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United States Department of Agriculture

Agricultural Research Service

Title: Failure of Short Term Feed Restriction to Effect Luteinizing Hormone Or Leptin Secretion and Subcutaneous Adipose Tissue Expression of Leptin Or Leptin Receptor in the Prepuberal Gilt

item Hart, Heather - UNIV. OF GEORGIA
item Azain, Michael - UNIV. OF GEORGIA
item Hausman, Gary
item Reeves, David - UNIV. OF GEORGIA
item Barb, Claude

Submitted to: Canadian Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 10, 2006
Publication Date: May 1, 2007
Citation: Hart, H.A., Azain, M.J., Hausman, G.J., Reeves, D.E., Barb, C.R. 2007. Failure of short term feed restriction to effect luteinizing hormone or leptin secretion and subcutaneous adipose tissue expression of leptin or leptin receptor in the prepuberal gilt. Canadian Journal of Animal Science. 87:191-197.

Interpretive Summary: Leptin, secreted by fat cells in response to changes in body weight and nutrition, regulates appetite and severs as a metabolic signal that directly effect brain and pituitary gland to regulate luteinizing hormone (LH) secretion, necessary for reproduction; reduced feed intake in the prepubertal gilt altered metabolism but failed to change LH or leptin secretion and fat cell function. The ability of the prepubertal gilt to maintain energy level in the normal range suggests the prepubertal animal is resistant to moderate reduction nutrition.

Technical Abstract: Ovariectomized prepuberal gilts averaging 164 days of age and 79.2 ± 3.8 kg body weight (BW) were either fed to appetite (FA; n = 6) or feed restricted (RST; 40% of FA diet; n = 6) for 7 seven days to determine the effects of feed RST on serum leptin concentrations, metabolism, leptin, Ob-r and transcription factor expression in subcutaneous back fat (BF). On day 8, blood samples were collected every 15 min for 8 h. Serum concentrations of glucose, T3, T4, NEFA, insulin, and leptin were determined. Real-time PCR was performed on mRNA extracted from subcutaneous adipose tissue collected on day 0 (start RST) and day 9. FA gilts gained (P<.0001) more BW (8.3 ± .6 kg) than RST (-2.5 ± .6 kg) gilts, however BF thickness did not change. A treatment x time interaction (P<.009) was detected for serum glucose concentrations. Serum insulin (P<.07), T3 (P<.08), and T4 (P<.04) concentrations were reduced and NEFA levels (P<.05) were greater during h 1, 6, 7 and 8 in RST gilts compared to FA animals demonstrating a metabolic response to RST. Serum leptin concentrations, leptin pulse amplitude, and leptin pulse frequency were not effected by RST. RST failed to effect subcutaneous BF leptin, Ob-r, AFABP (adipocyte fatty acid binding protein), C/EBP-alpha (CCAAT/enhancer binding protein alpha), or PPAR- gamma 2 (peroxisome proliferator activated receptor gamma 2) mRNA expression compared to FA gilts. These results may in part be related to the failure of RST of this duration to influence subcutaneous BF. Thus, the leptin response to RST may require energy levels and (or) BF reduction reaching a putative inhibitory threshold

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