Insulin Secretion and Insulin Sensitivity Pattern Is Different in Isolated Impaired Glucose Tolerance and Impaired Fasting Glucose

Abstract

OBJECTIVE -Isolated impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) are two risk categories for type 2 diabetes. This study compared both categories with respect to the degree of insulin secretion abnormalities and insulin resistance. RESEARCH DESIGN AND METHODS-This is a crossover comparison of a population at high risk for type 2 diabetes. The subjects were recruited from the Risk Factor in Impaired Glucose Tolerance for Atherosclerosis and Diabetes (RIAD) study. They underwent a 75-g oral glucose tolerance test, with measurement of specific insulin, C-peptide, proinsulin, and free fatty acids at baseline and every 30 min after load for 2 h. Factor analysis was performed to evaluate the importance of insulin resistance and secretion abnormalities in both categories.RESULTS -All categories of prediabetic hyperglycemia had a higher cardiovascular risk factor level when adjusted for sex, age, and BMI compared to control subjects with normal glucose tolerance. Subjects with isolated IFG were more insulin resistant than those with IGT. By contrast, subjects with isolated IGT exhibited a more severe deficit in early-and late-phase insulin secretion versus IFG subjects. As shown with factor analysis, in IFG the insulin resistance factor explained 28.4% of the variance, whereas in IGT the insulin secretion factor was dominant, explaining 31.1% of the total variance. CONCLUSIONS -Our cross-sectional data from the RIAD study demonstrate that isolated IFG and isolated IGT are different with respect to the degree of insulin resistance and anomalies in insulin secretion, and that subjects with IGT exhibit a deficit in the early and late phases of insulin secretion. This finding may be important for a differential approach in primary prevention of type 2 diabetes.

Differential relationship between physical activity and progression to diabetes by glucose tolerance status: the Inter99 Study

“…These findings suggest that individuals with i-IFG are characterised by predominantly hepatic insulin resistance compared with individuals with i-IGT, who have predominantly muscle insulin resistance. This is in accord with previous studies [12][13][14]16].…”

“…Although i-IFG and i-IGT both represent intermediate stages of glucose intolerance and are insulin-resistant states with impaired beta cell function, they are distinct conditions with different pathophysiological aetiologies [12][13][14][15]. Clinical studies suggest that the site of insulin resistance varies between the two disorders.…”

Different contributions of insulin resistance and beta‐cell dysfunction in overweight Israeli Arabs with IFG and IGT

“…Our results are consistent with other studies performed in other populations, which found that an increase in insulin resistance is the principal defect observed in subjects with IFG, while impairment in beta-cell function is the major pathology that leads to the development of IGT [8][9][10][11]. However, some other studies found opposite results [12][13][14].…”

“…Studies that aimed to clarify this question had conflicting results. Some studies reported an increase in insulin resistance as the main contributor to the development of IFG, while IGT was associated with impairment of betacell function [8][9][10][11]. Other studies demonstrated that subjects with IFG had mainly a reduction in insulin secretion, while IGT subjects had a reduction in insulin sensitivity [12][13][14].…”

Insulin sensitivity, insulin release and glucagon-like peptide-1 levels in persons with impaired fasting glucose and/or impaired glucose tolerance in the EUGENE2 study

“…Previous studies have given conflicting data on the association of IFG and IGT with insulin resistance and impaired insulin secretion [10][11][12][13][14][15][16][17][18][19][20]. In a study of Pima Indians, participants with isolated IFG and isolated IGT showed similar impairments in insulin sensitivity, but those with isolated IFG had a more pronounced defect in early insulin release and higher endogenous glucose output [10].…”