NIN study finds vitamin D deficiency linked to heart-cell stress in rats

A study by researchers at the ICMR-National Institute of Nutrition has linked vitamin D deficiency to cellular damage in rat heart tissue and laboratory-grown rat heart cells. The research examined normal, low and deficient dietary vitamin D levels in rats and investigated whether the vitamin could protect cardiac cells from oxidative stress. The findings were published in the journal Steroids, according to a press release.

Rats given food low in vitamin D showed higher levels of oxidative damage in heart tissue. They also had lower levels of glutathione, an important antioxidant, and reduced activity of enzymes that help protect cells from harmful molecules known as free radicals. The researchers found that deficiency impaired the Nrf2 pathway, a cellular defence mechanism involved in responding to oxidative stress.

They also observed increased markers of endoplasmic reticulum stress, autophagy and apoptosis in vitamin D-deficient hearts. Lead researcher Ayesha Ismail said prolonged oxidative stress associated with inadequate vitamin D could trigger a chain of cellular events contributing to heart-cell injury and death. Laboratory experiments produced similar results.

Rat cardiac cells exposed to oxidative stress had lower survival and more cellular damage. Treatment with the active form of vitamin D improved antioxidant responses and reduced markers associated with oxidative stress, endoplasmic reticulum stress and apoptosis. The findings add to evidence that vitamin D may have functions beyond bone health, including a possible role in maintaining heart-cell function.

However, the study did not establish that vitamin D deficiency causes the same effects in humans. ICMR-NIN director Bharati Kulkarni said the results were based on animal and cell models and that further human investigations were needed before direct conclusions could be drawn for people.