ArticleThe Journal of clinical endocrinology and metabolism2026
Effect of Osteocalcin on Insulin Sensitivity, Insulin Secretion, and β-cell Compensation in Mexican Americans.
Article in The Journal of clinical endocrinology and metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Differential Effects of Vitamin K Across Glycaemic Outcomes in Prediabetes and Type 2 Diabetes Mellitus.Nutrients · 2026Pooled it
- Osteocalcin Beyond Bone: Molecular Mechanisms, Endocrine Networks, and Translational Perspectives Across Metabolism, Neurobiology, and Chronic Disease.International journal of molecular sciences · 2026Review
- Effect of Osteocalcin on Insulin Sensitivity, Insulin Secretion, and β-cell Compensation in Mexican Americans.The Journal of clinical endocrinology and metabolism · 2026Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
contextPrevious animal studies show association between osteocalcin (OC) and type 2 diabetes-related quantitative traits (QTs), with some suggesting these effects being mediated by adipokines. Replication in humans has been inconsistent.
objectiveWe aimed to assess the association between osteocalcin and type 2 diabetes-related QTs and the roles of adipokines on the association between OC and glucose metabolism.
methodsWe used data from the BetaGene study, which is a cross-sectional family-based study of Mexican Americans from Los Angeles County. We tested the association between type 2 diabetes-related QTs and OC, including inactive (OC-inactive) and active (OC-active) forms, in 867 Mexican Americans without type 2 diabetes from 342 families. We also assessed the potential mediating effect of adipokines on these relationships.
resultsOC-active was negatively associated with insulin sensitivity (SI; P = 2.1 × 10-3) and positively associated with the insulinogenic index (P = 2.8 × 10-3). Acute insulin response was marginally significantly associated with OC-active (P = .07). Measures of β-cell compensation for insulin resistance were not associated with OC. There was no evidence of mediation by adipokines.
conclusionWe conclude OC-active is associated with SI, without mediation by adipokines or body fat. As there was no association with measures of β-cell compensation for insulin resistance, the association between OC-active and insulin secretion reflects the compensatory response to SI.
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