👤 Batakeh B Agoons

Introduction Insulin resistance (IR) and pancreatic B-cell dysfunction are fundamental disorders in the pathogenesis of type 2 diabetes. Recent evidence suggests that apolipoprotein B (Apo-B) may be related to the onset of type 2 diabetes. However, the mechanism explaining this association is unclear. Methods We analyzed data from 4888 normoglycemic adults pooled from the 2007-2016 National Health and Nutrition Examination Survey (NHANES). Participants were categorized by tertiles of Apo-B, and the main outcome measures were IR and pancreatic β-cell function ascertained by homeostasis model assessment for insulin resistance (HOMA-IR) and homeostasis model assessment for beta cell function (HOMA-β), respectively. Poisson and linear regressions were used to generate prevalence ratios (PRs) and β coefficients for IR and β-cell function, respectively. Results Among 4888 participants, the mean Apo-B was 0.85 ± 0.2 g/L, and 532 (10.8%) had IR. After adjusting for demographic variables, the PRs (95% CI) for IR comparing higher tertiles (T2 and T3) with the lowest tertile (T1) of Apo-B were 1.49 (1.19-1.88) and 1.92 (1.54-2.39), respectively. There was a significant increase in log HOMA-β for T2 and T3 compared to T1 of Apo-B, after adjusting for demographic variables (β 0.05 (95% CI: 0.01-0.09) and β 0.15 (95% CI: 0.11-0.19), respectively). Additional adjustment for lifestyle and metabolic variables did not change the significance of these findings. There was a significant graded increase in log HOMA-IR and HOMA-β from T2 to T3 (P for trend <0.001). Conclusion Apo-B was associated with increased IR and pancreatic β-cell function in normoglycemic adults independently of traditional risk factors for diabetes. These findings suggest that Apo-B may be associated with the development of glycemic dysregulation. Show less