Lean Genes - Discovered in Mice and Earthworms

I'm not sure if this is real, or a story from The Onion.

So, before eating earthworms, do you wait until they pass all the soil from
their body?

"Jim" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

Ever wish you were like some "intrinsically thin" people, who seem never
to put on fat? Maybe there is a genetic reason they are thin, a "Thin
Gene". New research may have discovered the "Thin Gene" in animals.

Reference: Suh et al.: "Adipose is a conserved dosage-sensitive
anti-obesity gene." Publishing in Cell Metabolism 6, 195--207, September
2007 DOI 10.1016/j.cmet.2007.08.001.

--- sprinkled quotes from news release -----

The gene involved is known a Adipose (Adp).

Animals without a working copy of the gene, known as Adipose (Adp), become
obese and resistant to insulin, while those with increased Adp activity in
fat tissue become slimmer, the researchers found. Moreover, the gene's
"dose" seems to determine how slender an animal turns out to be.

"We made mice that expressed Adp in fat-storing tissues, and lo and
behold, what happened"" Graff said. "They were skinny--weighed less with
markedly less fat--and their fat cells were smaller." Smaller fat cells
usually translate into better metabolic function, he said, including
better blood sugar control.

"It's a striking conservation of genes that restrain fat," he said. While
fat storage is an important mechanism for getting through lean times, "too
much fat in times of plenty has deleterious consequences."

The search for molecules underlying weight gain and poor blood sugar
control "has taken on additional urgency due to the recent dramatic
increase in obesity and diabetes," Graff said. But in a modern world where
many people have essentially unlimited access to food, it's a wonder that
even more people aren't overweight, he added. If this gene plays a similar
role in humans, "it may be that some people's Adp works very well."
=============================== Full News Release Below ===============
http://www.sciencedaily.com/releases/2007/09/070904122443.htm

Gene Therapy, Genes, Mice, Life Sciences, Diet and Weight Loss, Genetics
Anti-obesity Gene Keeps Mice And Worms Lean

Science Daily — Researchers have revealed an antiobesity gene that has
apparently been keeping critters lean during times of plenty since ancient
times. The gene, first discovered by another team in flies, also keeps
worms and mice trim, according to the new report in the September issue of
Cell Metabolism. If the gene works similarly in humans, the findings could
lead to a new weapon against our burgeoning waistlines, according to the
researchers.

Animals without a working copy of the gene, known as Adipose (Adp), become
obese and resistant to insulin, while those with increased Adp activity in
fat tissue become slimmer, the researchers found. Moreover, the gene's
"dose" seems to determine how slender an animal turns out to be.

"Maybe if you could affect this gene, even just a little bit, you might
have a beneficial effect on fat," said Jonathan Graff of the University of
Texas Southwestern Medical Center, noting that people often become
overweight very gradually--adding just one or two pounds a year. "After 30
years, that's a lot."

While worms and flies are routinely studied as models of human health and
disease, that trend has been less true in fat biology, Graff said. That's
because unlike mammals, worms and flies store their fat in multifunctional
cells rather than in dedicated fat cells known as adipocytes. However,
those differences didn't preclude the possibility that the animals might
use similar genes to accomplish their fat storage goals, he added.

In the new study, Graff's team found that worms lacking Adp activity
became fat, although they appeared to be otherwise healthy and fertile.
The researchers scoured the genetic database in search of related genes
and found one with "tremendous" similarity in flies.

Indeed, another scientist, Winifred Doane, had found a naturally occurring
strain of plump flies in Nigeria almost 50 years ago that carried a
mutation in their Adp gene. The flies lived in a climate marked by cycles
of famine, where they may have benefited from being highly efficient at
fat storage, Doane had suggested.

To explore Adp's function even further, Graff and his colleagues produced
a strain of mutant flies like those that Doane had found years earlier.
They found that the mutant flies were indeed fat and also had trouble
getting around. Flies with only one copy of the Adp mutation fell
somewhere in between the fat and normal flies, evidence that the gene's
effects are "dose dependent," they reported.

Treatments that increased Adp in the insects' fat tissue led them to lose
weight, evidence that the gene operates within fat cells themselves. In
mice that expressed the gene in fat-storing tissues, the same patterns
emerged.

"We made mice that expressed Adp in fat-storing tissues, and lo and
behold, what happened"" Graff said. "They were skinny--weighed less with
markedly less fat--and their fat cells were smaller." Smaller fat cells
usually translate into better metabolic function, he said, including
better blood sugar control.

"It's a striking conservation of genes that restrain fat," he said. While
fat storage is an important mechanism for getting through lean times, "too
much fat in times of plenty has deleterious consequences."

