In ovo leptin administration affects hepatic lipid metabolism and microRNA expression in newly hatched broiler chickens

Prenatally leptin-exposed chicks showed lower hatch weight, but higher liver weight relative to the body weight, compared to the control group. In ovo leptin treatment increased the hepatic content and serum concentration of leptin in newly hatched chickens. The hepatic contents of triglycerides (TG) and total cholesterol (Tch) were decreased, whereas the serum levels of TG, Tch and apolipoprotein B (ApoB) were increased. The hepatic mRNA expression of sterol regulator element binding protein 1 (SREBP-1c), SREBP-2, hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) and cholesterol 7α-hydroxylase 1 (CYP7A1) was significantly up-regulated, as was the protein content of both SREBP-1c and SREBP-2 in hepatic nuclear extracts of leptin-treated chickens. Moreover, out of 12 miRNAs targeting SREBP-1c and/or HMGCR, five were significantly up-regulated in liver of leptin-treated chicks, including gga-miR-200b and gga-miR-429, which target both SREBP-1c and HMGCR.These results suggest that leptin in ovo decreases hatch weight, and modifies hepatic leptin secretion and lipid metabolism in newly hatched broiler chickens, possibly via microRNA-mediated gene regulation.Leptin is involved in the regulation of food intake and energy balance in mammals [1,2]. Despite the current controversy over the existence of a leptin gene in the chicken genome [3], the existence of a leptin-like immunoreactive substance [4,5] and a functional leptin receptor (LEPR) has been confirmed [6]. Furthermore, exogenous murine or human leptin exerts similar effects on poultry as it does on mammals [7,8].Maternal leptin has been shown to program offspring obesity in mammals [9]. Fetal or neonatal abnormal nutritional environment induces leptin synthesis and secretion from adipocytes, and affects adipocyte morphology and metabolism, thus linking embryonic nutrition to adult obesity [10]. Manipulating either maternal plasma leptin or transplacental leptin transfer could impact the postnatal regulation of