Document Type : Original Article
Authors
1
Diabetes and Endocrinology unit, Department of Internal Medicine, Minia School of Medicine, Minia University, Egypt.
2
Department of Internal Medicine, Minia School of Medicine, Minia University, Egypt.
3
Department of Clinical Pathology, Minia School of Medicine, Minia University, Egypt.
4
Department of Biochemistry, Minia School of Medicine, Minia University, Egypt.
Abstract
DM is one of the five principal causes of death universally. It is a growing heath problem of
multifactorial origin, understanding its genetic background might help in early detection and disease
prevention. Obesity, especially visceral adiposity, and physical inactivity are major risk factors for
diabetes in Egypt. A 2010 World Health Organization (WHO) report indicated that 30.3% of
Egyptian adults are obese. Egypt currently has the third highest prevalence of obesity in the Middle
East and North Africa (MENA) region, after Saudi Arabia and United Arab Emirates. It has been
reported that genetic variations in the promoter region regulate tumor necrosis factor-α (TNFα)
production and transcription and, they influence susceptibility to inflammatory related diseases.
Single nucleotide polymorphism studies in the promoter region of TNFα (_238) have suggested its
role in increased insulin resistance. This is a prospective case control study aimed at detecting the
impact of TNF α 238 G/A rs 361525 gene polymorphisms in T2DM in Egyptian population. It
included 40 diabetic patients, and 40 apparently healthy unrelated volunteers. We underwent history
taking, clinical examination with detection of BMI and W/H ratio, laboratory investigations, (finger
prick test, 75 gram oral glucose tolerance test, HA1C, fasting and 2hPP blood glucose, and detection
of TNF -238G/A gene polymorphisms that was performed by using PCR/RFLP method. In respect to
the distribution of TNFα 238 G/A polymorphism genotypes: In patients with T2DM it was (GG
genotype: 75%, AA genotype 5%, and GA genotype: 20%). In control it was (GG genotype: 90%,
AA genotype: 2.5%, and GA genotype: 7.5%).
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