期刊
CURRENT OPINION IN LIPIDOLOGY
卷 20, 期 5, 页码 379-385出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MOL.0b013e32832fa5c4
关键词
atherosclerosis; insulin resistance; obesity; polyunsaturated fatty acids; saturated fatty acids; Toll-like receptor 4
资金
- National Institutes of Health [NIH-1K99HL096166-01, NIH-P01-HL49373]
- National Center for Complimentary and Alternative Medicine [NCCAM-P50AT002782]
- Intramural Research Program of the National Institutes of Health
- National Institute of Environmental Health Sciences
- NATIONAL CENTER FOR COMPLEMENTARY & ALTERNATIVE MEDICINE [P50AT002782] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL049373, R00HL096166, K99HL096166] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [ZIAES102005] Funding Source: NIH RePORTER
Purpose of review Dietary saturated fatty acids (SFAs) have been implicated in promoting the metabolic syndrome and atherosclerotic cardiovascular disease. Recent evidence suggests that SFAs promote the metabolic syndrome by activating Toll-like receptor 4 (TLR4). Here we examine emerging molecular evidence that SFAs directly engage pathways of innate immunity, thereby promoting inflammatory aspects of the metabolic syndrome. Recent findings Accumulation of SFA in the body is tightly regulated by stearoyl-CoA desaturase 1, an enzyme that converts endogenous SFA to monounsaturated fatty acids. Recent studies have demonstrated that the accumulation of SFA seen with genetic deletion or inhibition of stearoyl-CoA desaturase 1 promotes inflammation, TLR4 hypersensitivity, and accelerated atherosclerosis, Therefore, stearoyl-CoA desaturase 1 may play an unexpected role in suppressing inflammation by preventing excessive accumulation of endogenous SFA-derived TLR4 agonists. In parallel, several independent laboratories have demonstrated that TLR4 is necessary for dietary SFAs to induce obesity, insulin resistance, and vascular inflammation in rodent models. Summary The metabolic syndrome and atherosclerotic cardiovascular disease have long been linked to dietary SFA intake and inflammation. Recent mechanistic insights into how SFAs and downstream metabolites can potentiate inflammation-driven metabolic disease are discussed here.
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