This study examines the prevalence of, and risk factors for, diabetic retinopathy in Asian Indian, Chinese, and Creole Mauritians in whom there is an increasing prevalence of non-insulin-dependent diabetes mellitus (NIDDM). As part of a population-based survey on the Indian Ocean island of Mauritius in 1992, glucose tolerance was classified using a 75-g oral glucose tolerance test on 6,553 persons. Subjects with newly diagnosed (n = 358) or known diabetes (n = 388), and a random sample of one in four subjects with impaired glucose tolerance (n = 165), had stereoscopic 45 degrees retinal photographs taken of three fields in the right eye after mydriasis. Photographs were graded according to a modified version of the Airlie House criteria. The prevalence of nonproliferative and proliferative retinopathy was: 14.5% and 0.3%, respectively, in newly diagnosed diabetic subjects; 42.0% and 2.3%, respectively, in known diabetic subjects; and 9.1% and 0%, respectively, in persons with impaired glucose tolerance. Muslim Indians had the lowest prevalence of retinopathy (10.8% and 34.0% for new and known diabetes, respectively), but after adjusting for other factors, this was significantly different only to Creoles (18.8% and 53.8%, respectively). Univariate analysis revealed significant differences between diabetic subjects with and without retinopathy in mean age, body mass index, fasting and 2-hour plasma glucose levels, systolic and diastolic blood pressure, fasting triglycerides, serum creatinine, and urinary albumin levels. For known diabetes, mean duration of diabetes and the proportion using insulin were also greater in those with retinopathy. Multivariate analysis using logistic regression confirmed that increasing duration of diabetes, fasting plasma glucose, systolic blood pressure, and urinary albumin concentration, and decreasing body mass index, were independently associated with retinopathy. The high prevalence of diabetic retinopathy observed in all major ethnic groups in Mauritius portends a serious public health problem, given the relative recency of the NIDDM epidemic in that country and the limited resources for laser photocoagulation. Strategies to minimize this problem among those already known to have diabetes should include strict control of plasma glucose and blood pressure.

Diabetic retinopathy and albuminuria are common in Polynesian Western Samoans. Duration of diabetes and level of glycemia were the most important associated factors. These data underline the need for cost-effective programs for the detection and early treatment of diabetes in Western Samoa and other developing populations with high susceptibility to NIDDM.

The proportion of pyruvate dehydrogenase complex in the active, dephosphorylated form was decreased (compared with lean controls) in heart muscle in gold thioglucose-treated obese hyperinsulinaemic mice, and the extent of enzyme inactivation was significantly linearly correlated with both body weight and body fat content. A single oral dose (25 mg/kg body wt.) of the beta-oxidation inhibitor 2-tetradecylglycidic acid to obese animals restored pyruvate dehydrogenase complex activity to that of lean controls. It is suggested that increased fatty acid oxidation may be a major factor in mediating the phosphorylation and inactivation of pyruvate dehydrogenase complex in mouse heart muscle in obesity, and this may represent an important mechanism in the development and/or expression of insulin resistance in respect of abnormalities of cellular glucose homoeostasis in these animals.

Phosphorylation of the insulin receptor of isolated rat adipocytes in response to insulin has been studied. Immunoprecipitation of adipocyte membrane protein demonstrated increased incorporation of 32P after exposure to insulin for 15 min, but this was dependent on the presence of physiological concentrations of Ca2+ and Mg2+. Autoradiography of solubilized immunoprecipitated membrane protein after sodium dodecyl sulphate/polyacrylamide-gel electrophoresis revealed that most of the 32P incorporation occurred in a band corresponding to Mr 95 000, which has been identified previously as the beta-subunit of the insulin receptor. 32P incorporation was inhibited by 2,4-dinitrophenol and trifluoperazine. It is suggested that insulin-receptor phosphorylation is an energy-requiring process that is Ca2+-dependent and may be modulated by calmodulin. Phosphorylation may proceed independently of glucose transport.

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