Abstract
The objective of the present study was to identify the association of the TNF-α- 308G/A and leptin receptor (LEPR) Gln223Arg polymorphisms with the risk of development of type 2 diabetes mellitus (T2DM). Methods: A total of 160 volunteers were studied: 108 with T2DM and 52 participants as control, who served as the control group. Polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) for the genomic region of TNF-α- 308G/A and LEPR Gln223Arg were carried out. Results: The frequency of LEPR Gln223Arg genotypes in T2DM and control groups showed significant differences in the distribution of genotypes (p < 0.05). The frequency also of TNF-α- 308G/A genotypes in T2DM and control subjects showed significant differences in the distribution of genotypes (p < 0.05). Conclusion: Our results indicate that there are significant differences in the distribution of genotypes and alleles between the individuals with T2DM and control subjects (p < 0.05).
Highlights
Type 2 diabetes mellitus (T2DM) is characterized as a disorder of impaired energy metabolism caused by insufficient insulin production and/or decreased insulin sensitivity.The etiology remains unclear but many environmental and polygenic factors may contribute to the development of type 2 diabetes mellitus (T2DM)
All volunteers with GHbA1c > to 7.5% were considered as people with type 2 diabetes mellitus, while GHbA1c levels with normal fasting blood sugar levels and without any abnormal measurements in the past history were accepted as non-diabetic participants
We reported an association between the leptin receptor gene Q223R polymorphism and the Tumor necrosis factor-α (TNF-α) -308G/A in a sample of T2DM volunteers
Summary
Type 2 diabetes mellitus (T2DM) is characterized as a disorder of impaired energy metabolism caused by insufficient insulin production and/or decreased insulin sensitivity.The etiology remains unclear but many environmental and polygenic factors may contribute to the development of T2DM. Adipose tissue is a very active endocrine organ, secreting a number of hormones, such as adiponectin, leptin, resistin and visfatin, collectively with classical cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). All these adipocytokines play significant role in the regulation of energy metabolism, the metabolism of glucose and lipids, reproduction, cardiovascular function and immunity [3]. TNF-α plays a critical role in several autoimmune diseases, such as rheumatoid arthritis, and may mediate obesity-linked insulin resistance in type 2 diabetes. Upregulated expression of TNF-α plays a significant role in the induction of insulin resistance linked with obesity and
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