Association of G22A polymorphism of adenosine Deaminas with obesity in an Iranian population
- سال انتشار: 1395
- محل انتشار: اولین کنگره پزشکی شخصی
- کد COI اختصاصی: IPMCMED01_166
- زبان مقاله: انگلیسی
- تعداد مشاهده: 446
نویسندگان
Obesity and Eating Habits Research Center, Endocrinology and Metabolism Molecular -Cellular Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran
Metabolic Disorders Research Center, Endocrinology and Metabolism Molecular -Cellular Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran
Metabolic Disorders Research Center, Endocrinology and Metabolism Molecular -Cellular Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran
چکیده
Obesity is an important clinical and public health challenge and defined as an excess adipose tissue accumulation resulting from an imbalance in energy intake and energy expenditure. It is a forerunner for a variety of other disease such as type-2-diabetes, cardiovascular disease and can be fatal leading to premature death. Obesity is highly heritable and arises from the interplay of multiple genes and environmental factors. Adenosine deaminase, a key enzyme in purine metabolism, regulates extracellular and intracellular concentrations of adenosine by irreversible deamination of adenosine into inosine. ADA, present in all mammalian cells and its primary function in humans is development, differentiation, and maturation of the lymphoid system. ADA is encoded by the polymorphic ADA gene, which is located on chromosome 20q13.11. One of the commonest single nucleotide polymorphisms of ADA gene is the SNP G22A in exon1. This SNP results in the substitution of Asp amino acid (G allele) with Asn (A allele) amino acid in position 8 of the enzyme. The aim of the present study was to investigate the association between SNP G22A in the ADA gene with the obesity.کلیدواژه ها
obesity, adenosine deaminas (ADA), G22A polymprphismاطلاعات بیشتر در مورد COI
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