The search for molecules underlying weight gain and poor blood sugar
control "has taken on additional urgency due to the recent dramatic
increase in obesity and diabetes," Graff said. But in a modern world where
many people have essentially unlimited access to food, it's a wonder that
even more people aren't overweight, he added. If this gene plays a similar
role in humans, "it may be that some people's Adp works very well."

The researchers include Jae Myoung Suh, Daniel Zeve, Renee McKay, Jin Seo,
Zack Salo, Robert Li, Michael [censored], and Jonathan M. Graff of University of
Texas Southwestern Medical Center in Dallas.

This work was supported by awards to JMG from the NIH and the NIDDK.

Reference: Suh et al.: "Adipose is a conserved dosage-sensitive
anti-obesity gene." Publishing in Cell Metabolism 6, 195--207, September
2007 DOI 10.1016/j.cmet.2007.08.001.

Cubit said:

I'm not sure if this is real, or a story from The Onion.

Obviously, you failed to see the link to the press release from Science
Daily which I went to lengths to include.

http://www.sciencedaily.com/releases/2007/09/070904122443.htm

There is also the journal reference to the journal "Cell Metabolism"

You probably misunderstand a lot, don't you.

Actually, it seems more likely that you don't like to read long stuff
and make snap trivializing judgements -- which happens here sometimes.

Jim

Quoted message said:

So, before eating earthworms, do you wait until they pass all the soil from
their body?

"Jim" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

Ever wish you were like some "intrinsically thin" people, who seem never
to put on fat? Maybe there is a genetic reason they are thin, a "Thin
Gene". New research may have discovered the "Thin Gene" in animals.

Reference: Suh et al.: "Adipose is a conserved dosage-sensitive
anti-obesity gene." Publishing in Cell Metabolism 6, 195--207, September
2007 DOI 10.1016/j.cmet.2007.08.001.

--- sprinkled quotes from news release -----

The gene involved is known a Adipose (Adp).

Animals without a working copy of the gene, known as Adipose (Adp), become
obese and resistant to insulin, while those with increased Adp activity in
fat tissue become slimmer, the researchers found. Moreover, the gene's
"dose" seems to determine how slender an animal turns out to be.

"We made mice that expressed Adp in fat-storing tissues, and lo and
behold, what happened"" Graff said. "They were skinny--weighed less with
markedly less fat--and their fat cells were smaller." Smaller fat cells
usually translate into better metabolic function, he said, including
better blood sugar control.

"It's a striking conservation of genes that restrain fat," he said. While
fat storage is an important mechanism for getting through lean times, "too
much fat in times of plenty has deleterious consequences."

The search for molecules underlying weight gain and poor blood sugar
control "has taken on additional urgency due to the recent dramatic
increase in obesity and diabetes," Graff said. But in a modern world where
many people have essentially unlimited access to food, it's a wonder that
even more people aren't overweight, he added. If this gene plays a similar
role in humans, "it may be that some people's Adp works very well."
=============================== Full News Release Below ===============
http://www.sciencedaily.com/releases/2007/09/070904122443.htm

Gene Therapy, Genes, Mice, Life Sciences, Diet and Weight Loss, Genetics
Anti-obesity Gene Keeps Mice And Worms Lean

Science Daily — Researchers have revealed an antiobesity gene that has
apparently been keeping critters lean during times of plenty since ancient
times. The gene, first discovered by another team in flies, also keeps
worms and mice trim, according to the new report in the September issue of
Cell Metabolism. If the gene works similarly in humans, the findings could
lead to a new weapon against our burgeoning waistlines, according to the
researchers.

Animals without a working copy of the gene, known as Adipose (Adp), become
obese and resistant to insulin, while those with increased Adp activity in
fat tissue become slimmer, the researchers found. Moreover, the gene's
"dose" seems to determine how slender an animal turns out to be.

"Maybe if you could affect this gene, even just a little bit, you might
have a beneficial effect on fat," said Jonathan Graff of the University of
Texas Southwestern Medical Center, noting that people often become
overweight very gradually--adding just one or two pounds a year. "After 30
years, that's a lot."

While worms and flies are routinely studied as models of human health and
disease, that trend has been less true in fat biology, Graff said. That's
because unlike mammals, worms and flies store their fat in multifunctional
cells rather than in dedicated fat cells known as adipocytes. However,
those differences didn't preclude the possibility that the animals might
use similar genes to accomplish their fat storage goals, he added.

In the new study, Graff's team found that worms lacking Adp activity
became fat, although they appeared to be otherwise healthy and fertile.
The researchers scoured the genetic database in search of related genes
and found one with "tremendous" similarity in flies.

