Burning fats without producing ATP
mikalra at my-deja.com
mikalra at my-deja.com
Wed Jan 19 12:26:34 EST 2000
Tue, 18 Jan 2000 23:45:22 -0800
"Michael Sherman" <sherm at symdyn.com>
[I stumbled on the following abstract by accident. I think it says
that "NutriGuard Research" has discovered a novel and potentially
very lucrative way to modify the behavior of mitochondria
through supplementation. When burning fat, mitochondria
normally produce CO2 as a waste product and ATP as useful output.
This modification causes them instead to produce just CO2 and heat!
That means the body's fat is consumed without yielding any useful
energy, leading to "a remarkable rate of body-fat loss and
According to the abstract, this is accomplished by uncoupling of the
electron transport chain. My understanding is limited, but AFAIK this
means lots of state 4 activity -- mucho heat, mini ATP, and more freee
radicals than you can shake mtSOD at. The formula, in orther words, is
a recipe for accelerated aging, according to MiFR and others.
This might partly explain Hagen et al's results, in which ALCAR
supplementation INCREASED oxidative stress -- except that Hagen also
found increasesed ATP generation, so something else is going on.
The way I picture what they've done is: shift the mitochondria
into neutral and then step on the gas until the tank is empty.
Has anyone every heard of this outfit? Are they developing a product
which could cause people to burn up all their unwanted body fat by
taking a pill and running a fever? More importantly, should we be
investing in this company before the billions start to roll in?
Any molecular biologists out there care to comment on whether
this would really work in humans? Also, would the reaction
described be so dirty as to cause severe mitochondrial damage?
TI- Pyruvate and hydroxycitrate/carnitine may synergize to promote
electron transport in hepatocyte mitochondria, effectively
the oxidation of fatty acids.
AU- McCarty MF; Gustin JC
AD- NutriGuard Research, Encinitas, CA 92024, USA.
SR- Med Hypotheses, 52:407-16, 1999 May
AB- In a recent pilot study, joint administration of pyruvate,
hydroxycitrate (HCA), and carnitine to obese subjects was
a remarkable rate of body-fat loss and thermogenesis, strongly
of uncoupled fatty-acid oxidation. Hepatocytes possess an
mechanism--reverse electron transport--that enables fasting
to proceed independent of respiratory control. Electrons entering
respiratory chain at the coenzyme Q (CoQ) level via FAD-dependent
coA dehydrogenase, can be driven 'up' the chain by the
proton gradient to reduce NAD+; if these electrons are then
the cytoplasm, returning to the respiratory chain at the CoQ level,
net result is heat generation at the expense of the proton
enabling the uncoupled flow of electrons to oxygen. Pyruvate's
utility may stem from its ability to catalyze the rapid transport
high-energy electrons from mitochondria to the cytoplasm, thus
stimulating electron shuttle mechanisms. By enabling rapid
uptake of fatty acids and thus disinhibiting hepatocyte
HCA/carnitine should initiate reverse electron transport:
amplification of electron shuttle mechanisms by pyruvate can be
to accelerate this reverse electron transport, thereby decreasing
electrochemical proton gradient. As a result, hepatocytes may be
convert fatty acids to CO2 and heat with little net generation of
These considerations suggest that it may be feasible to render
hepatocytes functionally equivalent to activated brown fat, such
stored fat can be selectively oxidized in the absence of caloric
restriction. Other measures which enhance the efficiency of
electron shuttle mechanisms may increase the efficacy of this
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