Fasting rapidly increases fatty acid oxidation in white adipose tissue (269.2)

Abstract

Upregulating fatty acid oxidation in white adipose tissue in mice protects against diet‐induced obesity and excess plasma NEFA levels. At least part of this capacity results from the induction of brown‐like adipocytes within classical white depots, making it difficult to determine if white adipocytes contribute. Avian genomes lack a gene for uncoupling protein 1 and are devoid of brown adipocytes, making them a useful model in which to study lipid metabolism in white adipocytes. We recently reported that a brief (5 hr) period of fasting upregulated expression of genes involved in mitochondrial and peroxisomal fatty acid oxidation in white adipose tissue of broiler chickens. The objective of this study was to determine if the effects on gene expression manifested in increased rates of fatty acid oxidation. Abdominal adipose tissue was collected from 21 day‐old broiler chicks that fasted for 3.5, 5 or 7 hrs, or fed ad libitum. Fatty acid oxidation was determined by measuring and summing 14CO2 production and 14C‐labeled acid‐soluble metabolites from the oxidation of [1‐14C]palmitic acid. Citrate synthase activity was measured spectrophotometrically. Fasting induced a progressive increase in complete oxidation which was significantly different from controls in the 5.5 hr (p=0.0037) and 7 hr (p=0.0021) groups (1.14, 1.2, 1.49 and 1.95 nmol/mg protein/hr; control, 3.5, 5 and 7 hrs, respectively). Citrate synthase activity increased significantly after 7 hrs of fasting. Fasting did not significantly alter the production of acid soluble metabolites, an index of incomplete fatty acid oxidation. These results confirm that fasting rapidly increases fatty acid oxidation in white adipose tissue by upregulating the transcription of key regulatory enzymes and proteins. Identifying the underlying mechanism may provide new therapeutic targets through which to increase fatty acid oxidation in situ and protect against obesity and the detrimental effects of excess NEFA on adipocyte insulin sensitivity.