Leptin is involved in the effects of cysteamine on egg laying of hens, characteristics of eggs, and posthatch growth of broiler offspring.

Cysteamine has been reported to modulate energy homeostasis and exert significant growth-promoting effects in broiler chickens. However, little is known concerning its effects on egg production of hens and the growth rate of their offspring. In the present study, 67-wk-old broiler breeders were allotted at random to control and cysteamine-supplemented (400 mg/kg) groups for 8 wk. The hatchlings were fed under the same condition until 6 wk of age. Cysteamine significantly increased the average laying rate by 2.24% (P < 0.01), decreased dramatically the percentage of the broken eggs by 40.55% (P < 0.01), and increased that of the abnormal eggs by 20.15% (P < 0.05). Cysteamine did not alter the egg weight, egg quality, fertility, or hatch-ability but significantly increased eggshell weight (P < 0.05) and decreased albumin weight (P < 0.05). Serum concentrations of total thyroxine (P < 0.01) and leptin (P < 0.01) were significantly lower in cysteamine-treated hens, whereas total triiodothyronine (T(3)), free T(3), and glucagon were not affected. Western blot analysis with leptin-specific antibody detected a band of approximately 15 to 16 kDa in egg yolk and albumin extracts as well as in liver homogenates of hens. Cysteamine did not affect the yolk content of T(3), thyroxine, estradiol, or glucagon, but significantly increased leptin content in liver of hens (P < 0.05), as well as in yolk (P < 0.05) and albumin (P < 0.05) of eggs. These changes were accompanied by a significant downregulation of leptin receptor mRNA expression (P < 0.05) in the yolk sac of d-12 embryos. Female offspring hatched from cysteamine-treated eggs demonstrated significantly lower body weight at hatching (P < 0.01) and 42 d of age (P < 0.01). The results indicate that cysteamine improves laying performance of hens and affects the early posthatch growth of broiler offspring, in a sex-specific fashion. The modified leptin secretion and egg deposition, together with altered yolk sac leptin receptor expression, may be involved in such an effect.