| Decrease in hepatic very-low-density lipoprotein-triglyceride secretion after weight loss is inversely associated with changes in circulating leptin. | |
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MedLine Citation:
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PMID: 20590733 Owner: NLM Status: In-Process |
Abstract/OtherAbstract:
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AIM: Although weight loss usually decreases very-low-density lipoprotein-triglyceride (VLDL-TG) secretion rate, the change in VLDL-TG kinetics is not directly related to the change in body weight. Circulating leptin also declines with weight loss and can affect hepatic lipid metabolism. The aim of this study was to determine whether circulating leptin is associated with weight loss-induced changes in VLDL-TG secretion. METHODS: Ten extremely obese subjects were studied. VLDL-TG secretion rate and the contribution of systemic (derived from lipolysis of subcutaneous adipose tissue TG) and non-systemic fatty acids (derived primarily from lipolysis of intrahepatic and intraperitoneal TG, and de novo lipogenesis) to VLDL-TG production were determined by using stable isotopically labelled tracer methods before and 1 year after gastric bypass surgery. RESULTS: Subjects lost 33 +/- 12% of body weight, and VLDL-TG secretion rate decreased by 46 +/- 23% (p = 0.001), primarily because of a decrease in the secretion of VLDL-TG from non-systemic fatty acids (p = 0.002). Changes in VLDL-TG secretion rates were not significantly related to reductions in body weight, body mass index, plasma palmitate flux, free fatty acid or insulin concentrations. The change in VLDL-TG secretion was inversely correlated with the change in plasma leptin concentration (r = -0.72, p = 0.013), because of a negative association between changes in leptin and VLDL-TG secretion from non-systemic fatty acids (r = -0.95, p < 0.001). CONCLUSIONS: Weight loss-induced changes in plasma leptin concentration are inversely associated with changes in VLDL-TG secretion rate. Additional studies are needed to determine whether the correlation between circulating leptin and VLDL-TG secretion represents a cause-and-effect relationship. |
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Authors:
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F Magkos; E Fabbrini; J McCrea; B W Patterson; J C Eagon; S Klein |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Diabetes, obesity & metabolism Volume: 12 ISSN: 1463-1326 ISO Abbreviation: Diabetes Obes Metab Publication Date: 2010 Jul |
Date Detail:
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Created Date: 2010-07-01 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100883645 Medline TA: Diabetes Obes Metab Country: England |
Other Details:
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Languages: eng Pagination: 584-90 Citation Subset: IM |
Affiliation:
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Center for Human Nutrition, Washington University School of Medicine, St Louis, MO 63110, USA. |
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| Grant Support | |
ID/Acronym/Agency:
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DK-37948/DK/NIDDK NIH HHS; DK-56341/DK/NIDDK NIH HHS; RR 00954/RR/NCRR NIH HHS; UL1 RR024992/RR/NCRR NIH HHS |
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