Manipulating Adipose Tissue Fatty Acid Oxidation to Reduce Fatness in Broiler Chickens

Compared to rodents, broiler chickens, those reared for meat, are an attractive model for studies of adipose biology, and obesity development in children. The broiler chicken lacks the gene for uncoupling protein 1, the hallmark for brown adipose tissue making them a useful model to study lipid metabolism in white adipocytes. Two studies were performed to investigate if white adipose tissue had the metabolic ability for fatty acid oxidation (FAO), and to investigate the effects of dietary fatty acids on abdominal fat development of young broiler chickens as a model for childhood obesity. In study one, chickens were fasted for three, five, and seven hours. Afterwards, the oxidative flux from the citric acid cycle, and the citrate synthase enzyme activity were measured in white adipose tissue. In study two, young Cobb500 broilers, from age seven to 21 days, were fed isocaloric diets prepared using lard (primarily saturated), corn oil (primarily monounsaturated), flaxseed oil (enriched in alpha linolenic acid (ALA, 18:3, n-3)), or fish oil (enriched in eicosapentaenoic acid (EPA, 20:5, n-3) and docosahexaenoic acid (DHA, 22:6, n-3)), at 8% fat by weight. Physical characteristics, abdominal adipocyte histology, and abdominal adipose tissue gene expression profiles were altered due to dietary fatty acids. Collectively our studies confirm that white adipose tissue has the capacity to increase local FAO by increasing expression of key regulatory enzymes and proteins. Further, by altering the type of fatty acids consumed during childhood, adipose deposition and adipocyte size can be attenuated. These data confirm that FAO can be induced locally in white adipose tissue, dietary long chain n-3 polyunsaturated fatty acids promote reduced adipocyte size, and finally that these data could offer new therapeutic targets to reduce fatness in chickens and children.