Insulin resistance (IR) in type 1 diabetes mellitus (T1D) has significant cardiovascular and metabolic implications. Hypovitaminosis D has been linked to IR in various populations; however, its relationship with insulin sensitivity in T1D remains unclear. This review aimed to investigate the association between hypovitaminosis D and IR in individuals with T1D. Vitamin D may enhance glucose metabolism by protecting pancreatic β-cells, and therefore, insulin secretion. Animal studies and clinical trials have suggested that vitamin D supplementation improves β-cell survival and can slow disease progression when initiated soon after T1D diagnosis. Nevertheless, its impact on insulin secretion in established T1D is limited because of significant β-cell loss at diagnosis. Moreover, vitamin D can improve insulin sensitivity by attenuating renin-angiotensin system activity, enhancing insulin receptor expression, activating metabolic pathways such as peroxisome proliferator-activated receptor delta, and reducing inflammation by downregulating proinflammatory cytokines associated with IR. Studies have demonstrated an inverse relationship between serum 25-hydroxyvitamin D (25[OH]D) levels and IR in T1D, with higher vitamin D levels being associated with reduced IR odds across various age groups. However, factors such as the body mass index may influence this relationship, particularly in younger populations, indicating complex interactions. Despite preliminary evidence, the link between hypovitaminosis D and IR in T1D remains underexplored. The evidence reviewed in this work underscores the need for further research to clarify this relationship and explore the detailed mechanisms involved.

Insulin resistance in type 1 diabetes: is there a role for vitamin D? A systematic review of the evidence

Maria Grazia Tarsitano;Caterina Conte
2025-01-01

Abstract

Insulin resistance (IR) in type 1 diabetes mellitus (T1D) has significant cardiovascular and metabolic implications. Hypovitaminosis D has been linked to IR in various populations; however, its relationship with insulin sensitivity in T1D remains unclear. This review aimed to investigate the association between hypovitaminosis D and IR in individuals with T1D. Vitamin D may enhance glucose metabolism by protecting pancreatic β-cells, and therefore, insulin secretion. Animal studies and clinical trials have suggested that vitamin D supplementation improves β-cell survival and can slow disease progression when initiated soon after T1D diagnosis. Nevertheless, its impact on insulin secretion in established T1D is limited because of significant β-cell loss at diagnosis. Moreover, vitamin D can improve insulin sensitivity by attenuating renin-angiotensin system activity, enhancing insulin receptor expression, activating metabolic pathways such as peroxisome proliferator-activated receptor delta, and reducing inflammation by downregulating proinflammatory cytokines associated with IR. Studies have demonstrated an inverse relationship between serum 25-hydroxyvitamin D (25[OH]D) levels and IR in T1D, with higher vitamin D levels being associated with reduced IR odds across various age groups. However, factors such as the body mass index may influence this relationship, particularly in younger populations, indicating complex interactions. Despite preliminary evidence, the link between hypovitaminosis D and IR in T1D remains underexplored. The evidence reviewed in this work underscores the need for further research to clarify this relationship and explore the detailed mechanisms involved.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.12078/29266
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