Emerging evidence suggests a potential role of stearoyl-CoA desaturase (SCD)-1 in the control of body weight and energy homeostasis. The present study was conducted to investigate the effects of several energy balance-related factors (leptin, cerulenin, food deprivation, genotype, and gender) on SCD gene expression in chickens. In experiment 1, 6-week-old female and male broiler chickens were used. In experiment 2, two groups of 3-week-old broiler chickens were continuously infused with recombinant chicken leptin (8 μg/kg/h) or vehicle for 6 h. In experiment 3, two groups of 2-week-old broiler chickens received i.v. injections of cerulenin (15 mg/kg) or vehicle. In experiment 4, two broiler chicken lines (fat and lean) were submitted to two nutritional states (food deprivation for 16 or 24 h and feeding ad libitum). At the end of each experiment, tissues were collected for analyzing SCD gene expression. Data from experiment 1 showed that SCD is ubiquitously expressed in chicken tissues with highest levels in the proventriculus followed by the ovary, hypothalamus, kidney, liver, and adipose tissue in female, and hypothalamus, leg muscle, pancreas, liver, and adipose tissue in male. Female chickens exhibited significantly higher SCD mRNA levels in kidney, breast muscle, proventriculus, and intestine than male chickens. However, hypothalamic SCD gene expression was higher in male than in female (P < 0.05). Leptin increased SCD gene expression in chicken liver (P < 0.05), whereas cerulenin decreased SCD mRNA levels in muscle. Both leptin and cerulenin significantly reduced food intake (P < 0.05). Food deprivation for either 16 or 24 h decreased the hepatic SCD gene expression in fat line and lean line chickens compared with their fed counterparts (P < 0.05). The hypothalamic SCD mRNA levels were decreased in both lines only after 24 h of food deprivation (P < 0.05). In conclusion, SCD is ubiquitously expressed in chickens and it is regulated by leptin, cerulenin, nutritional state, and gender in a tissue-specific manner.
Sami Dridi, Mohammed Taouis, Arieh Gertler, Eddy Decuypere, and Johan Buyse
Els Willems, Astrid Koppenol, Bart De Ketelaere, Yufeng Wang, Lies Franssens, Johan Buyse, Eddy Decuypere, and Nadia Everaert
In mammalian models of prenatal undernutrition the maternal diet is manipulated, exerting both nutritional and hormonal effects on the offspring. In contrast, in the chicken, strictly nutritional effects can be applied. Prenatal protein undernutrition in chickens was induced by partial replacement of albumen with saline during early embryonic development (albumen-deprived group) and results were compared with a sham-manipulated and a non-manipulated group. Body weight of the albumen-deprived hens was reduced throughout the entire experimental period (0–55 weeks). The reproductive capacity was diminished in the albumen-deprived hens as reflected in the reduced number of eggs and lower egg weight. The plasma triiodothyronine levels were increased in the albumen-deprived group compared with the non-manipulated hens, but not the sham-manipulated hens. An oral glucose tolerance test (OGTT) at 10 weeks of age revealed a decreased glucose tolerance in the albumen-deprived hens. During adulthood, an age-related loss of glucose tolerance was observed in the hens, leading to disappearance of treatment differences in the OGTT. The offspring of the albumen-deprived hens (PA chicks) had reduced body weight until at least 3 weeks of age. In addition, the PA chicks had a decreased relative residual yolk weight at hatching. An insulin tolerance test revealed increased sensitivity to insulin for the PA chicks compared with the offspring of the non-manipulated (PN) and sham-manipulated hens (PS). In conclusion, prenatal protein undernutrition by albumen removal caused long-term effects on body weight, reproductive performance, and physiology.