Fructose consumption: potential mechanisms for its effects to increase visceral adiposity and induce dyslipidemia and insulin resistance
Year: 2008
Type: review
Abstract: PURPOSE OF REVIEW: Based on interim results from an ongoing study, we have reported that consumption of a high-fructose diet, but not a high-glucose diet, promotes the development of three of the pathological characteristics associated with metabolic syndrome: visceral adiposity, dyslipidemia, and insulin resistance. From these results and a review of the current literature, we present two potential sequences of events by which fructose consumption may contribute to metabolic syndrome. RECENT FINDINGS: The earliest metabolic perturbation resulting from fructose consumption is postprandial hypertriglyceridemia, which may increase visceral adipose deposition. Visceral adiposity contributes to hepatic triglyceride accumulation, novel protein kinase C activation, and hepatic insulin resistance by increasing the portal delivery of free fatty acids to the liver. With insulin resistance, VLDL production is upregulated and this, along with systemic free fatty acids, increase lipid delivery to muscle. It is also possible that fructose initiates hepatic insulin resistance independently of visceral adiposity and free fatty acid delivery. By providing substrate for hepatic lipogenesis, fructose may result in a direct lipid overload that leads to triglyceride accumulation, novel protein kinase C activation, and hepatic insulin resistance. SUMMARY: Our investigation and future studies of the effects of fructose consumption may help to clarify the sequence of events leading to development of metabolic syndrome.
Source: Current Opinion in Lipidology
Authors: Kimber L Stanhope, Peter J Havel
Institution: University of California, Davis
Language: English
Subfield: Endocrinology, Diabetes and Metabolism
Field: Medicine
Domain: Health Sciences
Open Access status: green
Funders: Office of Dietary Supplements, National Institutes of Health, Office of the President, University of California, National Institute on Aging, National Heart, Lung, and Blood Institute, National Institute of Child Health and Human Development, National Center for Research Resources, Office of Research on Women's Health, National Center for Complementary and Integrative Health, Eunice Kennedy Shriver National Institute of Child Health and Human Development
Awards: G1476214619, G223716007, Effects of 2wk fructose & HFCS consumption on lipid dysregulation & insulin resis, Dietary Fructose: Hormones & TG/Lipoprotein Metabolism, Effects of fish oil and alpha lipoic on the progression of insulin resistance, Stress, socioeconomic status, and obesity, UC Davis Clinical and Translational Science Center, Prevention of Diabetes with Nutritional Supplements, Fatty acid sources of fructose and HFCS-induced postprandial hypertriglyceridemia, G619771439, Effects of Chromium on Progression of Insulin Resistance, Building Interdisciplinary Research Careers in Women's Health at UC Davis, G8156748866
OpenAlex ID: W1967008598