The Correlation of genetic polymorphisms for leptin and leptin receptor, and serum level of leptin with hypertensive patients in Jenin رسالة ماجستير

Abstract

Background An endocrine hormone that functions as a significant regulator of food intake, neuroendocrine output, metabolism, and fat accumulation is the human homologue of the LEPTIN gene (LEP), which has been identified as an obesity gene. Through sympathetic activation in the circulation or at the renal level, leptin may also influence blood pressure and contribute to the development of hypertension, as demonstrated by certain experimental studies. Microinjections of leptin have also suggested that higher levels of leptin have greater effects on sympathetic activation. Objectives This study aimed to investigate the association between gene polymorphisms (LEP, LEPR) among hypertensive patients from Jenin, West Bank. Methodology This study was carried out on forty-five HBP patients with BMI>30 Kg/m2 and forty five HBP patients with BMI≤25 Kg/m2 . Blood samples were collected in EDTA and plain tubes for all patients. DNA was extracted from all EDTA blood samples. Polymorphisms of LEP, and LEPR genes were genotyped by using the restriction fragment length polymorphism (RFLP)-PCR. (The LEP gene SNP rs7799039 (2548G > A), while LEPR SNPs rs1137101 (þ668A > G). V Results Regarding the results of PCR-RFLP for LEP gene SNP rs7799039 (2548G > A), 0% of the cases were homozygous for the wild type genotype, compared to 20% in the normal BMI group. The heterozygous genotype was reported in 27% in cases, compared to 23% in the normal BMI group. The homozygous genotype was reported 18% in cases, compare to 13% in the normal BMI group. These results were statistically significant, with a higher frequency among patients (P=0.006). With no significance for LEP R SNPs rs1137101 (þ668A > G) polymorphism with P value (0.626456). The mean for leptin concentrations were 13.7 ± 12.5 (mean ± SD) for 45 patients with BMI>30 and 41.3 ± 17.7 for 45 patient with BMI<25. These results were highly statistically significant, with a higher frequency among patients (P<0.001). Conclusion In conclusion, our current findings provide conclusive proof that the LEP gene polymorphism is associated with susceptibility to HBP. This study suggests that having a LEP AA genotype is an independent risk factor for developing hypertension in obese individuals. To demonstrate a concrete link between these polymorphisms and HBP risk, further research should be conducted