The DOI matches its Crossref record; 24 of the 24 references it cites were found in a registry or an index.
Fructose consumption: potential mechanisms for its effects to increase visceral adiposity and induce dyslipidemia and insulin resistance
Open accessAbstract
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.
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Cites
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Cited by
Stanhope, K. L., Schwarz, J. M., Keim, N. L., Griffen, S. C., Bremer, A. A., Graham, J. L., Hatcher, B., Cox, C. L., Dyachenko, A., Zhang, W., et al. (2009) · Journal of Clinical Investigation · doi:10.1172/jci37385 · Cited by 1,765
Self-citationGepner, Y., Shelef, I., Schwarzfuchs, D., Zelicha, H., Tene, L., Yaskolka Meir, A., Tsaban, G., Cohen, N., Bril, N., Rein, M., et al. (2018) · Circulation · doi:10.1161/circulationaha.117.030501 · Cited by 279
Toward a unifying hypothesis of metabolic syndrome
Bremer, A. A., Mietus-Snyder, M., & Lustig, R. H. (2012) · PEDIATRICS · doi:10.1542/peds.2011-2912 · Cited by 186
Spruss, A., & Bergheim, I. (2009) · The Journal of Nutritional Biochemistry · doi:10.1016/j.jnutbio.2009.05.006 · Cited by 162
Bremer, A. A., Stanhope, K. L., Graham, J. L., Cummings, B. P., Wang, W., Saville, B. R., & Havel, P. J. (2011) · Clinical and Translational Science · doi:10.1111/j.1752-8062.2011.00298.x · Cited by 148
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Metadata
- Authors
- Stanhope, K. L., & Havel, P. J.
- Venue
- Current Opinion in Lipidology
- Published
- 2008-02
- Volume
- 19
- Issue
- 1
- Pages
- 16-24
- ISSN
- 0957-9672 (ISSN-L)
- OpenAlex
- W1967008598
- Cited by
- 269
- References
- 24
- FWCI
- 13.73
- Type
- journal article
- Language
- en
- Open access
- green
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