期刊
CELL METABOLISM
卷 24, 期 1, 页码 167-171出版社
CELL PRESS
DOI: 10.1016/j.cmet.2016.06.005
关键词
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资金
- United States Public Health Service [R01 DK-49230, R01 AG-23686, P30 DK-45735, SIG 11S10OD010613-01, UL1 RR-024139]
- Novo Nordisk Foundation Center for Basic Metabolic Research
- Distinguished Clinical Investigator Award from the American Diabetes Association
- Gilead Sciences Inc.
Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, and there is great interest in understanding the potential role of alterations in mitochondrial metabolism in its pathogenesis. To address this question, we assessed rates of hepatic mitochondrial oxidation in subjects with and without NAFLD by monitoring the rate of C-13 labeling in hepatic [5-C-13] glutamate and [1-C-13]glutamate by C-13 MRS during an infusion of [1-C-13] acetate. We found that rates of hepatic mitochondrial oxidation were similar between NAFLD and control subjects. We also assessed rates of hepatic pyruvate cycling during an infusion of [3-C-13] lactate by monitoring the C-13 label in hepatic [2-C-13] alanine and [2-C-13] glutamate and found that this flux was also similar between groups and more than 10-fold lower than previously reported. Contrary to previous studies, we show that hepatic mitochondrial oxidation and pyruvate cycling are not altered in NAFLD and do not account for the hepatic fat accumulation.
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