Abstract
The purpose of this screening and diagnostic study was to examine the accord among indices of glucose metabolism, including the Homeostatic Model Assessment for Insulin Resistance (HOMA), HOMA2, Matsuda Index, Quantitative Insulin-sensitivity Check Index (QUICKI), hemoglobin A1C (HbA1C), and fasting plasma glucose (FPG) against intravenous glucose tolerance test-measured insulin sensitivity (Si) in individuals with chronic motor complete SCI. Persons with chronic (≥12-months post-injury) SCI (n = 29; 79% men; age 42.2 ± 11.4; body mass index 28.6 ± 6.4 kg/m2; C4-T10) were included. Measures were compared using adjusted R2 from linear regression models with Akaike information criterion (AIC, a measure of error). QUICKI had the greatest agreement with Si (adjusted R2 = 0.463, AIC = 91.1, p = 0.0001), followed by HOMA (adjusted R2 = 0.378, AIC = 95.4, p = 0.0008), HOMA2 (adjusted R2 = 0.256, AIC = 99.7, p = 0.0030), and the Matsuda Index (adjusted R2 = 0.356, AIC = 95.5, p = 0.0004). FPG (adjusted R2 = 0.056, AIC = 107.5, p = 0.1799) and HbA1C (adjusted R2 = 0.1, AIC = 106.1, p = 0.0975) had poor agreement with Si. While HbA1C and FPG are commonly used for evaluating disorders of glucose metabolism, QUICKI demonstrates the best accord with Si compared to the other measures.
Highlights
Insulin resistance, or decreased insulin sensitivity (Si), is defined as the decreased responsiveness to the metabolic actions of insulin and the pathophysiological response to insulin-mediated glucose uptake in tissue [1,2]
Our results demonstrate Quantitative Insulin-sensitivity Check Index (QUICKI) has the strongest agreement with Si compared to Homeostatic Model Assessment for Insulin Resistance (HOMA), HOMA 2 (HOMA2), Matsuda Index, fasting plasma glucose (FPG), and hemoglobin A1C (HbA1C)
This study demonstrates a difference between the performance of clinical versus nonclinical indices of glucose metabolism
Summary
Decreased insulin sensitivity (Si), is defined as the decreased responsiveness to the metabolic actions of insulin and the pathophysiological response to insulin-mediated glucose uptake in tissue [1,2]. Cragg et al [9] and Lai et al [10] reported greater odds and adjusted hazard ratios, respectively, in persons with SCI compared to nondisabled controls, and Peterson et al [11] recently calculated an incidence almost double that of persons without SCI. These data underscore that glucose dysregulation is a profound public health issue in the SCI population that warrants universal surveillance
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