New research suggests that vitamin D supplementation may improve blood sugar control and reduce inflammation in type 2 diabetes, offering a promising addition to current treatments.
Study: Vitamin D Supplementation: Shedding Light on the Role of the Sunshine Vitamin in the Prevention and Management of Type 2 Diabetes and Its Complications. Image Credit: Natalya Bardushka/Shutterstock.com
A recent study published in Nutrients reviewed the role of vitamin D (VD) in type 2 diabetes mellitus (T2DM) management and prevention.
Background
Diabetes is among the major causes of morbidity, premature death, and severe outcomes like kidney failure and amputation, among others. T2DM accounts for over 90% of diabetes cases, mounting a significant burden on healthcare systems.
It is characterized by pancreatic β-cell malfunction and insulin sensitivity. VD has gained considerable attention for its pleiotropic effects beyond skeletal health.
Deficient VD levels are reported to elevate the risk of diabetes. Further, VD is speculated to exert anti-diabetic properties through various mechanisms. While studies support its role in glucose homeostasis, findings remain inconsistent.
As such, in the present study, researchers investigated the protective effects of VD on pancreatic β-cells, focusing on the benefits of VD on glycemic control and diabetes.
VD and diabetes
VD is well known for its role in calcium metabolism, and VD deficiency can lead to impaired bone development. However, VD’s role in improving insulin sensitivity and β-cell function is less recognized.
VD stimulates insulin secretion by activating β-cell VD receptors (VDRs). Further, VD supplementation improves glycated hemoglobin (HbA1c) and fasting glucose levels and reduces T2DM risk.
A meta-analysis confirmed that VD sufficiency helps mitigate cellular pathology associated with insulin resistance. This is achieved by sustaining minimal levels of radicals and reactive species, reducing pro-inflammatory cytokines, increasing anti-inflammatory cytokines, and facilitating normal calcium signaling.
The binding of 1,25-dihydroxyvitamin D, the active form of VD, to VDRs activates genes responsible for the growth of β-cells, glucose transport, and insulin synthesis. VD also influences insulin secretion via non-genomic mechanisms. It depolarizes β-cell membranes, opening calcium channels and increasing calcium influx, which triggers insulin release.
VD supplementation for glycemic control
Various studies have reported on the effects of VD supplementation on HbA1c levels. A randomized controlled trial (RCT) observed decreased HbA1c levels following VD administration. Another trial revealed significantly reduced HbA1c with combined VD and calcium intake but not with VD alone.
One study reported improved HbA1c and fasting blood glucose levels following a high-dose VD injection in T2DM patients.
Further, one study found that calcium and VD supplementation could prevent glucose elevations and insulin resistance in individuals with impaired glucose levels. A meta-analysis also revealed a significant effect of VD supplementation on fasting glucose; however, another study observed that VD supplementation had little impact on fasting blood glucose levels.
While a few trials have observed no improvements in insulin resistance with VD supplementation, others have reported substantial reductions.
These discrepancies arise from methodological limitations and individual factors, such as genetic variations, responsiveness, and baseline VD levels. Of note, VD has specific effects on different populations, such as older adults, children, and adults.
For instance, a trial showed that VD supplementation significantly reduced HbA1c and fasting glucose levels in older individuals with prediabetes.
Moreover, in adolescents and children with T1DM or T2DM and VD deficiency, VD supplementation was associated with a clinically meaningful reduction in HbA1c and a significant decrease in body mass index and alanine aminotransferase levels.
VD supplementation and T2DM complications
VD’s effects on the risk of diabetes complications and cardiovascular disease remain contentious. An RCT with over 25,000 participants showed that VD treatment over five years had no significant protective benefits against cardiovascular events. By contrast, mechanistic studies have highlighted the essential role of VD in vascular regeneration and protection.
Furthermore, one trial involving older adults showed that VD supplementation led to a significant reduction in heart failure events; however, there were no differences in the incidence of stroke or myocardial infarction.
The effects of VD on hypertension are unclear, albeit studies suggest that high-dose VD supplementation could result in short-term improvements. Various studies suggest links between age-related macular degeneration and VD deficiency.
One study noted an inverse correlation between 1,25-dihydroxy vitamin D levels and diabetic retinopathy (DR). Another study reported a significant association between DR prevalence and serum 25-hydroxyvitamin D levels in a diabetes cohort. Further, a meta-analysis demonstrated that patients with VD deficiency and diabetes were at a higher risk of developing DR.
Concluding remarks
VD influences diabetes pathophysiology by improving insulin production, secretion, and sensitivity and reducing inflammation and oxidative stress.
Its impact on glucose metabolism and T2D incidence has been inconsistent across trials. Moreover, VD supplementation has substantial benefits against diabetes-related complications.
Notably, the considerable variability across studies complicates the formulation of definitive conclusions and clinical recommendations.
As such, further studies are necessary to elucidate the relationship between VD and glucose metabolism, emphasizing individual responses to VD supplementation.
