±5.25	0.6282)
MD (95% CI)	0.01(—0.22, 0.24)	—0.11 (—0.52, 0.26)
P-value3)	0.995	0.523
WC (cm)
Baseline	97.20±12.19	96.78±11.22	0.8971)
After 6 weeks	97.01±9.76	96.35±10.68	0.8552)
MD (95% CI)	—0.19 (—1.47, 1.07)	—0.43 (—1.93, 1.07)
P-value3)	0.760	0.560
WHR
Baseline	0.90±0.06	0.89±0.06	0.7781)
After 6 weeks	0.90±0.06	0.89±0.06	0.8482)
MD (95% CI)	0.01 (—0.01, 0.02)	0.00 (—0.02, 0.01)
P-value3)	0.941	0.894

Values are presented as mean±standard deviation.

P<0.05 was considered significant.

¹⁾P-values indicate comparison between groups (independent sample t-test at baseline).

²⁾P-values indicate comparison between groups (and analysis of covariance test, adjusted for baseline values, after 6 weeks).

³⁾P-values indicate comparison within groups (paired t-test).

BMI, body mass index; WC, waist circumference; WHR, waist to hip ratio; MD, mean difference; CI, confidence interval.

Table 3.

Dietary intake of the study subjects at baseline and after 6 weeks of coriander seed powder supplementation

Variable	Placebo group (n=20)	Coriander seed group (n=20)	P-value
Energy (kcal/d)
Baseline	1,949.73±68.39	1,955.50±96.14	0.8201)
After 6 weeks	1,961.58±90.02	1,961.58±90.02	0.5312)
MD (95% CI)	11.85 (—24.83, 48.53)	6.08 (—36.65, 48.81)
P-value3)	0.818	0.553
Carbohydrate (g/d)
Baseline	275.70±17.78	277.50±17.59	0.8221)
After 6 weeks	276.65±19.38	276.40±17.96	0.7432)
MD (95% CI)	0.95 (—7.58, 9.48)	—1.10 (—9.26, 7.06)
P-value3)	0.490	0.753
Protein (g)
Baseline	81.42±11.31	78.35±11.45	0.8661)
After 6 weeks	81.40±9.32	78.00±8.03	0.7552)
MD (95% CI)	—0.02 (—4.77, 4.73)	—0.35 (—4.89, 7.06)
P-value3)	0.533	0.633
Fat (g)
Baseline	63.91±5.85	63.80±6.35	0.3261)
After 6 weeks	63.12±5.78	63.60±6.36	0.7552)
MD (95% CI)	—0.79 (—3.46,1.88)	—0.20 (—3.12, 2.72)
P-value3)	0.125	0.855
Vitamin E (mg/d)
Baseline	3.85±1.81	3.60±1.94	0.5881)
After 6 weeks	3.50±2.10	3.80±2.20	0.3462)
MD (95% CI)	—0.35 (—1.25, 0.55)	0.20 (—0.75, 1.15)
P-value3)	0.685	0.786
Vitamin C (mg/d)
Baseline	121.17±68.45	113.67±70.54	0.7351)
After 6 weeks	112.36±65.00	119.13±45.43	0.5322)
MD (95% CI)	—8.81 (—39.44, 21.82)	5.46 (—21.76, 32.68)
P-value3)	0.402	0.943

Values are presented as mean±standard deviation.

P<0.05 was considered significant.

¹⁾P-values indicate comparison between groups (independent sample t-test at baseline).

²⁾P-values indicate comparison between groups (and analysis of covariance test, adjusted for baseline values, after 6 weeks).

³⁾P-values indicate comparison within groups (paired t-test).

MD, mean difference; CI, confidence interval.

