Open AccessRelationship Research of PPAR-r Gene Polymorphisms with Adiponectin and Leptin in Type 2 Diabetes Mellitus
Author(s) -
Jianhua Feng,
Shujin Wang,
Hong Zuo,
Xufeng Liu,
Guohong Li,
Niou Yu
Publication year - 2020
Publication title -
journal of clinical and nursing research
Language(s) - English
Resource type - Journals
eISSN - 2208-3693
pISSN - 2208-3685
DOI - 10.26689/jcnr.v4i4.1378
Subject(s) - adiponectin , medicine , endocrinology , leptin , type 2 diabetes , type 2 diabetes mellitus , triglyceride , diabetes mellitus , gene polymorphism , leptin receptor , peroxisome proliferator activated receptor , dyslipidemia , polymorphism (computer science) , allele , obesity , cholesterol , biology , receptor , insulin resistance , gene , genetics
Objective: To investigate the peroxisome proliferator-activated receptor-? (peroxisome) in patients with type 2 diabetes mellitus. Proliferators-activated receptors-?, PPARs-? (?) gene polymorphisms about serum lipofuscin and leptin. Methods: One hundred and twenty patients with type 2 diabetes admitted to our hospital from June 2015 to June 2018 were selected. The patients were divided into an obese group and a non-obese group of 60 patients each according to their waist circumference. A polymerase chain reaction-length polymorphism protocol was implemented in all patients to explore the PPAR-? gene polymorphism, and blood glucose, lipid, adiponectin and leptin levels were measured in both groups. Results: PPAR-? gene polymorphisms in type 2 diabetic patients were dominated by wild-type homozygous; The levels of total cholesterol, triglyceride and LDL cholesterol in the obese group were significantly higher than those in the non-obese group, while the levels of HDL cholesterol were lower than those in the non-obese group. There is significant difference in comparison between groups (P<0.05) Those carrying the A allele had a significant lipid disorder profile and decreased adiponectin levels. Conclusions: PPAR-? gene polymorphisms in type 2 diabetes are not significantly associated with adiponectin and leptin, and only in the obese group, the patients with the Allele A showed significant dyslipidemia and a declining trend of adiponectin levels.