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Vitamin D may prevent blocked blood vessels in diabetics

Published on

30 November 2012

Diabetic patients who have adequate blood vitamin D concentrations are less likely to develop clogged arteries compared to vitamin D deficient diabetics, suggests a new US study.

In the study, blood samples of 43 participants with type 2 diabetes, and 25 healthy controls of the same age, sex, and weight were analyzed for vitamin D serum levels and the property of immune cells (macrophages) to adhere to walls of blood vessels (1). The results showed that in the diabetic patients with vitamin D levels less than 30 ng/mL, macrophage cells were more likely to attach to blood vessel walls. Only vitamin D levels, but not blood pressure, cholesterol, blood sugar or body weight, showed correlation with the level of immune cell adhesion to blood vessel walls.

The researchers commented that the adherence of macrophage cells to blood vessels triggers the cells to become loaded with cholesterol. The build-up of cholesterol in arteries eventually causes the vessels to stiffen and block blood flow. This risk seems to increase with lower blood concentrations of vitamin D. In future research, the scientists hope to determine whether vitamin D treatment can help to prevent the deposit of cholesterol in the blood vessels and/or to reverse other risk factors associated with reduce blood pressure and lessen the likelihood that diabetics will develop atherosclerosis or other vascular complications, the scientists noted.

About 26 million Americans have type 2 diabetes and as obesity rates rise, it is expected that even more people will develop diabetes in the future. Diabetics are more likely to experience heart problems due to an increase in vascular inflammation. Previous studies have linked vitamin D deficiency in diabetic patients to increases in cardiovascular disease and mortality. Other work has suggested that vitamin D may improve insulin release from the pancreas and insulin sensitivity.

REFERENCES

  1. Riek A. E. et al. Vitamin D suppression of endoplasmic reticulum stress promotes an anti-atherogenic monocyte/macrophage phenotype in type 2 diabetic patients. Journal of Biological Chemistry. 2012; 287(46):38482–38494.

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