Objective.Obesity is a complex heterogeneous disease that is caused by genes, environmental factors, and the interaction between the two. The leptin (LEP) and leptin receptor (LEPR) genes have been evaluated for polymorphisms that could potentially be related to the pathophysiology of obesity and its complications. The aim of this study was to investigate the role ofLEPG2548A andLEPR668A/G polymorphisms in the pathogenesis of obesity.Subjects.The study included 127 patients with obesity and 105 healthy controls. Polymerase chain reaction and restriction fragment length analysis forLEPG2548A andLEPR668A/G polymorphisms were applied.Results.There was no statistically significant difference in the genotype frequencies of theLEPgene polymorphism between patients and control groups (P>0.05). We found a difference in theLEPRgenotypes between patients and controls, but this was not statistically significant (P=0.05). Additionally, we found an increased risk of obesity in theLEP/LEPRGG/GG combined genotype (P<0.05).Conclusion.Our findings indicate that theLEPG2548A polymorphism is not a relevant obesity marker and that theLEPR668A/G polymorphism may be related to obesity in a Turkish population. Further researches with larger patient population are necessary to ascertain the implications ofLEPandLEPRpolymorphisms in obesity.

Diabetes mellitus (DM) is a serious and common in the world health problem that leads to different complications. Changes in oxidative stress and antioxidant capacity play an important role in the pathogenesis of DM. The purpose of this study was to investigate ellagic acid (EA) treatment in diabetes induced testicular damage. In our study, 24 male Sprague Dawley rats were divided into four groups. Group 1: Control (n = 6), Group 2: EA (n = 6), Group 3: Diabet (n = 6), Group 4: Diabet + EA (n = 6). Diabetes was induced by intraperitoneal injection of streptozocin (STZ) (55 mg/kg) to group 3 and 4. EA was given 100 mg/kg/day group 2 and 4 for 35 days by oral gavage. We used that Hematoxylen-Eosin (H&E) and Johnsen’s scoring to determine histological change. The terminal-deoxynucleoitidyl-transferase mediated nick end-labeling assay (TUNEL) was used for apoptosis. Oxidative stress markers were determined by qRT-PCR and immunexpression of Nrf2 was evaluated in testicular tissue. In conclusion, EA administration on the diabetes model has changed the histopathological features, apopotosis and oxidative stress marker genes in the testis and may have an effect on the reduction of diabetes induced testicular damage.