Hypovitaminosis D and Insulin Resistance in Type 1 Diabetes Mellitus: A Systematic Review of Clinical and Mechanistic Evidence

Type 1 diabetes mellitus (T1DM) involves autoimmune β-cell destruction, but insulin resistance may also influence disease outcomes. Vitamin D modulates insulin sensitivity and immune function, and hypovitaminosis D is common in T1DM. This systematic review evaluates clinical and mechanistic evidence on the association between hypovitaminosis D and insulin resistance in T1DM. A Preferred Reporting Items for Systematic Reviews and Meta‑Analyses (PRISMA) framework was applied for a systematic search of PubMed®, BMJ Journals, Scopus®, IEEE Xplore®, and Web of Science™, including articles published until 7 March 2026. Studies assessing vitamin D status and insulin resistance measures in T1DM populations were included. Risk of bias was evaluated using the Cochrane Risk of Bias 2 tool and the Newcastle-Ottawa Scale. Narrative synthesis was performed due to methodological heterogeneity. Eight studies (one controlled trial, two prospective cohorts, and five cross-sectional) were included. Hypovitaminosis D prevalence ranged from 47 to 79%. Six studies reported significant associations between low vitamin D levels and markers of insulin resistance, including a positive correlation with estimated glucose disposal rate (eGDR), as well as associations with higher insulin requirements and greater odds of insulin resistance. Mechanistic studies demonstrated preserved β-cell function with sufficient vitamin D and identified vitamin D receptor (VDR) polymorphisms as effect modifiers. Supplementation trials showed conflicting results, and longitudinal analysis revealed no significant association over time. Risk of bias was low in one study, good in five, and fair in two. Hypovitaminosis D is prevalent in T1DM and associated with insulin resistance in cross-sectional studies, with supportive mechanistic evidence. However, interventional and longitudinal data remain inconsistent. Vitamin D may be a marker of metabolic dysregulation, but its therapeutic role in improving insulin resistance requires further robust investigation.