Background. Type 2 diabetes mellitus (T2DM) is the most common metabolic disorder and its pathogenesis is characterized by a combination of peripheral insulin resistance and impaired insulin secretory capacity of pancreatic β cell. Genetic predisposition interacts with environmental factors including diet, physical activity, and age leading to the development of diabetes.Objective. To determine the proportion of overweight and obese persons with type 2 diabetes and to compare the fasting blood sugar, fasting serum insulin, insulin resistance and β-cell function in G972R carrier and non-carrier overweight and obese persons with type 2 diabetes.Methodology. One hundred overweight and obese patients with T2DM were recruited from persons with diabetes attending the Diabetes Outpatient Department of Yangon General Hospital. History taking and physical examination were done and blood samples were collected. Plasma glucose level was determined by the glucose oxidase method and fasting serum insulin was measured by enzyme linked immunoassay (ELISA) kit method. Polymerase chain reaction and Restriction Fragment Length Polymorphism were done for genetic polymorphism.Results. Among 100 overweight and obese subjects with T2DM, 81 patients were of homozygous (G/G) genotype, 18 patients were of heterozygous (G/A) and only one patient of homozygous (A/A) genotype. There was no statistically significant difference in the proportion of genotypes between overweight and obese subjects with T2DM.There was no significant difference in fasting blood sugar (FBS), fasting serum insulin, HOMA-IR, β-cell function, lipid parameters between IRS-1 (G972R) carriers and non-carriers. There is significant negative correlation between insulin resistance and TG level (r 2 =0.0529, p=0.01). Conclusion.It was concluded that IRS-1 G972R polymorphism was not important in insulin resistance, β-cell function and lipid parameters in overweight and obese T2DM. There could be a number of candidate genes in the pathophysiology of diabetes mellitus, genetic sequencing of IRS-1 and other genes in the insulin signaling pathway, and finding out the alteration in their genetic patterns would provide clues for the association of the site-specific polymorphisms of these genes with insulin resistance in T2DM.

Background: Thalassemia constitutes a major public health problem causing a significant burden on children and their families. Zinc deficiency plays an important role in many thalassemia-related complications like growth retardation, hypogonadism and delayed puberty which are frequently noted in adolescent age. Although zinc is supplemented to thalassemic patients visiting Day Care Center, Yangon Children Hospital (YCH), Myanmar, a report concerning serum zinc level of these patients is still lacking. This study, therefore, aimed to assess serum zinc status in thalassemic adolescents attending Day Care Center, YCH. Materials and Methods: This hospital-based cross-sectional study was conducted on 99 thalassemic adolescents. Mean age of diagnosis was 5.1±2.1 years. Non-fasting serum zinc concentration was determined by atomic absorption spectrophotometry. According to National Health and Nutrition Examination Survey data, zinc deficiency was defined as serum zinc concentration < 66 μg/dL (female) and < 70 μg/dL (male). Results: Serum zinc concentration (μg/dL) was 57.35 (47.30-80.14) (median, interquartile range) with maximum, 195.05 and minimum, 28.83. Zinc deficiency was observed in 69.7% (69 out of 99; 35 males and 34 females) of the patients. The associations of zinc deficiency with gender, phenotype and the use of chelator were non-significant (P>0.05). Conclusion: In spite of zinc supplementation, nearly 70% of the thalassemic adolescents showed zinc deficiency. Zinc deficiency in these adolescents might not be related to gender, phenotypes or the use of chelator. Poor compliance to take zinc supplementation and/or irregular blood transfusion could partly be attributable to zinc deficiency in these adolescents. Providing health education on the importance of regular intake of adequate zinc is advisable and periodic evaluation of zinc levels is recommended for thalassemic adolescents.

Aim: Type 2 diabetes mellitus (T2DM) is the most common metabolic disorder and its pathogenesis is characterized by a combination of peripheral insulin resistance and impaired insulin secretary capacity of pancreatic β cell. Over the years, there has been increasing deaths from T2DM. In Myanmar, there is little information on its causes, due to few published data on the prevalence of MS and its association with T2DM. This study aims at identifying the metabolic risk markers leading to MS in T2DM, as well as the impact of MS on the insulin resistance.Methods: Hundred T2DM patients were recruited from Diabetic Clinic, Yangon General Hospital. The clinical evaluation consisted of waist circumference, blood pressure, height and weight measurements; the biochemical analysis included determination of fasting plasma glucose, serum insulin and fasting lipid profile. Plasma glucose level was determined by the glucose oxidase method and fasting serum insulin was measured by enzyme linked immunoassay (ELISA) kit method. Insulin resistance (HOMA IR) was calculated using formula by Matthews et al in 1985. Metabolic syndrome was defined as International Diabetes Federation (IDF) criteria. Results:In the present study, MS was not significantly associated with insulin resistance (84.72% in the insulin resistance group vs 75% in the non-insulin resistance group). There were no significant differences in metabolic risk markers between the insulin resistance and non-insulin resistance groups. Present study showed 80% of insulin resistance male patients and 85% of insulin resistance female patients had MS, and also 83% of non-insulin resistance male patients and that of female patients had 64% of MS, respectively. There was no significant association between each group. Conclusion:Metabolic syndrome was found in 83 patients in the present study, and of which 61 patients were found to show insulin resistance. Metabolic syndrome was not significantly associated with presence or absence of insulin resistance.