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Clinical Science| Volume 62, ISSUE 6, P786-792, June 2013

Nondiabetic patients with either subclinical Cushing's or nonfunctional adrenal incidentalomas have lower insulin sensitivity than healthy controls: Clinical implications

Published:January 18, 2013DOI:https://doi.org/10.1016/j.metabol.2012.12.006

      Abstract

      Objective

      The aim of this study was to estimate insulin sensitivity (IS) in nondiabetic patients with adrenal incidentalomas (AI): nonfunctional adrenal incidentalomas (NAI) and patients with AI and subclinical Cushing's syndrome (SCS).

      Methods

      Based on the inclusion criteria (normal fasting glucose levels, no previous history of impaired fasting glucose and/or diabetes, and no medications or concomitant relevant diseases) and the exclusion criteria (pheochromocytoma, overt hypercortisolism, hyperaldosteronism, adrenal carcinoma, metastasis of extra-adrenal tumors, extra-adrenal malignancies), 142 subjects were drawn from a series of patients with AI. The subjects were age-, sex- and body mass index (BMI)-matched: 70 with NAI (50 women and 20 men), 37 with AI and SCS (31 women and 6 men) and 35 healthy control (HC) subjects (30 women and 5 men).
      The oral glucose tolerance test (OGTT) and several indices of insulin sensitivity (IS) were used: homeostasis model assessment (HOMA), quantitative insulin sensitivity check index (QUICKI), triglycerides and glucose index (TyG), index of whole-body insulin sensitivity (ISI-composite) and glucose to insulin ratio (G/I).

      Results

      There was a significant difference in IS between subjects with NAI and HC (HOMA, p=0.049; QUICKI, p=0.036; TyG, p=0.002; ISI-composite, p=0.024) and subjects with SCS and HC (AUC insulin, p=0.01; HOMA, p=0.003; QUICKI, p=0.042; TyG, p=0.008; ISI-composite, p=0.002). There was no difference in the tested indices of IS between subjects with NAI and SCS (p>0.05). However, subjects with SCS had a significantly higher prevalence of impaired glucose tolerance and higher area under the curve for glucose than subjects with NAI (p=0.0174). The linear regression analysis showed that 1 mg-DST cannot be used as a predictor of HOMA (R2=0.004, F=0.407, p=0.525). Significant relationship was found between 1 mg-DST and ISI-composite (R2=0.042, F=4.981, p=0.028) but this relationship was weak and standard error of estimate was high. The linear regression model also showed that ACTH cannot be used as a predictor of HOMA (R2=0.001, F=0.005, p=0.943) or ISI-composite (R2=0.015, F=1.819, p=0.187).

      Conclusions

      Insulin resistance is a major cardiovascular risk factor; therefore, the assessment of IS in patients with AI, even nonfunctional, has a valuable place in the endocrine workup of these patients.

      Abbreviations:

      AI (adrenal incidentalomas), SCS (subclinical Cushing's syndrome), NAI (nonfunctional adrenal incidentaloma), HC (healthy control), IS (insulin sensitivity), IR (insulin resistance), HOMA (homeostasis model assessment), QUICKI (quantitative insulin sensitivity check index), G/I (glucose to insulin ratio), TyG (the product of triglycerides and glucose), ISI-composite (whole-body insulin sensitivity), OGTT (oral glucose tolerance test), ACTH (adrenocorticotrophic hormone), IGT (impaired glucose tolerance), IFG (impaired fasting glucose), 1mg-DST (overnight low dose dexamethasone suppression test), MSC (midnight serum cortisol), AUC (area under the curve), BMI (body mass index), CV (coefficient of variance)

      Keywords

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