Effect of peripheral administration of lamprey GnRH-III on gonadotropin secretion and a biomedical model to study obesity-related traits

The secretory profiles of gonadotropin differ in response to several physiological factors. Differential release of LH and FSH may be dynamically regulated by signals from distinct pathways selectively activated by GnRH or other hormone regulators. In mammals, the general idea is that release of FSH and LH is mainly regulated by GnRH-I; however, lamprey GnRH-III also is present in the mammalian hypothalamus and both peptides are involved in the control of gonadotropin secretion. Nonetheless, there are contradictory results regarding the function of (l)GnRH-III. Our results showed that exogenous infusion of (l)GnRH-III stimulated LH secretion in barrows. A greater rise in serum LH was induced when (l)GnRH-III was infused at high doses (10.0 ìg/kg of BW). The concentrations of FSH in serum were not changed, even at the highest doses of (l)GnRH-III. In conclusion, our results do not support the hypothesis that (l)GnRH-III might be the FSH-releasing factor, but a preferential release of LH was observed at high doses of (l)GnRH-III. Hormonal interactions among ghrelin, growth hormone, insulin, and other hormones contribute to the regulation of food intake and body weight. Obesity is the result of the impaired regulation of these hormones, and obesity is related to the development diabetes and cardiovascular diseases. Similar to insulin, ghrelin circulates in relation to energy stores and might regulate growth hormone and glucose metabolism. Results of our experiment indicate that ghrelin, growth hormone, and insulin concentrations were not influenced during the experiment by the full feed (FF) and restricted (RES) treatments and during fasting conditions (FC) and after feeding (AF) periods; however, plasma concentrations of ghrelin and growth hormone in the beginning of the experiment were greater in FC compared with AF. The pig might offer a suitable model of how the human could react to changes in metabolism caused by obesity. Nonetheless, we must also consider that a biomedical model used for clinical testing might not reflect the disease as it occurs in humans, which could account for why there were no statistical differences between treatments in our experiment. Further research should be conducted in healthy and obese pigs to determine the effects of these hormones on the underlying physiological pathogenesis of obesity