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The intense genetic selection for rapid growth in broilers has resulted in an increase in voluntary feed intake and growth rate, accompanied by increased fat deposition in adipose tissue depots throughout the body. Adipose tissue expansion is a result of the formation of adipocytes (several processes collectively referred to as adipogenesis) and cellular accumulation of triacylglycerols inside lipid droplets. In mammals, different anatomical depots are metabolically distinct. The molecular and cellular mechanisms underlying adipose tissue development have been characterized in mammalian models, whereas information in avian species is scarce. The purpose of this review is to describe factors regulating adipogenesis in chickens, with an emphasis on dietary factors and the broiler. Results from many studies have demonstrated effects of dietary nutrient composition on adipose tissue development and lipid metabolism. Transcription factors, such as peroxisome proliferator-activated receptor γ, CCAAT/enhancer-binding proteins α and β, and sterol regulatory element binding proteins orchestrate a series of cellular events that lead to an increase in activity of fatty acid transport proteins and enzymes that are responsible for triacylglycerol synthesis. Understanding the mechanisms underlying adipose tissue development may provide a practical strategy to affect body composition of the commercial broiler while providing insights on diets that maximize conversion into muscle rather than fat and affect depot-dependent deposition of lipids. Because of the propensity to overeat and become obese, the broiler chicken also represents an attractive biomedical model for eating disorders and obesity in humans.
Wang et al. (Thu,) studied this question.
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