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Scientists Identify Vitamin A Role in Energy Production

Lee Swanson Research Update

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According to findings published in the FASEB Journal, vitamin A (retinol) may play a role in the synthesis of ATP in mitochondria—the power plant of the cells—and when vitamin A is deficient the production of energy is reduced by 30%.

Researchers led by Ulrich Hammerling from the Institute for Cancer Research, New York, found that when vitamin A supplies are adequate, the preferred energy sources are glycolysis and pyruvate production. On the other hand, when the vitamin is scarce the body turns to fat reserves, preparing the organism to win energy from fat oxidation.

However, when cells are deprived of retinol, the synthesis of ATP decreases as does respiration. But such declines were reversed when retinol levels were restored, and no conversion to other retinoids was observed, showing the effect was related purely to retinol.

"Bioenergetics is fundamental to all cells," wrote the researchers. "In view of this tenet, it is puzzling why metabolic regulation by the pathway described in this report depends on retinol that vertebrates cannot synthesize de novo (anew).

"In limiting vitamin A to nutritional sources, there must be an evolutionary advantage of such import as to override the physiological needs for vitamin A in vision and retinoic acid-dependent transcription.

"The answer may lie in the scenario that finite amounts of vitamin A are subject to depletion during periods of severe starvation when an organism is forced to conserve energy. Our observation that in the absence of vitamin A energy generation by respiration adapts downwards appears relevant in this context," added the researchers.

Data from vitamin A-deficient mice has previously indicated that triglycerides accumulate in the liver and may signify a switch to fat for energy generation, said the researchers, in order to offset the limited use of glycolysis and pyruvate production.

"It is also predictable that chronic deviations of vitamin A transport will lead to metabolic disease," Hammerling and his co-workers added.

FASEB Journal 24(2):627-626, 2010

March, 2010

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