Prevalence and pathophysiology of impaired glucose tolerance in three different high-risk white groups

Page, R. C.L., Walravens, E. K.N., Levy, J. C., Stratton, I. M. and Turner, R. C. (1993) Prevalence and pathophysiology of impaired glucose tolerance in three different high-risk white groups. Metabolism, 42 (8), 932-938. (doi:10.1016/0026-0495(93)90003-7).

Abstract

Insulin resistance and β-cell function were assessed by a continuous infusion of glucose in the following three groups of white subjects at risk of developing impaired glucose tolerance and diabetes: 41 subjects who were the offspring of patients with type II diabetes, 26 general-population subjects with an increased fasting plasma glucose level of at least 5.6 mmol/L on screening, and 22 subjects who had had gestational diabetes but were now nondiabetic. Subjects had a mean (± 1 SD) age of 43 ± 9 years and a body mass index (BMI) of 27 ± 5 kg/m². Subjects with previously increased fasting glucose levels were significantly more insulin resistant than a control group, taking into account BMI, age, and gender (% normal insulin sensitivity [%S], 59 [50 to 79] v 87 [73 to 96]; P < .005), and previously gestationally diabetic subjects showed greater impairment of β-cell function (% normal β-cell function [%β], 69 [60 to 87] v 97 [89 to 105]; P < .005). Diabetes (defined by World Health Organization criteria) or impaired glucose tolerance (defined as an achieved plasma glucose concentration [APG]>95th percentile of an age-and weight-matched population) was identified in 22% of family members, 31% of fasting hyperglycemic subjects, and 41% of previously gestationally diabetic subjects. Twenty-two subjects with impaired glucose tolerance from all the groups were compared with their normoglycemic counterparts and were characterized by greater obesity (29 ± 7 v 25 ± 3 kg/m², P < .05), impaired insulin sensitivity [%S, 46 [23 to 78] v 81 [51 to 128]; P < .001), impaired β-cell function (%β, 83 [63 to 110] v 95 [65 to 141]; P < .05), and decreased suppression of nonesterified fatty acids ([NEFA] 40 [38 to 50] v 66 [50 to 77] % decrease in NEFA, P < .001). After taking into account BMI, gender, and age, the decrease in β-cell function of the impaired-glucose tolerance group was more apparent (P < .01) and there continued to be a difference in insulin sensitivity, implying non-obesity-associated insulin resistance in the impaired-glucose tolerance group (P < .001). In conclusion, although subjects with impaired glucose tolerance from each of the three different at-risk groups showed similar phenotypic characteristics with obesity being a major feature, we have identified in a single study using a single investigative technique more marked impairment of β-cell function in previously gestationally diabetic subjects and more insulin resistance in subjects with a previously increased fasting plasma glucose level. Impaired glucose tolerance is thus a multifactorial disease in which genetic or environmental contributions vary between different at-risk groups and between different individuals.

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Contributors

Author: I. M. Stratton

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