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Vitamin A derivative potentially treats type 2 diabetes and prevents its complications
Date:6/16/2014

and has many mitochondria, the energy factories of cells. Vitamin A derivatives stimulate a mitochondrial uncoupling protein (UCP1) that allows uncoupling of the mitochondria pathway (oxidative phosphorylation ), which uses energy from the oxidation of nutrients for the production of adenosine triphosphate (ATP). For a period of time, they generate heat (thermogenesis) instead of ATP, which is traditionally the energy required for active metabolism. Exposure to cold leads to the stimulation of brown fat and white fat, promoting the conversion of triglycerides to free fatty acids and glycerol. However, in brown adipocytes, these fatty acids are rapidly oxidized in the mitochondria and produce heat (under the influence of the UCP1 protein). Brown fat thus helps to increase basal energy metabolism. As a result, hibernating mammals fatten in the fall without developing diabetes and lose weight without moving too much in the winter (while warming their den). They are also the animals that accumulate the most Vitamin A in their livers. Retinoic acid (a Vitamin A derivative) is recognized for its involvement in cell maturation and differentiation and may guide pre-adipocytes to become brown (or beige) instead of white. It is as if "boilers" were installed directly in reserves of white fat to melt it on the spot and prevent it from over-accumulating.

"Vitamine A is a bioactive nutrient. The originality of our project is in addressing obesity and type 2 diabetes through the involvement of retinoids. We have attracted international attention and were named among 12 teams in the world to bring conclusive data in this regard," says Dr. Pangala V. Bhat.

"Our studies on animals show that retinoic acid induces normalization of blood glucose and reduction of obesity. It is an important contribution to understanding RA action on the liver, fat, muscles, and the heart, and on retinoid metabolism, energy metabolism, fatty acid oxidation, and insulin resistance. Our
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Contact: Benjamin Augereau
benjamin.augereau@umontreal.ca
514-343-6796
University of Montreal
Source:Eurekalert

Page: 1 2 3

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