Association of Leptin Receptor Gene Polymorphisms with Blood Glucose Concentration and Obesity
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422
144
Biochemistry and Molecular Biology (Science Publishing Group)
2022
English
Myanmar
Abstract
Obesity has become a global epidemic and is a known risk factor for several adverse health outcomes. Single Nucleotide Polymorphism (SNP) in leptin receptor genes become interesting candidates as susceptibility genes for obesity and glucose homeostasis. The present study intended to explore the genetic analysis of LEPR gene K109, Q223R, and K656N polymorphisms and their relation to obesity and fasting plasma glucose (FPG) concentration in the Myanmar population. One hundred and fifty diagnosed obese subjects and 150 healthy non-obese controls were included. Fasting plasma glucose (FPG) was measured and LEPR gene K109R, Q223R, and K656N polymorphisms were detected by DNA analysis. Data were analyzed by chi-square and one-way ANOVA tests. Each genotype frequency distribution of LEPR gene (K109R, Q223R, and K656N) polymorphisms was not associated with obesity (p > 0.05), as well as each allele frequency distribution also similar outcome (p > 0.05). FPG levels of the study population showed no significant differences between each genotype of LEPR gene polymorphisms (p > 0.05). The K109R, Q223R, and K656N polymorphisms of the LEPR gene were not linked to obesity or FPG levels in the population of Myanmar, according to our findings. Therefore, it does not seem that these polymorphisms have an equivalently significant role for the people of Myanmar. To completely understand the unique genetic variables that predispose to obesity in humans, an ongoing study of diverse obesity phenotypes and related gene mutations is necessary as our understanding of the genes causing obesity increases as a result of new findings.
Obesity, Fasting Plasma Glucose, LEPR Gene K109R SNP, LEPR Gene Q223R SNP, LEPR Gene K656N SNP
Obesity has become a global epidemic and is a known risk factor for several adverse health outcomes. Single Nucleotide Polymorphism (SNP) in leptin receptor genes become interesting candidates as susceptibility genes for obesity and glucose homeostasis. The present study intended to explore the genetic analysis of LEPR gene K109, Q223R, and K656N polymorphisms and their relation to obesity and fasting plasma glucose (FPG) concentration in the Myanmar population. One hundred and fifty diagnosed obese subjects and 150 healthy non-obese controls were included. Fasting plasma glucose (FPG) was measured and LEPR gene K109R, Q223R, and K656N polymorphisms were detected by DNA analysis. Data were analyzed by chi-square and one-way ANOVA tests. Each genotype frequency distribution of LEPR gene (K109R, Q223R, and K656N) polymorphisms was not associated with obesity (p > 0.05), as well as each allele frequency distribution also similar outcome (p > 0.05). FPG levels of the study population showed no significant differences between each genotype of LEPR gene polymorphisms (p > 0.05). The K109R, Q223R, and K656N polymorphisms of the LEPR gene were not linked to obesity or FPG levels in the population of Myanmar, according to our findings. Therefore, it does not seem that these polymorphisms have an equivalently significant role for the people of Myanmar. To completely understand the unique genetic variables that predispose to obesity in humans, an ongoing study of diverse obesity phenotypes and related gene mutations is necessary as our understanding of the genes causing obesity increases as a result of new findings.
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