Significance of Vitamin A (Retinol) in Ageing

Abstract

Summary:In recent years, studies involving animal models, case reports, and some epidemiological studies have indicated that an accumulation of vitamin A in the liver is linked to low bone mineral content, fracture risk, and hence osteoporosis. While vitamin A in its physiological level acts as an inducer of bone matrix protein (osteocalcin) and matrix GLA protein in the osteoblast cells (bone formation), excess reinoic acid (a metabolic product of vitamin A) supresses osteoblastic activity and stimulates osteoclast formation (bone degradation). There also appear to have an antagonistic or synergistic interactions between vitamins A and D, influencing bone metabolosm; such effects are dose related. These effects could be of concern, especially for the older persons, because of the age-associated cumulation of vitamin A in the liver. The vitamin A status in elderly population, however, has not been as well documented as in an earlier age. In effect, the Food and Nutrition Board of National Academy's Institute of Medicine has not made any differenciation in it's recommendation for the Dietary Reference Intake (DRI) of vitamin A between 14 years and >70 years old individuals. This report will delineate the ageing differences in metabolic availability of vitamin A and that such differences are independent of its intake. The report will also attempt to formulate a hypothesis that in old age, deficiency of vitamin A is not a concern but its potential toxicity involving bone.

Relation of retinol binding protein4, visfatin and vitamin a in obese and non obese Iraqi patients with non alcoholic fatty liver disease

“…The HSCs activated and rapidly loss their vitamin A contents in response to liver injury and this process linked to Chronic liver diseases including NAFLD (31,32). It is unclear, the level of hepatic retinoid are reduced in high fat diet, NAFLD (33)(34)(35)(36), and acute liver injury (37). The level of hepatic retinoid were inversely correlated with hepatic steatosis and NAFLD, this suggesting that ectopic hepatic lipid itself perhaps an early excite hepatic retinoid losing before the onset of HSC activation (38).…”