Put the "A" to the "D": Very High Dietary Vitamin A (Retinol, not Beta Carotene!) Content Ameliorates Visceral Adiposity and Improves Insulin Sensitivity in Obesity Prone Rats
What's the first letter in the alphabet? "D"? Well if you look at current research on vitamins, you would think so. Vitamin D is everywhere, vitamin A - if anything - its toxic antagonist. You, as a faithful student of the SuppVersity know better anyway: balance is where the magic lies; and thus you probably won't be surprised that not vitamin D, but vitamin A supplementation improves insulin sensitivity and ameliorates weight gain in a group of obesity prone rats on their favorite fattening stock-diet (Jeyakumar. 2011).
In the Journal of Diabetes, Obesity and Metabolism, Jeyakumar et al. published the results of an early 3-months intervention with a vitamin A-enriched diet (129mg vitamin A/kg diet) on visceral obesity and insulin sensitivity in 50days old obesity prone (WNIN/ob strain) rats:
The scientists explain their observations by another observation they made. Compared to rats fed the standard stock-diet, the vitamin A group exhibited an increased phosphorylation of the insulin receptor on the soleus muscle (this was the one the scientists used to access muscular insulin sensitivity via measuring gene transcription). By decreasing protein tyrosine phosphatase1B (PTP1B), consequently increasing insulin receptor phosphorylation and thus locally increasing insulin sensitivity, vitamin A had a glucose repartitioning effect, shuttling blood sugar into the muscle instead of having it converted to triglycerides that would consecutively be stored in the form of unhealthy visceral fat depots.
Although news like this usually go unrecognized, this is by far not the first study showing beneficial effect in obesity prevention and even treatment. In a 2005 study published in the Journal of Molecular Endocrinology, Jeyakumar et al. had already published similar findings, indicating that an increase in dietary Vitamin A intake resulted "in a significant reduction in the adiposity index and retroperitoneal white adipose tissue (RPWAT) weight in obese rats" (Jeyakumar. 2005).
Jeyakumar et al.'s results stand in line with previous largely unrecognized studies on the effects of low vitamin A levels on adipose tissue development about which Ribot et al. (Ribot. 2001) write in the research journal Obesity:
After all, that seems not so bad for a "vitamin", the reputation of which is almost as bad as that of the most fundamental building block of all your hormones: cholesterol. And guess what, foods such as eggs, liver and other organ meats are high in both: Vitamin A (as retinol not beta carotene, which many people have a hard time to convert) and cholesterol! Wouldn't this be a good reason to (re-)introduce these traditional, once highly appreciated foods back into your diet? One or two eggs a day (of course including the yolk), some liver once a week and a lot of sun and outdoor activity to bolster up both your vitamin A and D levels - what more could you ask for?
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| Image 1: Molecular structure of all-trans retinol |
Compared to stock diet-fed obese rats, vitamin A-enriched diet fed-obese rats had reduced body weight gain, visceral adiposity and improved insulin sensitivity as evidenced by decreased fasting plasma insulin and unaltered glucose levels.
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| Image 2: WNIN obese (A) and normal rat (B) aged 12 months (image from Reddy. 2009) |
Although news like this usually go unrecognized, this is by far not the first study showing beneficial effect in obesity prevention and even treatment. In a 2005 study published in the Journal of Molecular Endocrinology, Jeyakumar et al. had already published similar findings, indicating that an increase in dietary Vitamin A intake resulted "in a significant reduction in the adiposity index and retroperitoneal white adipose tissue (RPWAT) weight in obese rats" (Jeyakumar. 2005).
Jeyakumar et al.'s results stand in line with previous largely unrecognized studies on the effects of low vitamin A levels on adipose tissue development about which Ribot et al. (Ribot. 2001) write in the research journal Obesity:
Vitamin A-deficient diet feeding led to a marked increase of adiposity and to a small increase of body weight. Hypertrophy of white adipose tissue depots correlated with enhanced PPAR-gamma-2 expression. Hypertrophy of BAT, in contrast, correlated with a decrease of PPAR-gamma-2 expression that may contribute to the known reduced thermogenic potential of BAT under conditions of vitamin A restriction. Treatment with tRA [trans retinoic acid =vitamin A] triggered a reduction of adiposity and body weight that correlated with a down-regulation of PPAR-gamma-2 expression in all adipose tissues.And in July 2003 Felipe et al. (Felipe. 2004) submitted a paper to the American Diabetes Association describing how
RA [retinoic acid] administration to normal mice resulted in reduced resistin mRNA levels in brown and white adipose tissues, reduced circulating resistin levels, reduced body weight, and improved glucose tolerancein mice. While there appear so be a difference in the localization of resistine expression in rodents and humans (in rodents it is mainly released by fat cells, in humans and primates primarily by immune and epithelial cells), the negative effects of high serum levels of resistin on insulin sensitivity appears to be same in both species.
After all, that seems not so bad for a "vitamin", the reputation of which is almost as bad as that of the most fundamental building block of all your hormones: cholesterol. And guess what, foods such as eggs, liver and other organ meats are high in both: Vitamin A (as retinol not beta carotene, which many people have a hard time to convert) and cholesterol! Wouldn't this be a good reason to (re-)introduce these traditional, once highly appreciated foods back into your diet? One or two eggs a day (of course including the yolk), some liver once a week and a lot of sun and outdoor activity to bolster up both your vitamin A and D levels - what more could you ask for?