The key metabolic outcomes revealed marked improvements in the coriander group compared to the placebo: FBS decreased by 25.85 mg/dL (P<0.001), insulin by 0.60 µU/mL (P=0.003), and HOMA-IR by 1.30 units (P<0.001; Table 4). Lipid profile modifications included reductions in the levels of TC (−38.65 mg/dL), TG (−22.10 mg/dL), and LDL-C (−15.95 mg/dL) (P<0.001). The coriander group also exhibited an enhanced antioxidant capacity, indicated by a TAC increase of 0.04 mmol/L (P<0.001) and reduced OS, suggested by a decrease in the MDA contents of 0.15 nmol/mL (P<0.001). In contrast, the placebo group exhibited only a small but statistically significant enhancement in TC by 5.85 mg/dL (P=0.042). Moreover, clinically meaningful improvements in critical metabolic parameters: FBS reduction of 25.85 mg/dL (∼16% decrease), approached the 30 mg/dL threshold, suggesting meaningful diabetes management. The 9% reduction in MDA exceeded the 5% threshold linked to improved endothelial function in T2DM. The observed reduction in FBS at 25.85 mg/dL (∼16%) represents a clinically significant improvement, consistent with the American Diabetes Association’s recommendations on achieving glycemic targets that reduce the risk of diabetes-associated complications (American Diabetes Association Professional Practice Committee, 2024). Moreover, an LDL-C reduction by 16.0 mg/dL aligned with the 15－20 mg/dL target set for dietary interventions in CVD prevention (Jacobson et al., 2015). All inter-group variations were statistically significant (P<0.001) for glycemic, lipid, and OS parameters after adjustment for baseline values and potential confounders (age, sex, medications, and physical activity) using ANCOVA.

Table 4.

Serum glycemic indices, lipid profiles, and oxidative stress-indicative parameters of the study subjects at baseline and after 6 weeks of coriander seed powder supplementation

Variable	Placebo group (n=20)	Coriander seed group (n=20)	P-value
FBS (mg/dL)
Baseline	161.15±25.17	156.15±23.19	0.5171)
After 6 weeks	160.85±26.01	130.30±21.15	<0.0012)
MD (95% CI)	—0.30 (—1.83, 1.23)	—25.85 (—32.63, —19.07)
P-value3)	0.685	<0.001
Insulin (µU/mL)
Baseline	17.80±0.50	17.72±0.47	0.6281)
After 6 weeks	17.92±0.63	17.12±0.76	0.0012)
MD (95% CI)	0.12 (—0.27, 0.52)	—0.60 (—0.98, —0.22)
P-value3)	0.514	0.003
HOMA-IR
Baseline	7.08±1.12	6.82±0.95	0.4361)
After 6 weeks	7.13±1.27	5.52±0.99	<0.0012)
MD (95% CI)	0.05 (—0.10, 0.20)	—1.30 (—1.60, —1.01)
P-value3)	0.514	<0.001
TC (mg/dL)
Baseline	155.73±68.39	183.85±55.68	0.1621)
After 6 weeks	161.58±69.02	145.20±31.36	<0.0012)
MD (95% CI)	5.85 (0.24, 11.46)	—38.65 (—58.35, —18.95)
P-value3)	0.042	<0.001
TG (mg/dL)
Baseline	170.70±77.78	152.50±37.59	0.3541)
After 6 weeks	171.65±79.38	130.40±27.96	<0.0012)
MD (95% CI)	0.95 (—4.13, 6.03)	—22.10 (—32.03, —12.17)
P-value3)	0.700	<0.001
LDL-C (mg/dL)
Baseline	133.35±21.31	127.35±23.45	0.4021)
After 6 weeks	133.00±21.03	111.40±25.71	<0.0012)
MD (95% CI)	—0.35 (—1.38, 0.68)	—15.95 (—20.79, —11.11)
P-value3)	0.487	<0.001
HDL-C (mg/dL)
Baseline	33.80±6.35	33.21±5.85	0.7641)
After 6 weeks	33.60±6.36	33.12±5.78	0.7822)
MD (95% CI)	—0.20 (—0.56, 0.16)	—0.10 (—0.36, 0.16)
P-value3)	0.258	0.428
TAC (mmol/L)
Baseline	1.88±0.14	1.93±0.12	0.2101)
After 6 weeks	1.88±0.14	1.97±0.09	<0.0012)
MD (95% CI)	0.001 (—0.003, 0.004)	0.04 (0.02, 0.06)
P-value3)	0.789	<0.001
MDA (nmol/mL)
Baseline	1.67±0.14	1.65±0.15	0.6131)
After 6 weeks	1.68±0.14	1.49±0.15	<0.0012)
MD (95% CI)	0.01 (—0.01, 0.02)	—0.15 (—0.22, —0.09)
P-value3)	0.213	<0.001

Values are presented as mean±standard deviation.

P<0.05 was considered significant.

¹⁾P-values indicate comparison between groups (independent sample t-test at baseline).

²⁾P-values indicate comparison between groups (and analysis of covariance test, adjusted for baseline values, after 6 weeks).

³⁾P-values indicate comparison within groups (paired t-test).

FBS, fasting blood serum; HOMA-IR, homeostatic model assessment for insulin resistance; TC, total cholesterol; TG, triglyceride; LDL-C, low-density lipoprotein cholesterol; HDL-C, high-density lipoprotein cholesterol; TAC, total antioxidant capacity; MDA, malondialdehyde; MD, mean difference; CI, confidence interval.

