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Testosterone and Fat Loss- Greater Benefits Than Realized |
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Written by Dan Gwartney, MD
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Sunday, 04 January 2009 |
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Page 4 of 5
cAMP and Phosphoinositide
As was mentioned earlier, leptin is a hormone produced by fat cells. Theoretically, when leptin levels are high, the body receives signals to eat less and the metabolic rate is increased to facilitate calorie burning and weight loss. Yet, women have naturally higher levels of leptin and testosterone has been shown to lower leptin production.4 The basic understanding of leptin would lead one to believe that women would then be leaner and more capable of maintaining lower body fat content. Again, there’s a yet-to-be understood disparity, proving that fat loss and weight maintenance remain a mystery at the bio-molecular level.
Genomic effects, such as LPL and leptin require the affected cells to create new proteins and the effects are generally not seen for days to weeks. Non-genomic effects are much more rapid, showing an effect in minutes to hours.18 Non-genomic effects of steroids occur when receptors embedded in the cell membrane interact with steroids circulating in the blood. When this occurs, other nearby receptors or proteins are altered, so that the cell becomes more responsive to non-steroid hormones. Two examples to demonstrate the non-genomic effects of steroids include cAMP and phosphoinositide. Cyclic-AMP, known as cAMP, is a secondary messenger in cells that carry the signal from membrane receptors to functions inside the cell. Epinephrine, the fight-or-flight hormone that makes the heart race when scared or excited, causes a potent fat release from fat cells that’s dependent on cAMP. When fat cells are pre-exposed to estrogens, the fat release effect of epinephrine is lessened.19 In part, this may be due to an estrogen-stimulated increase in ?-2-adrenoreceptors; a subclass of receptors that block lipolysis (fat release). Testosterone increases cAMP-dependent lipolysis, an effect clearly demonstrated in female-to-male transsexuals.20
Phosphoinositides are also secondary messengers. Fat cells exposed to insulin store fat more easily and precursor cells mature into full-grown fat cells, due to the signal generated by phosphoinositides. For what they’re worth, rat studies have shown that estrogens increase phosphoinositides, promoting fat cell growth; androgens have the opposite effect.21
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Research and Review 
