Effect of Vitamin D on Fat Storage
A quick preface
Adipogenesis is the process of cellular differentiation (a less specialized cell becomes a more specialized cell type) by which pre-adipocytes (undifferentiated fibroblasts that can be stimulated to form adipocytes) become adipocytes (also known as lipocytes or fat cells).
Adipocytes stay in a dynamic state, they start expanding and storing lipids (fats) when the energy intake is higher than the expenditure and undergo mobilization (emptying) when the energy expenditure exceeds the intake. This process is constantly happening and is highly regulated by counter regulatory hormones to which these cells are very sensitive.
Now that all the technical stuff is out of the way, it seems that adequate Vitamin D convinces fibroblasts to turn into muscle rather than intramuscular fat, inadequate Vitamin D on the other hand convinces the fibroblasts to turn into fat cells which can then fill up with a calorie excess , it is likely that the mechanism behind this (although slightly complex), is that when winter approaches we get less Vitamin D and this deficiency causes the fibroblasts to make fat cells within the muscle and store energy for the coming winter.
So what you might say, well any extra fat in the body in the form of intramuscular fat makes it harder for you to burn off the Subcutaneous Fat that is stopping you from looking good naked. Intramuscular triacylglycerol (Fat) serves as an energy store that can be used during exercise, it may contribute up to one fifth of total energy turnover but without it or with less of it, your body will need to source energy elsewhere when you are doing low level cardiac exercise, most likely from Subcutaneous Fat or Visceral Fat.
On top of all that Adipose tissue (fat cells), is the greatest peripheral source of Aromatase in males, which is what converts Testosterone into Estradiol (and we don’t want that).
So will Vitamin D help you lose weight? Possibly, but it is more likely that it will stop you from putting on the extra fat that our ancestors needed to survive the winter, which will in turn make it easier to tone up for summer. While we are on the subject, excess accumulation of intramuscular fat in overweight people has been associated with conditions such as insulin resistance and type 2 diabetes. So lower your Intramuscular fat with more Vitamin D this coming winter (and summer) and give yourself a better chance at staying in shape.
The link to the study,
And the important part that explains it,
It is difficult to extrapolate from this study to the likely effects of VitD deficiency on the level of transdifferentiation of muscle precursor cells to adipocytes that occur in muscle in vivo. Our findings suggest that low (deficient) levels (Zittermann et al. 2009) of 1,25(OH)2D3 (i.e. 10−13 M) may actually enhance adipogenic transdifferentiation, whereas high (sufficient) levels (i.e. 10−9 M) inhibit adipogenesis, thereby potentially impacting on fat infiltration and muscle function. A number of studies have demonstrated the ability of primary muscle cells to form adipocytes, but the mechanisms involved are not clear (Asakura et al. 2001, Csete et al. 2001, Aguiari et al. 2008). However, the C2C12 cell model is likely to be a conservative model of adipogenic transdifferentiation, as primary satellite cells isolated from pig muscle demonstrate a much higher degree of plasticity with a greater number of adipocytes and a lower number of myotubes formed in response to adipogenic media (Redshaw et al. 2010). The exposure of myogenic precursor cells to adipogenic regulatory factors may be an important factor in contributing to the increased fat infiltration seen in muscle, for example during ageing and VitD deficiency, although infiltration by already committed adipocyte populations is also possible. VitD has been shown to play a key regulatory role in myogenesis and is likely to be important in muscle fibre repair (Capiati et al. 1999, Garcia et al. 2011).
A speculative interpretation of the bimodal response of C2C12 cells to 1,25(OH)2D3 observed in vitro is that it represents an energy-conserving mechanism in vivo that has evolved in response to the changing seasons and enables extra energy to be repartitioned into fat depots. Certainly for our ancestors, a significant quantity of VitD was primarily obtained from exposure to u.v./sunlight, which induces the conversion of 7-dehydrocholesterol to VitD3. Low levels of VitD in the body, which possibly occur during periods of low u.v. exposure such as winter (Moosgaard et al. 2005, Aguiari et al. 2008), may act as an important regulatory cue in inducing muscle precursor cells to form adipocytes rather than myofibres and enable extra fat depots to be stored in the body during periods of austerity. This speculative hypothesis needs testing in an appropriate animal model.
In conclusion, this is the first study to show that low physiological concentrations (0.1–10 pM or 10−13–10−11 M) of 1,25(OH)2D3, which may represent a VitD-deficient state, induce myoblasts to transdifferentiate into the adipogenic lineage and appears to involve activation of PPARγ2. These findings have implications for muscle health and function as well as whole-body energy metabolism because an increase in fat infiltration within skeletal muscle has been linked with a decrease in functional strength and impairment of glucose tolerance, leading to an increased susceptibility to obesity and type II diabetes (Goodpaster et al. 2003, Hilton et al. 2008). High concentrations (1 nM or 10−9 M and above) of 1,25(OH)2D3 appeared to block adipogenic transdifferentiation, suggesting that changes in physiological concentrations of 1,25(OH)2D3 have a major impact on the determination of cell fate of myogenic precursor cells.
Furthermore, our data indicate that levels of 1,25(OH)2D3 in the serum and muscle are likely to be important biomarkers linking VitD intakes and optimal muscular health. Given the widespread prevalence of VitD deficiency, particularly in the elderly population, understanding the role of this vitamin in muscle differentiation processes throughout life will be key to defining nutritional parameters for maintaining life-long health and well-being.
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