In addition to the importance of adipose tissue (AT) mass and distribution in type 2 diabetes (T2D) etiology, there is increasing interest in AT function, including insulin resistance and inflammation. Little information is available, however, on the associations of AT insulin resistance (AT-IR) and AT inflammation with glycemic deterioration in large cohort studies. Our objective was to assess the longitudinal associations of AT-IR and inflammation with incident dysglycemia using a novel AT-IR index and sCD163, a marker of AT macrophage activation due to inflammation.


Adults ≥30 years old at-risk for T2D in the Prospective Metabolism and Islet Cell Evaluation (PROMISE) cohort (n=468) had four assessments over 9 years. AT-IR was calculated as the product of baseline serum fasting insulin and non-esterified fatty acids. Fasting serum was used to measure sCD163 as a measure of AT inflammation. Incident dysglycemia was defined as onset of impaired fasting glucose, impaired glucose tolerance, or T2D during follow-up. Associations of AT-IR and sCD163 with incident dysglycemia were estimated using generalized estimating equations (GEE) logit models, adjusted for demographic and lifestyle covariates.


Baseline AT-IR and sCD163 were moderately correlated (r=0.23, p<0.05). Further, AT-IR and sCD163 were positively correlated with BMI, waist circumference, and fasting glucose, and negatively correlated with physical activity (all p<0.05). In separate GEE models, baseline AT-IR and sCD163 were independently associated with incident dysglycemia after full adjustment (odds ratio (OR) 1.21 (95%CI, 1.15-1.29) and OR 1.04 (95%CI, 1.02-1.06), respectively). When included in the same fully adjusted model, these variables remained significantly associated with incident dysglycemia (AT-IR, OR 1.09 (95%CI, 1.06-1.12); sCD163, OR 1.07 (95%CI, 1.04-1.11)).


Our findings demonstrate that AT insulin resistance and AT inflammation are independent predictors of glycemic deterioration over time.