Ghrelin and Leptin role in Fructose-Induced Insulin–Resistant Rats

CABRAL AGUSTINA; RASCHIA AGUSTINA; MARQUES LORENA; SUESCUN MARIA OLGA

Ciudad autónoma de Buenos Aires

Jornada; XI Jornadas de la Sociedad Argentina de Biología; 2009

Sociedad Argentina de Biología

GhRelin and Leptin RolE in Fructose-Induced Insulin–Resistant Rats.Cabral A, Raschia A, Marques L, Suescun MO, IMBICE, CIC CONICET,CCT-La Plata Chair of Endocrinology-UNLP, CENEXA-CCT-UNLP, Argentine                                                      Leptin (Lp) and Ghrelin (Gh) have been reported to play a role in the interaction among the metabolic syndrome (MS), insulin resistance (IR), and testicular function. Fructose-rich diet (FRD) is a good experimental model of MS and IR. We have previously observed lower in vitro steroidogenic response in FRD than in Control(C) rats, and an inhibitory effect of Lp and Gh on hCG-stimulated testosterone production by both FRD and C Leydig cells. However Gh inhibitory effect was higher in FRD group. Aim: Assessment of eventual differences in the expression of Gh, Lp and its specific receptor GHSr-1a, and Ob-Rb in testicular tissue from FRD and C rats. Methodology: Normal male rats were fed with a standard commercial diet and water without (C) or with 10% fructose (FRD) for three weeks. Blood glucose, triglycerid and insulin levels were measured at sacrifice. Gh, GHSr-1a, Lp and Ob-Rb expression (relative to β actina expression) was evaluated by RT-PCR real time in testicular tissue aliquots from both groups. Results: FRD rats showed normoglycemia but impaired glucose tolerance, hypertriglyceridemia, and hyperinsulinemia. GHSr-1a expression was higher in FRD than in C testicular tissue and the opposite was observed for Ob-Rb expression (p<0.05). Gh and Lp expression showed low decrease and increase respectively in FRD. Discussion: Present results confirm the significant role played by Lep and Gh in testicular dysfunction observed during SM and IR. Changes in Ob-Rb  and GHSr-1a expression in testicular tissue may reflect hyperleptinemia characteristic of FRD and could explain the high Gh inhibition on hCG-stimulated testosterone production found in vitro.