Hypothalamic pro-opiomelanocortin (POMC) neurons help regulate long-term energy stores. POMC neurons are also found in the nucleus tractus solitarius (NTS), a region regulating satiety. We show here that mouse brainstem NTS POMC neurons are activated by cholecystokinin (CCK) and feeding-induced satiety and that activation of the neuronal melanocortin-4 receptor (MC4-R) is required for CCK-induced suppression of feeding; the melanocortin system thus provides a potential substrate for integration of long-term adipostatic and short-term satiety signals.
A single nucleotide polymorphism (SNP) in the corticotrophin-releasing hormone gene (CRH C22G) alters the fourth amino acid in the signal sequence from proline to arginine. Two other SNPs (CRH A145G and C240G) occur in the propeptide region at residue positions 45 and 77, respectively, that result in serine/asparagine and histidine/aspartic acid substitutions respectively. These SNPs, as well as SNPs in pro-opiomelancortin (POMC), leptin (LEP) and melanocortin-4 receptor (MC4R), were evaluated for associations with average daily gain, end-of-test rib-eye area, shipping weight and hot carcass weight in a group of 256 steers using a general linear model. The CRH C22G SNP was associated with end-of-test rib-eye area (P < 0.034) and hot carcass weight (P < 0.0015). The SNP in POMC was associated with shipping weight (P < 0.0078) and hot carcass weight (P = 0.006) while it approached significance for average daily gain (P < 0.07). The SNP in MC4R approached significance for hot carcass weight (P < 0.085) while no significance was observed between the leptin SNP and the above listed traits. Because both CRH and POMC regulate appetite, potential interaction effects between these two genes were assessed. The absence of an interaction effect between CRH and POMC with hot carcass weight suggests that these genes act independently to increase carcass yield. These gene effects used singularly or together could result in an economic benefit to the beef industry.
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