Study On The Relationship Between Serum Leptin Levels In Dietetic Obese Rats And Obesity, Polycystic Ovary Syndrome

Polycystic ovary syndrome (PCOS) affects >5% of women ofreproductive age. It is characterized by both gynaecological andendocrine symptoms, including chronic anovulation, hyperandrogenism,insulin resistance, and the metabolic syndrome. PCOS is also one ofthe leading causes of infertility and involuntary childlessness ,which represent major stress factors in female life. Effects onphysical appearance, including obesity, hirsutism, cystic acne,seborrhoea and hair loss can also cause psychological distress anddecrease quality of life, possibly by influencing feminine identity .Further, it is also the metabolic syndrome ,and it had sequelae,e.g. type 2 diabetes mellitus, hypertension, lipid disorders,atherosclerosis. Obesity has the symptoms above also, so we thinkthat obesity correlatived with PCOS.Pathogeny of pcos is not very clearly, but we know that serumhigh leptin level is one of incretion characteristic of PCOS.Leptinis a 16 kDa pleiotrophic protein encoded by the obese(ob) gene, whichis mainly produced by white adipocytes.The most important biologicalproperties attributed to leptin are its effects on feeding,metabolism. However, several independent studies reported thatleptin play an important role in procreation and PCOS. So we wantto study the correlation between obesity and PCOS via leptin.Objective Observed the serum levels of leptin, estradiol(E2),testosterone(T), insulin(INS), glucose(GLU) in dietetic obese ratsand ovary development to study the correlation between obesity andPCOS.Methods Dietetic obese model were established in 60 femaleWister rats. Three groups were used (20 rats one group) :control group(IIgroup, the rats were feed with normal dieat), obesity group(Iagroup , fat-enriched diet),and reducing group (fat-enriched dietfor 6 weeks, then replaced by a normal diet), then were sacrificedat 13 weeks after the start of the experiment. We measured the serumlevels of leptin, estradiol, testosterone, insulin, glucose andobserved ovary development by microscope.Results Mean body weight of obese rats was over 20% than thatof control group at the end of experiment. The serum leptin levels ,E2, T , INS and GLU in obese group were obviously higher than thatin control group(P<0.05). They showed a positive correlation withleptin and body weight, leptin and INS, T and INS. At the same timethey show a negtive correlation with leptin and insulin sencibilityindices﹙ISI﹚.Experimental result display that ovary histology of each groupis normal. Obesity group rats' ovary weight is higher than controlgroup and reducing group. They were more mature ovarian follicle inobesity group,but development of them were bad than that of controland reducing groups by microscopy. The shape of reducing group ovaryapproach it of control group.Conclusion (1) The leptin level of obesisty group is higher thancontrol group and reducing group. So we say the leption level ofobesity rat is not reducing ,but increasing. Normal biology effectof leptin is not displayed, consequently that results in obesity andcompensational high leptin disease. It shows a positive correlationwith leptin and body weight ,and that prompts us serum leptin levelwas affected by weight. The prevenient results indicate that highserum leptin level conduces PCOS because it likelihood counteractthe action of insulin-like grouth factor-1 (IGF-1) in preponderantfollicle. High leptin level in folliculiar fluid may impact granularcell differentiation, follicular maturity and ovulation. Obesity cancause high serum leptin level,and we have known high serum leptinlevel can conduce PCOS, so we speculate that obesity can conduce PCOSby the change of leptin. (2) Serum glucose and insulin level ofobesity group are apparently higher than reducing group and controlgroup, and ISI is lower. That shows us rats of obesity group havehyperinsulinemia and insulin resistance. The experiment shows apositive correlation with leptin and insulin, and a negativecorrelation with ISI. So there are intimate contact between leptinand insuline and ISI. Insulin is the ovary functions' regulator, andobesity can conduce hyperinsulinemia and insulin resist. In theduring the form of hyperinsulinemia and insulin resist, Leptin playan important role . (3) Serum testosterone level of obesity groupis apparently higher than reducing group and control group, and ithas positive correlation with insulin level. That shows us obesistycan conduce hyperandrogenism, which relates with high serum leptinlevel. Serum high level of Leptin , hyperinsulinemia and hyper-androgenism interact all together, then speed the formation ofPCOS.(4) Serum high leptin level participate the formation of hyper-insulinemia , insulin resist and hyperandrogenism besides itself canconduce PCOS. And hyperinsulinemia , insulin resist and hyper-androgenism are all characteristics of PCOS. So we say obesityparticipate in the formation and development of PCOS via the laterof these incretionary characteristic , and leptin play a role ofbridge or ligament .(5) The incretionary characteristics in reducinggroup are better than in obesity group ,and close to control group.So we speculate on banting can rectify the change of theseincretionary characteristics. That offers an proof for treatment ofwomen with PCOS.