Table 1.

Preclinical and clinical studies evaluating fructose consumption on cardiometabolic parameters.

Study	Year	Primary Endpoint	Main Findings
Teff KL et al. [8] Dietary fructose decreases the circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women	2004	Testing whether meals high in fructose (HFr) would result in lower leptin concentrations than meals containing the same amount of glucose (HGl)	Consuming HFr beverages with meals results in lower circulating insulin and leptin concentrations and higher ghrelin and triglyceride levels compared with consumption of HGl beverages
Aeberli I et al. [29] Fructose intake is a predictor of LDL particle size in overweight schoolchildren	2007	To determine whether LDL particle size is associated with fructose intake in normal-weight and overweight children	Greater total and central adiposity are associated with smaller LDL size and lower HDL cholesterol. Additionally, higher fructose intake predicts smaller LDL particle size
Stanhope KL et al. [25] Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans	2009	To assess the relative effects of fructose-sweetened and glucose-sweetened beverages on lipid and glucose metabolism in humans, overweight, and obese subjects	Dietary fructose increases hepatic de novo lipogenesis, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults
Cox CL et al. [26] Consumption of fructose- but not glucose-sweetened beverages for 10 weeks increases circulating concentrations of uric acid, retinol-binding protein-4, and gamma-glutamyl transferase activity in overweight/obese humans	2012	Investigating the relative effects of 10 weeks of fructose or glucose consumption on plasma uric acid, retinol binding protein-4, and liver enzyme activities in men and women	Consumption of fructose, but not glucose, led to significant increases in 24-h uric acid profiles and retinol binding protein-4 concentrations, as well as plasma gamma-glutamyl transferase activity
de Castro UG et al. [11] Age-dependent effect of high-fructose and high-fat diets on lipid metabolism and lipid accumulation in liver and kidney of rats	2013	Evaluating biochemical, physiological, histological, and biometric parameters in rats with a high-fat or high-fructose diet	High-fructose diet caused the most significant change in the metabolism of serum lipids and lipid accumulation in the liver and kidney, while a high-fat diet induced elevation of arterial pressure and heart rate and increased visceral lipid stores
Morenga LA et al. [24] Dietary sugars and cardiometabolic risk: systematic review and meta-analyses of randomized controlled trials of the effects on blood pressure and lipids	2014	Systematic review and meta-analysis of randomized controlled trials that examined effects of the modification of dietary free sugars (mostly fructose) on blood pressure and lipids	Higher intake of sugars is associated with increased concentrations of triglycerides, total and LDL cholesterol, and blood pressure (this last effect was significant in studies of a longer duration only)
Yoo S et al. [21] High dietary fructose intake on cardiovascular disease-related parameters in growing rats	2016	Determining the effects of a high-fructose diet on cardiovascular disease-related parameters in growing rats	High-fructose diet increased total-fat weight and serum triglyceride levels. Negative effects were found in abdominal aortic thickness, as well as endothelial nitric oxide synthase and endothelin-1 mRNA expression
Gungor A et al. [31] The relationship between daily fructose consumption and oxidized low-density lipoprotein and low-density lipoprotein particle size in children with obesity	2021	To investigate the relationship between fructose consumption and obesity and the role of fructose consumption in development of atherosclerosis in obese and healthy children	The overconsumption of fructose in children triggers atherogenic diseases by increasing the levels of small, dense LDL