An adipocyte-derived peptide, adiponectin (also known as GBP28), is decreased in subjects with type 2 diabetes. Recent genome-wide scans have mapped a diabetes susceptibility locus to chromosome 3q27, where the adiponectin gene (APM1)

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In a 5-12 year follow-up study of 288 subjects with impaired glucose tolerance after a 100-g glucose load, 48 worsened to overt Type 2 (non-insulin-dependent) diabetes with the elevation of fasting blood glucose. The initial level of blood glucose was a major predictor of subsequent worsening to diabetes. In addition, subjects with a lower insulin response to glucose showed a higher incidence of worsening to the disease, irrespective of blood glucose levels. Multivariate analysis indicated that a diminished insulin response and a high maximal body weight index, as well as a high level of fasting and 2-h glucose values at the initial 100-g oral glucose tolerance test were significant independent risk factors for the development of diabetes in Japanese subjects.

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The changes in insulin response to a 100 g glucose tolerance test after treatment by diet, sulphonylurea and insulin were compared in non-ketotic diabetic patients who had fasting blood glucose concentrations higher than 160 mg/100 ml. Patients were selected so that their pre-treatment and post-treatment blood glucose levels were comparable between different treatment groups. Their insulin responses were poor initially but increased significantly when the diabetic state was improved by each treatment. The degree of improvement of insulin response was similar between different treatment groups, when their fasting blood glucose decreased below 140 mg/100 ml and the glucose tolerance curves were improved to a similar extent. Pre- and post-treatment sigma IRI values (sum of insulin values during glucose tolerance test, mean +/- SD) were 102 +/- 50 and 200 +/- 37 microU/ml in diet-treated group (n = 28), 90 +/- 40 and 195 +/- 53 microU/ml in sulphonylurea-treated group (n = 48), and 83 +/- 28 and 193 +/- 38 microU/ml in insulin-treated group (n = 13), respectively. The data suggest that the poor insulin response in overt diabetes results not only from an inherent insensitivity of B-cells to glucose but also from the metabolic derangement of diabetes. Poor insulin response and overtly diabetic metabolism seems to form a vicious cycle.

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Insulin secretory responses during the 100-gm. glucose tolerance test (GTT) were studied in subjects who had or had had glucose intolerance. Patients who had metabolic diseases other than diabetes were excluded. The ratio (AIRI/ABS) of increments of blood insulin to blood sugar 30 minutes after glucose load was used as the most sensitive index to detect the abnormality of early Insulin release In diabetes. In patients with definite diabetes (i.e., those whose fasting blood sugar values (FBS) were or had been higher than 140 mg./lOO ml. or who had diabetic retinopathy), AIRI/ABS ratios were almost invariably subnormal regardless of FBS levels and the types of glucose tolerance at the time of GTT. In the rest of the patients (equivocal diabetics), AIRI/ABS ratios were either normal or subnormal. The decrease in AIRI/ABS was a fairly stable characteristic of each individual; in 330 equivocal diabetics, only 28 cases (8.4 per cent) moved between high-and low-insulin-responder groups during the follow-up. In 39 patients who had equivocal diabetes at the Initial examination but subsequently developed definite diabetes (20 who began to have FBS above 140 mg./lOO ml. and 19 who developed retinopathy), the Insulin response were already subnormal at the initial GTT and remained low throughout the follow-up periods, although their glucose tolerance varied between normal, borderline, and diabetic types. Thus, definite diabetes occurred exclusively in the lowinsulln-responder group among equivocal diabetics. The decrease in insulin response to glucose seems to be a more Inherent, specific, and stable feature of true diabetes than glucose intolerance, because it precedes the occurrence and persists after the remission of derangement of carbohydrate metabolism in definite diabetes.DIABETES 26:944-52,October, 1977.

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