The E23K variant of the Kir6·2 gene has been shown to be associated with type 2 diabetes mellitus in Caucasian subjects. Because offspring of type 2 diabetic patients have a genetically increased risk of developing diabetes, we sought to identify the E23K variant of the Kir6·2 gene in offspring of Caribbean patients with type 2 diabetes and assess the contribution of this variant to impaired glucose tolerance in these subjects. Forty-six offspring of patients with type 2 diabetes and 39 apparently healthy subjects whose immediate parents were not diabetic ('control') were studied after an overnight fast. Anthropometric indices were measured and blood samples were collected. Fasting and 2 h plasma glucose, insulin and lipids were subsequently determined. Insulin resistance was calculated using the homeostatic model assessment technique. The offspring and control subjects had similar frequencies of the E23K polymorphism (52·6 vs 45·5%, P>0·05) and the frequency of the E23K variant did not differ significantly between gender and ethnic distributions, irrespectively of a family history of diabetes (P>0·05). There were no significant differences in biochemical risk factors for developing diabetes in offspring carriers of the E23K variant compared with offspring non-carriers of the mutation. Offspring with the E23K mutation had even significantly higher 2 h insulin concentrations when compared with control subjects. It is concluded that the presence of the Kir6·2 E23K genotype in Caribbean subjects with an immediate positive family history of diabetes does not confer significantly higher levels of biochemical risk factors for the development of type 2 diabetes.

Reports from developing countries indicate that a rise in the socioeconomic level is a risk factor for metabolic disorders. We aimed to assess the indices of obesity, dyslipidemia, and insulin resistance among fairly literate healthy adults in a multidisciplinary institution in Trinidad. The study included 156 volunteers (46 males and 110 females, 17-40 years old). The subjects provided information on age, ethnicity, educational attainment, and occupation in self-administered, closed-ended questionnaires. Waist and hip circumferences (cm), weight (kg), and height (m) were measured. Fasting blood samples were taken for glucose, insulin, and lipid determinations in 78 subjects who volunteered for laboratory measurements. Insulin resistance was determined with homeostasis model assessment (HOMA). Of the 156 subjects studied, 83% had received tertiary education, and had no previous record of body mass index (BMI); 8% were obese, 17% were overweight, and 27% were underweight. Laboratory measurements in 78 subjects revealed 28% hypercholesterolemia and 20% hyperinsulinemia. There were no significant gender-related differences in these prevalence rates (P>0.05). The identification of obesity, underweight, hyperinsulinemia, and hypercholesterolemia in this healthy population suggests that screening for the indices of metabolic disorders in a healthy population would be potentially useful for the early identification and treatment of metabolic-related disorders.

The correlation between adiponectin and some known biochemical risk factors for developing diabetes and cardiovascular disease in the offspring of patients with diabetes warrants further study to evaluate its potential in assessing the risk of developing these disorders.

Low adiponectin levels are associated with elevated plasma alanine aminotransferase, a marker of reduced hepatic insulin sensitivity and a risk factor for type 2 diabetes. This study aims to determine the relationship between serum adiponectin level and alanine aminotransferase in diabetic and non-diabetic subjects. Fifty-six type 2 diabetic patients and 33 non-diabetic subjects participate in the study. Baseline plasma concentrations of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and glucose are measured on a chemistry analyser. Insulin and adiponectin are measured using enzyme-linked immunoassay techniques and insulin resistance is determined using the homeostatic model assessment method. Diabetic patients showed significantly lower levels of serum adiponectin than did the non-diabetic subjects, whereas levels of alanine aminotransferase and alkaline phosphatase were similar in both groups. While female non-diabetic subjects showed higher serum adiponectin levels than did female diabetic patients, alanine aminotransferase level did not differ (P>0.05). No significant relationship was seen between adiponectin and alanine aminotransferase in diabetic and non-diabetic subjects (P>0.05). Serum adiponectin levels were higher in non-diabetic subjects but there was no significant correlation between adiponectin and alanine aminotransferase in both groups of subjects. The data suggest that low serum adiponectin level may not be a suitable marker for impaired liver function in diabetic patients.

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