ArticleCureus2025
Apolipoprotein B and Glycemic Indices in Normoglycemic Adults: Analysis of the National Health and Nutrition Examination Survey, 2007-2016.
Article in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Apolipoprotein B in cardiovascular risk assessment: beyond traditional lipid markers.Frontiers in cardiovascular medicine · 2026Review
- Associations of apolipoprotein A1, apolipoprotein B, and their ratio with novel cardiometabolic indices in adults with coronary artery disease.Frontiers in cardiovascular medicine · 2026Article
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Authors and funding
2 authors.
Funding
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Abstract
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.
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