Fructose, weight gain, and the insulin resistance syndrome.

By Sharon S Elliott, N. Keim, J. Stern, K. Teff, P. Havel. American Journal of Clinical Nutrition, 2002

1,126 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Physiology

View Paper: https://www.semanticscholar.org/paper/c2933d7749264677e66716e444efd4d0e36b9bbe

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Citations in the corpus

Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. (2004, methodology): “Peak values of the active form of GLP-1, GLP-1(7-36), after meals did not differ between HFr and HGl days; however, GLP-1(7-36) levels remained elevated for a longer period (up to 120 min) after HFr than after HGl meals (Fig.”
Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. (2007, background): “In 2002, Havel’s group (37) made the case that the fructose content of sugar may be the critical component associated with the risks of obesity and heart disease.”
Sugar-sweetened beverages and risk of obesity and type 2 diabetes: Epidemiologic evidence (2010, background): “Fructose, which is a constituent of both sucrose and HFCS in relatively equal parts is preferentially metabolized to lipid in the liver, leading to increased hepaticdenovo lipogenesis, dyslipidemia and insulin resistance [89–92].”
Dietary fructose: implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism. (2005, background): “The effects of dietary sugars on insulin action in animals and humans have been examined in several recent reviews.(2,70-72) When compared with studies conducted in experimental animals, much more limited data are available concerning the effects of fructose consumption on insulin action in humans.”
Mechanisms (2019, neutral): “in Sf20 – 400 lipoprotein-TG ( mol/L) 3 (3) where multiplication by 3 is used to account for the number of”
Pharmacological actions and potential uses of Momordica charantia: a review. (2004, background): “A fructose rich diet in rats has been shown to induce syndrome X—constituting hyperglycemia associated with hyperinsulinemia, hypertriglyceridemia and obesity ( Elliot et al., 2002).”
Crop domestication in the Compositae: a family-wide trait assessment (2008, background): “Humans however have a limited ability to metabolize fructose and if over-consumed it can potentially have detrimental effects on human health (Fields 1998; Elliott et al. 2002; Basciano et al. 2005).”
INCREASED FRUCTOSE CONSUMPTION IS ASSOCIATED WITH FIBROSIS SEVERITY IN PATIENTS WITH NAFLD (2010, result): “In this regard, our findings reproduce other reports that have linked such metabolic derangements with increased consumption of fructose.(4,5,29-34) Moreover, after controlling for factors that have been shown to influence NAFLD (such as age, sex, BMI, Hispanic ethnicity, and total calorie intake), ”
Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. (2004, background): “A recent review described many facets of this issue (3).”
Honey for Nutrition and Health: A Review (2008, background): “A surplus consumption of fructose in today’s American diet, mainly in the form of high-fructose corn syrup, is suspected to be one of the main causes for overweight problems [55].”
Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. (2008, background): “Several studies have correlated the rise in the incidence of obesity with an increase in sugar consumption (Bray et al., 1992; Elliott et al., 2002; Howard and Wylie-Rosett, 2002; Ludwig et al., 2001).”