Neural levels of cholecystokinin peptide and mRNA during dietary stimulation of growth and LH secretion in growth-retarded lambs.
Chronic feed restriction of prepubertal male lambs adversely affects reproductive development by inhibiting the pulsatile release of luteinizing hormone (LH). Because this effect can be reversed by ad libitum feeding, the associations between diet-induced increases in LH release and concurrent changes in body weight gain, serum glucose. CCK peptide, and CCK mRNA were examined. Neonatally castrated male lambs received a restricted ration to maintain their respective weaning weights beginning at 8 wk of age. At 23 wk of age, lambs were assigned randomly to receive additional feed equivalent to 0%, 50%, or 100% of their previous daily intake. Serum profiles of LH and glucose were determined 2 and 4 wk after onset of the increased intakes. At 27 wk of age, lambs were euthanized and both hypothalamic and cerebral cortical tissues were collected for analysis of CCK peptide and CCK mRNA. With additional intakes, body weight gain increased (P < 0.001) proportional to the graded increases in feed intake. Mean serum LH concentrations, LH peak frequencies, and serum glucose concentrations also increased (P < 0.05) progressively among the 0%, 50%, and 100% dietary intake groups. Neither CCK peptide nor CCK mRNA differed (P > 0.05) among dietary groups suggesting that endogenous CCK in the whole hypothalamus did not change with the feeding-induced increase in LH release. Concentrations of CCK peptide in cerebral cortex were greater (P < 0.05) than hypothalamic concentrations, but there were no differences between hypothalamus and cerebral cortex in the relative abundance of CCK mRNA. In summary, dietary stimulation of growth-retarded male lambs resulted in progressive increases in body weight gain, mean serum LH, serum glucose, and LH peak frequencies. Because hypothalamic levels of CCK peptide and CCK mRNA did not change during feeding-induced secretion of LH, endogenous CCK in the hypothalamus seems unlikely as a chronic mediator of nutrition-sensitive LH release.
Holmberg
B J
BJ
Department of Animal Sciences, Purdue University, West Lafayette, IN 47907, USA.
Malven
P V
PV
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D002540:Cerebral Cortex / Q000378:metabolism; D002766:Cholecystokinin / Q000235:genetics* / Q000378:metabolism*; D004032:Diet; D005508:Food Deprivation; D007987:Gonadotropin-Releasing Hormone / Q000494:pharmacology; D007031:Hypothalamus / Q000378:metabolism; D007986:Luteinizing Hormone / Q000097:blood / Q000378:metabolism*; D008297:Male; D016202:N-Methylaspartate / Q000494:pharmacology; D009919:Orchiectomy; D012333:RNA, Messenger / Q000378:metabolism*; D012756:Sheep / Q000254:growth & development* / Q000378:metabolism
D001786:Blood Glucose; D012333:RNA, Messenger; D007987:Gonadotropin-Releasing Hormone; D016202:N-Methylaspartate; D007986:Luteinizing Hormone; D002766:Cholecystokinin