J A Marshall1, S Hoag, S Shetterly, R F Hamman. 1. Department of Preventive Medicine and Biometrics, University of Colorado Health Sciences Center, Denver 80262.
Abstract
OBJECTIVE: To determine if dietary fat intake measured at a baseline exam in subjects with impaired glucose tolerance (IGT) predicted the subsequent development of non-insulin-dependent diabetes mellitus (NIDDM). RESEARCH DESIGN AND METHODS: Based on an oral glucose tolerance test (OGTT) (World Health Organization criteria), we identified 134 eligible subjects with IGT from a geographically based sample of subjects with no prior history of diabetes. One to three years after the baseline exam, 123 subjects (92%) had a repeat OGTT. Diet was assessed by a 24-h diet recall reported before the baseline OGTT. RESULTS: The mean percentage of energy eaten as fat was 43.4% in 20 people subsequently developing NIDDM compared with 40.6% in 43 people remaining IGT and 38.9% in 60 subjects who subsequently reverted to normal glucose tolerance. In comparing the 20 subjects who developed NIDDM with the 103 who remained IGT or normal, an increase in fat intake of 40 g/day was associated with an increase in risk of NIDDM of 3.4-fold (95% confidence interval [CI] 0.8-13.6) adjusted for energy intake, age, sex, ethnicity, and obesity. The odds ratio increased to sixfold (95% CI 1.2-29.8) after adjustment for fasting glucose, insulin, and 1-h insulin. CONCLUSIONS: Fat consumption significantly predicts NIDDM risk in subjects with IGT after controlling for obesity and markers of glucose metabolism.
OBJECTIVE: To determine if dietary fat intake measured at a baseline exam in subjects with impaired glucose tolerance (IGT) predicted the subsequent development of non-insulin-dependent diabetes mellitus (NIDDM). RESEARCH DESIGN AND METHODS: Based on an oral glucose tolerance test (OGTT) (World Health Organization criteria), we identified 134 eligible subjects with IGT from a geographically based sample of subjects with no prior history of diabetes. One to three years after the baseline exam, 123 subjects (92%) had a repeat OGTT. Diet was assessed by a 24-h diet recall reported before the baseline OGTT. RESULTS: The mean percentage of energy eaten as fat was 43.4% in 20 people subsequently developing NIDDM compared with 40.6% in 43 people remaining IGT and 38.9% in 60 subjects who subsequently reverted to normal glucose tolerance. In comparing the 20 subjects who developed NIDDM with the 103 who remained IGT or normal, an increase in fat intake of 40 g/day was associated with an increase in risk of NIDDM of 3.4-fold (95% confidence interval [CI] 0.8-13.6) adjusted for energy intake, age, sex, ethnicity, and obesity. The odds ratio increased to sixfold (95% CI 1.2-29.8) after adjustment for fasting glucose, insulin, and 1-h insulin. CONCLUSIONS: Fat consumption significantly predicts NIDDM risk in subjects with IGT after controlling for obesity and markers of glucose metabolism.
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