Abstract P289: In Africans With Abnormal Glucose Tolerance the Triglyceride-Glucose Index is a Feasible, Effective Way to Distinguish Between Beta-Cell Failure and Insulin Resistance

Abstract

Background: With the prevalence of abnormal glucose tolerance (Abnl-GT) soaring in sub-Saharan Africa, there is a growing appreciation that the major etiology of Abnl-GT in Africans may be beta-cell failure rather than insulin resistance (IR). As optimal therapy depends on etiology, distinguishing between beta-cell failure and IR is critical. However, identifying IR with formulas such as the Matsuda Sensitivity Index which requires insulin to be assayed in plasma, is expensive and rarely available in medical clinics in most African countries. Therefore, our goal was to use data from the Matsuda Index as the diagnostic standard, and determine how well the widely available, low-cost Triglyceride-Glucose Index (TyG) performs in distinguishing between beta-cell failure and IR in Africans with Abnl-GT. Methods: OGTTs and fasting triglyceride (TG) levels were obtained in 589 African immigrants living in the Washington DC area (Male: 64%, Age: 39±11, (mean±SD) range 20 -69y; BMI 27.9±4.5 kg/m 2 range 19.5-41.9). Glucose tolerance status was determined by ADA criteria for the OGTT. IR was defined as the lowest quartile of the population distribution of the Matsuda Index (≤2.89). As a primary etiology, beta-cell failure was defined as Abnl-GT in the absence of IR. Insulin secretion was calculated using the insulinogenic index. The formula for TyG was: ln(fasting glucose & fasting TG)/2. IR by TyG was defined by the highest quartile of its distribution across the cohort(≥3.38). Results: Abnl-GT occurred in 39% (228/589) of the enrollees. Among participants with Abnl-GT, the prevalence of beta-cell failure and IR were: 59% (134/228) vs. 41% (94/228), P <0.001, respectively. Compared to Africans with Abnl-GT and IR, Africans with Abnl-GT and beta-cell failure had less IR & lower insulin secretion (both P<0.001). Overall, with data from the Matsuda Index as the diagnostic standard, TyG correctly identified the etiology of Abnl-GT in 90% (205/228) of the participants with Abnl-GT, specifically 93% (125/134) with beta-cell failure and 85% (80/94) of participants with IR. Conclusions: As the TyG correctly identified the etiology of Abnl-GT in 90% of Africans, it may be a feasible, economically viable alternative to the Matsuda Index in determining whether Africans with Abnl-GT have beta-cell failure or IR. With correct information about Abnl-GT etiology, therapy for can be optimized.