Abstract
People with type 1 diabetes mellitus (T1D) have reduced insulin sensitivity (IS), which partially explains their increased risk of cardiovascular disease. However, there is limited data on how weight gain alters IS in T1D, and so this study aimed to analyze the effect of weight change on IS components in T1D and non-diabetic (non-DM) adults. This study included 1133 adults (T1D=528 and non-DM n=605) with a mean ± SD age of 38 ± 9 years from the Coronary Artery Calcification in Type 1 Diabetes cohort, examined at baseline and after 6.2±0.6 years. Weight change was categorized as follows: weight loss (WL), lost > 2%), weight stable (WS), within 2% of baseline, and weight gain (WG), > 2%. Estimated IS (eIS) was calculated by a model derived from a clamp study (Table) at each visit. Multiple age and sex adjusted least squares means were calculated by weight change group and diabetes status, and progression of coronary artery calcium (CAC) was examined by logistic regression. There was a significant improvement in eIS in the T1D WL group, along with a greater reduction in triglycerides and insulin dose and increase in adiponectin compared to the other weight change groups (Table). There was significant increase in eIS among the non-DM WL group, along with a reduction in triglycerides, fasting glucose, HbA1c and DBP and an increase in adiponectin. For each 2% increase in weight, the odds ratio (OR) for progression of CAC was 1.23 (95% CI 1.1-1.4, p=0.002), after adjusting for age, sex, diabetes status, and baseline BMI and CAC. The odds of CAC progression were decreased by 40% (OR 0.6, 95% CI 0.5-0.8, p=0.0007) for each SD increase in eIS, adjusting for the same variables. In conclusion, over 6 years of follow-up, weight loss increased eIS and related factors in both people with and without T1D, but was not associated with improved Hba1c in T1D. Additionally, weight gain was associated with a greater risk and eIS with a lower risk for CAC progression, demonstrating the importance of avoiding weight gain in prevention of subclinical cardiovascular disease.
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