Expression patterns of AMPK and genes associated with lipid metabolism in newly hatched chicks during the metabolic perturbation of fasting and refeeding.

Fasting-refeeding perturbation has been extensively used to reveal specific genes and metabolic pathways that control energy metabolism in chickens. In this study, 200 chickens were randomly assigned to 2 groups after hatching: the control group (C, fed ad libitum) and the fasting-refeeding group (T, water ad libitum). The chicks in Group T were fasted for 72 h, and then fed for another 48 h. Liver, hypothalamus, and adipose samples were collected at 0 (F0), 24 (F24), 48 (F48), and 72 h (F72) after fasting and 4 (FR4), 12 (FR12), 24 (FR24), and 48 h (FR48) after refeeding, respectively. Results showed that Group T had a significantly higher number of liver vacuoles (P < 0.05 or P < 0.01) and a significantly lower gray value of Sudan IIIstained sections (P < 0.05 or P < 0.01) than Group C at F48-FR48. In addition, compared with the Group C, fasting and refeeding reduced the expression of stearoyl CoA desaturase (SCD) mRNA (P < 0.05 or P < 0.01) in the liver and adipose tissues, the expression of glucocorticoid receptor (GR) mRNA (P < 0.05 or P < 0.01) in the liver, adipose, and hypothalamus tissues, and the expression of fatty acid synthase (FAS) mRNA (P < 0.05 or P < 0.01) in the liver at F24-FR24. Moreover, relative to those in Group C, fasting and refeeding increased the mRNA expression levels of adenosine monophosphate-activated protein kinase (AMPK) α, AMPKβ, and AMPKγ in the hypothalamus (P < 0.05 or P < 0.01) at F24-FR24. In conclusion, fasting and refeeding increased the fat content of the liver, and the expression of lipolytic genes in the hypothalamus (e.g., AMPKα, AMPKβ, and AMPKγ) but decreased the expression of fat synthesis genes in the liver (e.g., SCD, GR, and FAS), adipose (SCD and GR), and hypothalamus (GR).