DISCUSSION

This study prepared coriander seed powder under standardized conditions using an electric mill with a 0.5 mm mesh to ensure a consistent particle size. The powder was administered at a dose of 1,000 mg/d－as two 500 mg capsules taken 30 min before lunch and dinner－for 6 weeks. This protocol was designed based on previous clinical trials conducted by Parsaeyan (2012) and preclinical studies by Aissaoui et al. (2011) that demonstrated the beneficial effects of this dosage and duration on metabolic parameters in diabetic patients (Aissaoui et al., 2011; Parsaeyan, 2012). This dose translates to 14－17 mg/kg BW for a 60－70 kg individual, aligning with the effective ranges reported in diabetic models. The improvements in glycemic control (16% reduction in FBS) and lipid profile (12.5% decrease in LDL-C) observed can be attributed to coriander’s bioactive compounds, including polyphenols (e.g., quercetin and rutin) and linalool, which exert their influence through multiple mechanisms (Laribi et al., 2015; Mahmoud et al., 2022). Findings suggested an acceptable efficacy of coriander seed powder supplementation among the T2DM study population. Our results align with the historical uses of coriander in traditional medicine in regions like the Mediterranean and South Asia, where it has been employed for its metabolic benefits. Such cultural familiarity not only supports the biological plausibility of our results but also underscores the potential for higher adherence and accessibility in communities where coriander is already integrated into the daily diet and health practices (Jabeen et al., 2009; Laribi et al., 2015; Sobhani et al., 2022). Serum glucose levels declined remarkably in the coriander group compared to the baseline measurements and those in the placebo group. In consistency, Aissaoui et al. (2011) indicated significant post-intervention changes with coriander seed supplementation (after a single oral dose, daily for 30 days) in obese hyperlipidemic and hyperglycemic rats. Similar results were also discussed by Parsaeyan (2012) in T2DM patients, indicating the hypoglycemic influence of coriander seeds (2 capsules for 6 weeks). These included a stimulation of glucose utilization by peripheral tissues, especially muscles and adipose tissue, and a modulation of hepatic glucose metabolism through elevated glycogen storage and suppressed gluconeogenesis (Kondeti et al., 2010; Aissaoui et al., 2011; Parsaeyan, 2012). Moreover, a recent study by Jin et al. (2025) indicated that coriander-derived polysaccharides possessed marked hypoglycemic activity by enhancing insulin sensitivity and glucose uptake in the peripheral tissues. Additionally, these compounds demonstrate a potent antioxidant capacity, supporting their role in mitigating OS in diabetes-associated conditions (Jin et al., 2025). Furthermore, inhibiting glucosidase and amylase activities, glucose release, and absorption through the gastrointestinal tract via a suppression of the SGLT1 transporter may also play a role in reducing glycemia (Parsaeyan, 2012). In contrast, Al-Suhaimi (2008) reported no changes in the serum glucose levels after coriander seed administration of healthy, adult male rabbits at 250 mg/kg BW for 7 days. In contrast to the present findings, Nyakudya et al. (2014) suggested increased serum glucose levels after coriander intervention (500 mg/kg BW for 5 weeks), though statistically insignificant. The present results indicated that coriander seed supplementation remarkably decreased the serum insulin levels compared to the baseline and placebo group (Al-Suhaimi, 2008; Nyakudya et al., 2014). A statistically insignificant reduction in serum insulin was also observed post-coriander seed supplementation (Aissaoui et al., 2011). Additionally, insulin resistance improved remarkably in the treatment group compared to the baseline and placebo group. This finding was also in accordance with those of a previous investigation (Aissaoui et al., 2011). Thus, coriander seeds may elevate insulin signaling, thereby reducing insulin resistance via enhancing insulin sensitivity (Aissaoui et al., 2011).

