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Using the hormone-like messenger protein leptin to
shrink your fat cells is an intriguing, potentially key new concept in
weight loss. Diminishing the body’s cravings that lead to overeating is
another critical, new concept.
And with more and more of us dining out on, or taking
out, industrialsized meal portions, it is clear that
shrinking our fat cells and reducing cravings that lead to overeating
are potentially two very good things.
So what if we really could safely shrink our fat cells
(without losing muscle)? What if we simply could
safely lose the cravings that cause us to overeat?
The science of slimming is now on the verge of such
breakthroughs. We cannot assure everyone reading this report that the
information we present will result in weight loss or conversion of fat
to lean muscle, because the information is preliminary (and also
individual biochemistry affects all outcomes).
But, many of us welcome all the help we can get when it
comes to appetite control and weight loss. Our mission is to keep you
informed of cutting edge breakthroughs in health. Anecdotal reports are
coming
in now from individuals who are losing weight and/or becoming more trim
with the use of a leptin-based
colostrum formula from TBR Labs. It is called Lepti-Trim. So we want to
present this information. It may prove helpful to many of you.
Scientists Say
Leptin Works
As a longtime consultant to the dairy industry, Dr. Al
Fox has seen firsthand the beneficial impact of leptin on body mass
composition. “I have been involved in studies with lean body mass and
calves, and we have demonstrated that supplemental colostrum aids lean
body mass. It seems likely that it is the combination of leptin and
insulinlike growth factor-I (IGF-I) in colostrum that helps to create
lean body mass,” says Fox, one of the world’s leading experts on
colostrum, its formulation, utilization and applications. Dr. Fox is
scientific consultant to TBR Labs.
“Leptin directs how you actually use fatty acids,” he
continues. “Large fat cells indicate a leptin deficiency or
an inability to properly use leptin due to faulty cell receptors or
other feedback mechanisms. It’s a vicious cycle. Once you get a lot of
large fat cells you have inefficient uses of leptin and you end up with
more fat cells and even more leptin because your body is no longer
responding. But as people lose weight, their leptin levels decrease,
making it difficult to reach ideal body weight. What we do know is that
supplemental
leptin seems to work.”
Most telling is a 1999 study from the Journal of the
American Medical Association that found that leptin not
only resulted in significant weigh loss, “more than 95% of weight loss
was fat loss,” note researchers.
Meanwhile, researchers at the Howard Hughes Medical
Institute have been using genechip technology—
a powerful tool for analyzing the expression patterns of thousands of
genes at a time—and have identified a
number of genes that are specifically regulated by the hormone leptin.
Identifying genes regulated by leptin will improve
knowledge of how leptin causes its effects on weight and appetite, and
may also offer new targets for drugs designed to stimulate weight loss.
Since the discovery of leptin in 1994, many have hoped that the
hormone would be a promising weight-loss treatment for humans.
Studies of the hormone’s weight-reducing effects in humans are
underway, but researchers still have a way to go before they fully
comprehend how the hormone affects the brain and other tissues.
In experiments described in the April 15, 2000, issue of
the journal Genes & Development, Dr. Jeffrey M.
Friedman, an HHMI investigator at The Rockefeller University, and
Rockefeller colleagues Alexander
Soukas, Paul Cohen and Nicholas D. Socci report that they are beginning
to probe the genetic program orchestrated by leptin to induce weight
loss.
FYI
Leptin Background
Leptin, a hormone-like messenger protein (known technically as a
cytokine), is produced in relatively large
amounts by fat tissue and in smaller amounts by other peripheral
organs, and then secreted into the bloodstream, where it travels to the
brain and other tissues, causing fat loss and decreased appetite.
Once leptin has been secreted by your fat cells, it
travels to the hypothalamus—the part of your brain that has an
influence on eating behavior. In the medial hypothalamus, leptin
activates “anorectic” nerve cells, which serve to suppress your
appetite. At the same time, leptin prevents “orexigenic” cells from
stimulating your appetite.
Leptin (from the Greek leptos, meaning thin) first came
to national attention in 1994 when the obesity gene and its product
leptin were discovered. It was shown then that obese mice dropped 40
percent of their body weight after only one month of treatment with
leptin. Leptin also improved symptoms of diabetes.
Recently, the taste organ was found to be one of the
peripheral targets for leptin. The hormone specifically inhibits sweet
taste responses in lean mice. Thus, leptin appears to act as a
modulator of sweet taste.
Leptin also suppresses a gene that produces an enzyme
known as acetyl-CoA carboxylase, or ACC, which is essential for fat
production. When researchers injected laboratory mice with leptin,
previously obese mice became as thin as rodent track stars. Some
researchers believe that leptin works, in part, by inhibiting the
synthesis of fat in fat cells and increasing the burning of fat in
muscle cells—that it works at an enzymatic, cellular level.
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