Glycerol-3-phosphate Acyltransferase Isoform-4 (GPAT4) Limits Oxidation of Exogenous Fatty Acids in Brown Adipocytes

摘要: Glycerol-3-phosphate acyltransferase-4 (GPAT4) null pups grew poorly during the suckling period and, as adults, were protected from high fat diet-induced obesity. To determine why Gpat4−/− mice failed to gain weight these two periods of feeding, we examined energy metabolism. Compared with controls, metabolic rate fed a 45% diet was 12% higher. Core body temperature 1 oC higher after feeding. Food intake, absorption, and activity similar in both genotypes. Impaired did not result increased heat loss, because cold tolerance response β3-adrenergic agonist Because GPAT4 comprises 65% total GPAT brown adipose tissue (BAT), characterized BAT function. A expression peroxisome proliferator-activated receptor α (PPAR) target genes, Cpt1α, Pgc1α, Ucp1, mitochondria oxidized oleate pyruvate at rates than suggesting that fatty acid signaling flux through TCA cycle enhanced. assess role directly, neonatal preadipocytes differentiated adipocytes. adipocytes incorporated 33% less into triacylglycerol 46% more pathway β-oxidation. The oxidation due solely an increase exogenous acids. These data suggest absence exposure, limits excessive detrimental induction hypermetabolic state.