Marked declines in the serum levels of TC, TG, and LDL-C were observed in the intervention group supplemented with coriander seed powder compared to the baseline and placebo group. In line with our findings, previous studies in animal models have also demonstrated a similar result in serum cholesterol after coriander seed administration (Dhanapakiam et al., 2008; Aissaoui et al., 2011; Joshi et al., 2012; Hosseinzadeh et al., 2014). Furthermore, the findings of the clinical trial by Parsaeyan (2012), reporting similar potential effects of coriander seed supplementation in lowering serum cholesterol contents in T2DM patients, support our results. Conversely, another study reported no significant alterations (Al-Suhaimi, 2008), which contrasts with our outcomes. Such a discrepancy may be attributed to several factors: (1) the relatively low dose used (250 mg/kg) compared to effective doses reported in other studies in diabetic animal models (Aissaoui et al., 2011), which were typically 500－1,000 mg/kg; (2) the short intervention duration of 7 days vs. 4－6 weeks in most positive studies; and (3) differences in the metabolic status of healthy animals vs. diabetic/hyperlipidemic models. Our study employed a dose of 1,000 mg/d in human subjects (14－17 mg/kg BW for a 60－70 kg individual), which aligned with the effective doses employed in previous clinical trials (Parsaeyan, 2012). Cholesterol-lowering mechanisms of coriander seed powder are presumably attributable to a suppression in cholesterol biosynthesis, particularly by inhibiting β-hydroxy β-methylglutaryl-CoA reductase (a key enzyme of the cholesterol biosynthesis pathway), increasing the degradation of cholesterol into fecal bile acids, and enhancing lecithin-cholesterol acyl transferase activity (Joshi et al., 2012; Parsaeyan, 2012). Additionally, flavonoids and polyphenols present in coriander seeds may be responsible for their hypolipidemic and hypoglycemic effects (Parsaeyan, 2012). A decrease in serum LDL-C can also be due to suppressed LDL biosynthesis or elevated LDL metabolism (Joshi et al., 2012). Moreover, such a reduction in serum TG levels may be due to a stimulation of TG degradation through increased lipoprotein lipase expression and activity, as well as decreased TG synthesis and its secretion (Joshi et al., 2012). However, inconsistent with our results, Al-Suhaimi (2008) revealed no decline in serum cholesterol levels in healthy male rabbits after intervention. Such a lack of cholesterol reduction might be attributed to the low dose of coriander seeds used. In our study, the changes in serum HDL-C levels were insignificant compared to the baseline and the placebo group. These findings were in line with a study of Parsaeyan (2012), who reported no significant changes in serum HDL-C after coriander seed supplementation. Our study was not similar to Dhanapakiam et al. (2008), who proved that HDL-C contents elevated after coriander seed consumption, probably due to a reduction in the tissue cholesterol and directing it to the liver by HDL-C (Dhanapakiam et al., 2008). Additionally, Aissaoui et al. (2011) indicated that coriander seeds decreased serum HDL-C markedly, which was probably due to large changes in blood cholesterol levels.

Lipid peroxidation can produce various compounds, including MDA, the most important toxin. The plasma concentrations of MDA were elevated markedly in patients with DM (Černe and Lukač-Bajalo, 2006; Braxas et al., 2019). To the best of our knowledge, the present study is the first research to assess the impacts of coriander seed supplementation on T2DM. In this study, coriander seeds remarkably increased serum TAC and decreased serum MDA levels compared to the baseline and the placebo group. Animal studies showed the role of coriander seeds in scavenging superoxide anion and hydroxyl radicals (Deepa and Anuradha, 2011; Joshi et al., 2012; Msaada et al., 2017). This observation indicates that coriander seed powder might interact with peroxyl radicals, modulating their accumulation and acting as a chain-breaking antioxidant against lipid peroxidation (Deepa and Anuradha, 2011). The active components of coriander seed can participate as electron donors, which can react with free radicals to generate their stable forms and thereby terminate the chain reaction of radicals (Deepa and Anuradha, 2011).

Coriander seed powder supplementation was well tolerated throughout the study period. No adverse events or side effects were reported by any of the intervention group participants. This favorable safety profile was corroborated by a stabilization of the key biochemical indices post-intervention. Furthermore, these findings align with those of animal and human studies, which reported no significant adverse effects following coriander seed consumption (Aissaoui et al., 2011; Parsaeyan, 2012), supporting its potential as a safe complementary approach to T2DM management.

The limitations of the current study were a small number of participants and a short duration of supplementation. Moreover, dietary intake of other antioxidants was not quantitatively assessed due to limitations in the composition data of these compounds in local foods. The strengths of our study were conducting a double-blind, randomized, placebo-controlled design. We evaluated dietary energy and nutrient intake at baseline and at the end of the trial to find any confounders. Coriander seed powder seemed to be well tolerated by participants. In conclusion, the present study demonstrated that coriander seed powder supplementation markedly decreased serum glucose, insulin, insulin resistance, TC, TG, LDL-C, and MDA levels and increased serum TAC levels in T2DM patients. These findings suggest that coriander seed powder can be useful in the management of diabetic patients.