Background: The leptin receptor (LEPR) gene, is a member of the class I cytokine receptor superfamily, with six known isoforms. Animal as well as human modal both studies indicate that LEPR have important and powerful roles in the mechanism of obesity. This study aims to determine the correlation of the LEPR genetic variant with obesity and leptin level in the obese and control groups in the northern Indian population. Methods: 109 fertile controls and 120 unexplained infertile cases were recruited. Serum leptin level was measured by active human ELISA kit using an ELISA reader. Leptin receptor gene polymorphism A668G, A326G and G1968C were analyzed by polymerase chain reaction (PCR) followed by restriction fragment length polymorphism (RFLP). Results: The anthropometric parameters are slightly higher in obese cases as compared to control group (p > 0.005), whereas waist circumference and hip circumference shows a significant p-value (p < 0.005) between obese cases and controls. The leptin level is found increased in obese cases than controls and this difference is significant with p < 0.05. The higher frequency of GG genotype of (Gln223Arg) variant in obese cases with significant difference found in between obese cases and control groups p < 0.001. Similarly GG and CC genotype of (Lys109Arg) and (Lys656Asn) respectively found higher frequency with significantly different p < 0.001 in obese group as compared to control group. Conclusion: Genetic variants (Gln223Arg), (Lys109Arg) and (Lys656Asn) in LEPR gene are significantly associated with anthropometric parameter obesity and leptin level in northern Indian population.

Objective The aim of the present study was to examine the relation between the PON1 polymorphisms and recurrent pregnancy loss (RPL). Methods In a cross-sectional study, blood samples were collected from 100 females. DNA was extracted and PON1 genotypes were determined by polymerase chain reaction (PCR) amplification. Results Regarding PON1 L55M, the mutated allele (M) frequency was found in 70.5% in RPL and in 53.5% in controls; the M allele was significantly associated with an increased risk of RPL (adjusted odds ratio [ORadj] = 2.07; 95% confidence interval [CI]; p < 0.001). However, regarding PON1 Q192R, the R mutated allele frequency was found in 28.5% in RPL and in 33% in controls. The R allele did not show any risk for RPL (ORadj 0.81; 95%CI; p = 0.329). Conclusion The present study suggests that there is an effect of genetic polymorphism on RPL and provides additional evidence that combines with the growing information about the ways in which certain PON1 genotypes can affect the development of the fetus in the uterus.