期刊
CELL REPORTS
卷 22, 期 7, 页码 1745-1759出版社
CELL PRESS
DOI: 10.1016/j.celrep.2018.01.067
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资金
- Australian NHMRC [1126724, 1084344, APP1077703]
- COBRE center grant from the NIH [NIH 8P20GM103528]
- NORC center grant from the NIH [NIH 2P30-DK072476-11A1]
- Australian Government Research Training Program scholarship
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico-CNPq Brazil
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK072476] Funding Source: NIH RePORTER
AgRP neurons control peripheral substrate utilization and nutrient partitioning during conditions of energy deficit and nutrient replenishment, although the molecular mechanism is unknown. We examined whether carnitine acetyltransferase (Crat) in AgRP neurons affects peripheral nutrient partitioning. Crat deletion in AgRP neurons reduced food intake and feeding behavior and increased glycerol supply to the liver during fasting, as a gluconeogenic substrate, which was mediated by changes to sympathetic output and peripheral fatty acid metabolism in the liver. Crat deletion in AgRP neurons increased peripheral fatty acid substrate utilization and attenuated the switch to glucose utilization after refeeding, indicating altered nutrient partitioning. Proteomic analysis in AgRP neurons shows that Crat regulates protein acetylation and metabolic processing. Collectively, our studies highlight that AgRP neurons require Crat to provide the metabolic flexibility to optimize nutrient partitioning and regulate peripheral substrate utilization, particularly during fasting and refeeding.
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