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UCP-3’s Role In Enhancing Fat Oxidation |
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Written by Robbie Durand
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Thursday, 12 February 2009 |
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Page 3 of 5
Tripping Mice And Increased UCP-3 Activity
DNP was the first drug to stimulate UCP activity, but others drugs do as well. MDMA or “ecstasy” is a drug that acts as both a stimulant and psychedelic, producing an energizing effect. I don’t know if you have been to a rave, but those people twirling glow sticks are usually sweating their ass off! Side effects of ecstasy are a noticeable rise in body temperature, faster heartbeat, skin tingles, sudden sweating and dilated pupils. So why all the sweating and increased body temperature? A recent in mice examined how ecstasy affected UCP activation. Mice treated with ecstasy underwent rapid increases in rectal and muscle temperature. Ecstasy also caused intense sympathetic activation and increased UCP-3 activity in muscle, which may partly explain the rapid increases in body temperature. In the second part of the study, the researchers administered ecstasy to UCP-3-deficient mice; UCP-3-deficient mice did not have any rise in body temperature, demonstrating UCP-3’s role in stimulating metabolism.20 This demonstrates that large increases in sympathetic activity increase UCP-3 activity. Don’t be a dumb ass and start trying ecstasy to increase UCP-3. There are much safer ways!
Catecholamines Increase UCP-3
Drugs that increase the activity of the central nervous system are a potential therapeutic pharmacological treatment for obesity. Two drugs that stimulate metabolism and have profound effects on increasing UCP-3 are thyroid and sympathetic agents, such as beta-agonists (drugs that stimulate catecholamines). 18 Treatment with ß2-adrenergic agonists (salbutamol, formoterol) has been demonstrated to increase UCP-3 expression in muscle fibers.30 Both thyroid and catecholamines are potent stimulators of metabolism. A recent study found that having a low resting metabolic rate is predictive of obesity. Muscle accounts for 20 percent of the basal metabolic rate, so increasing muscle metabolism enhances fat oxidation. A significant portion of the variation in metabolic rate between humans can be accounted for by differences in the amount of skeletal muscle energy expenditure and supports the probable role of skeletal muscle in mediating thermogenesis.
Caffeine And Growth Hormone Increases UCP-3 Activity
Resting metabolic rate can be increased by 30 percent by the sympathetic nervous system agents27 and by about 15 percent by growth hormone (GH).28 GH has also been shown to increase UCP-3 in muscle, which may be a part of GH’s powerful effect on fat loss.39, 40 Any supplement that increases adrenaline should increase UCP-3 activity. UCP-3 activity varies between people; research has demonstrated that of all of these possible regulators of the expression of the UCP3 between people, only norepinephrine (a sympathetic catecholamine) could explain part of the variability between UCP-3 expression in subjects. Interestingly, norepinephrine urinary excretion also correlated with resting energy expenditure.34 It should be of no surprise that many of the fat-loss supplements target fat loss by increasing norepinephrine levels. Basically, the higher your norepinephrine levels are, the higher your resting energy expenditure and UCP-3 activity will be. Caffeine is a potent stimulator of norepinephrine and increases fatty acid mobilization, which has also been shown to increase UCP-3 activity.38 I suspect the combination of caffeine with ephedrine and yohimbine would also increase UCP-3 activity as well as increase norepinephrine levels, but no research is available.
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Research and Review 
