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A1CR
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Joined: 18 Jan 2006
Posts: 559
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 Posted: Sun Feb 19, 2006 8:03 pm Post subject: Mechanism for "thrifty" vs. "burner" phe |
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[posted on behalf of CRON4healthyfuture; 2002-07-11]
There is [an] article in Science detailing a specific mechanism that
can explain the differences observed between organisms in regards to the
relationship observed between body fat and caloric intake.
An enzyme, SCD-1, which I suppose is Stearoyl-Coa desaturase, has a
negative relationship with leptin, which is generated from fat cells. When
knockout mice were bred without SCD-1, they were thinner than the control
mice, DESPITE IDENTICAL FOOD INTAKE.
SCD-1 is therefore related to fat storage. In a normal wild-type organism,
the enzyme functions in a negative feedback loop with leptin. When you are
fat, SCD-1 is downregulated, and fat deposition slows. When you are
skinny, SCD-1 is upregulated, and fat deposition accelerates. If you
knockout SCD-1, then you are perpetually skinny, no matter how much you eat.
However, they also observed that the SCD-1 knockout mice had no hair, so
they surmised that SCD-1 also functions in skin and hair integrity. This
particular facet of the observed phenomena could have implications in
regards to individuals who are practicing severe caloric restriction who
report thinning hair and deteriorated skin, as perturbed lipid metabolism
could be one of the causal factors, among others. If you restrict to the
point that little to no fat can be synthesized despite elevated SCD-1
expression, then perhaps skin and hair deterioration can be expected.
Enzymes have to have a substrate.
In any case, this SCD-1 discovery could be a large piece of the puzzle in
regards to the whole speculation about the "thrifty" versus "burner"
phenotypes that everyone is so interested in.
SOURCE: Science 2002;297:240-243.
The following is from Reuters......
| Quote: |
Scientists May Have Found Way to Boost Metabolism
Thu Jul 11, 5:55 PM ET
By Linda Carroll
NEW YORK (Reuters Health) - An enzyme called SCD-1 may act as a switch to
turn metabolism up or down, new study findings suggest.
Researchers found that mice that were missing the enzyme tended to stay
thin, even if they overate, according to the report published in Science.
The research may help scientists devise treatments for obesity, study co-
author Dr. James M. Ntambi, a professor of biochemistry and nutritional
sciences at the University of Wisconsin, Madison, said in an interview with
Reuters Health.
The amount of SCD-1 in an animal's body appears to be regulated, at least
in part, by the hormone leptin, Ntambe said. When levels of leptin
increase, levels of SCD-1 decrease.
Leptin is released by fat cells. And the larger fat cells get, the more
leptin they release. Normally, when the brain gets a surge of leptin, it
concludes that the body has a safe store of fat and it sends out a message
to dampen appetite. The hormone also appears to regulate metabolism, but
until now, nobody knew how.
In 1994, when researchers discovered leptin, they thought they might have
come up with a cure for obesity. But when scientists tried giving
overweight people more leptin to see if it would kill appetite and cause
weight loss, the experiments were a dismal failure.
"Most obese people already have high levels of leptin," study co-author Dr.
Jeffrey M. Friedman, an investigator with the Howard Hughes Medical
Institute at The Rockefeller University in New York City, said in an
interview with Reuters Health. "For reasons we don't completely understand,
leptin doesn't seem to work well enough for them."
But Friedman and his colleagues suspect that SCD-1 may give obesity
researchers a way to skip past leptin and turn up metabolism, allowing
people to lose weight.
In the new study, researchers compared mice that were deficient in leptin
to mice that were deficient in both leptin and SCD-1. Mice with no or low
levels of leptin tend to be obese.
The first thing the scientists noticed was that the SCD-1-deficient mice
were thinner than those with normal levels of the enzyme. When they checked
to see whether the SCD-1-deficient mice were eating less, there was a
surprise. These mice, though thinner than their counterparts, were actually
consuming more food.
Apparently, the body needs SCD-1 in order to store fat. Without the enzyme,
most fat is burned instead of being stashed away.
There is a catch, however. The enzyme is necessary for maintenance of
healthy hair and skin. Mice that were completely deficient in SCD-1 tended
to lose their hair, Ntambe said.
So scientists would need to design a therapy that only cut back production
of SCD-1, instead of completely knocking it out, he added. |
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