Abstract | OBJECTIVE: RESEARCH DESIGN AND METHODS: We recruited obese subjects who met criteria for bariatric surgery with (n = 16) or without (n = 15) NAFLD and assessed 1) insulin-mediated regulation of hepatic and peripheral glucose metabolism using hyperinsulinemic-euglycemic clamps with [6,6-2H2] glucose, 2) fasting and carbohydrate-driven hepatic DNL using deuterated water (2H2O), and 3) hepatocellular insulin signaling in liver biopsy samples collected during bariatric surgery. RESULTS: CONCLUSIONS: Acute increases in lipogenesis in humans with NAFLD are not explained by altered molecular regulation of lipogenesis through a paradoxical increase in lipogenic insulin action; rather, increases in lipogenic substrate availability may be the key.
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Authors | Kasper W Ter Horst, Daniel F Vatner, Dongyan Zhang, Gary W Cline, Mariette T Ackermans, Aart J Nederveen, Joanne Verheij, Ahmet Demirkiran, Bart A van Wagensveld, Geesje M Dallinga-Thie, Max Nieuwdorp, Johannes A Romijn, Gerald I Shulman, Mireille J Serlie |
Journal | Diabetes care
(Diabetes Care)
Vol. 44
Issue 2
Pg. 489-498
(02 2021)
ISSN: 1935-5548 [Electronic] United States |
PMID | 33293347
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
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Copyright | © 2020 by the American Diabetes Association. |
Chemical References |
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Topics |
- Diabetes Mellitus, Type 2
(metabolism)
- Humans
- Insulin
(metabolism)
- Insulin Resistance
- Lipogenesis
- Liver
(metabolism)
- Non-alcoholic Fatty Liver Disease
(metabolism)
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