Indeed, another scientist, Winifred Doane, had found a naturally occurring
strain of plump flies in Nigeria almost 50 years ago that carried a
mutation in their Adp gene. The flies lived in a climate marked by cycles
of famine, where they may have benefited from being highly efficient at
fat storage, Doane had suggested.

To explore Adp's function even further, Graff and his colleagues produced
a strain of mutant flies like those that Doane had found years earlier.
They found that the mutant flies were indeed fat and also had trouble
getting around. Flies with only one copy of the Adp mutation fell
somewhere in between the fat and normal flies, evidence that the gene's
effects are "dose dependent," they reported.

Treatments that increased Adp in the insects' fat tissue led them to lose
weight, evidence that the gene operates within fat cells themselves. In
mice that expressed the gene in fat-storing tissues, the same patterns
emerged.

"We made mice that expressed Adp in fat-storing tissues, and lo and
behold, what happened"" Graff said. "They were skinny--weighed less with
markedly less fat--and their fat cells were smaller." Smaller fat cells
usually translate into better metabolic function, he said, including
better blood sugar control.

"It's a striking conservation of genes that restrain fat," he said. While
fat storage is an important mechanism for getting through lean times, "too
much fat in times of plenty has deleterious consequences."

The search for molecules underlying weight gain and poor blood sugar
control "has taken on additional urgency due to the recent dramatic
increase in obesity and diabetes," Graff said. But in a modern world where
many people have essentially unlimited access to food, it's a wonder that
even more people aren't overweight, he added. If this gene plays a similar
role in humans, "it may be that some people's Adp works very well."

The researchers include Jae Myoung Suh, Daniel Zeve, Renee McKay, Jin Seo,
Zack Salo, Robert Li, Michael [censored], and Jonathan M. Graff of University of
Texas Southwestern Medical Center in Dallas.

This work was supported by awards to JMG from the NIH and the NIDDK.

Reference: Suh et al.: "Adipose is a conserved dosage-sensitive
anti-obesity gene." Publishing in Cell Metabolism 6, 195--207, September
2007 DOI 10.1016/j.cmet.2007.08.001.

Jim said:

Ever wish you were like some "intrinsically thin" people, who seem
never to put on fat? Maybe there is a genetic reason they are thin,
a "Thin Gene". New research may have discovered the "Thin Gene" in
animals.

There's amazing stuff going on in gene research. (I'm no expert, just
someone who's interested in the subject.) It doesn't get nearly as
much press as it deserves, because when you talk about genetic
differences you're often talking about race and that's the most
dangerous topic there is; but the discoveries are coming fast and
furious.

It seems self-evident that body shape is genetic to a great extent,
but it's still useful to track down the specific genes if we want to
find ways to treat it directly. Now if they could just find the gene
for laziness, I'd be all set....

That reminds me: about a month ago, I wrote about how almost all the
kids at the county fair were quite slender, so I wondered where the
childhood obesity epidemic was. Well, I was at Burger King this
weekend, and now I know.

Quoted message said:

Reference: Suh et al.: "Adipose is a conserved dosage-sensitive
anti-obesity gene." Publishing in Cell Metabolism 6, 195--207,
September 2007 DOI 10.1016/j.cmet.2007.08.001.

--- sprinkled quotes from news release -----

The gene involved is known a Adipose (Adp).

Animals without a working copy of the gene, known as Adipose (Adp),
become obese and resistant to insulin, while those with increased Adp
activity in fat tissue become slimmer, the researchers
found. Moreover, the gene's "dose" seems to determine how slender an
animal turns out to be.

"We made mice that expressed Adp in fat-storing tissues, and lo and
behold, what happened"" Graff said. "They were skinny--weighed less
with markedly less fat--and their fat cells were smaller." Smaller fat
cells usually translate into better metabolic function, he said,
including better blood sugar control.

"It's a striking conservation of genes that restrain fat," he
said. While fat storage is an important mechanism for getting through
lean times, "too much fat in times of plenty has deleterious
consequences."

The search for molecules underlying weight gain and poor blood sugar
control "has taken on additional urgency due to the recent dramatic
increase in obesity and diabetes," Graff said. But in a modern world
where many people have essentially unlimited access to food, it's a
wonder that even more people aren't overweight, he added. If this gene
plays a similar role in humans, "it may be that some people's Adp
works very well."
=============================== Full News Release Below ===============
http://www.sciencedaily.com/releases/2007/09/070904122443.htm

Gene Therapy, Genes, Mice, Life Sciences, Diet and Weight Loss, Genetics
Anti-obesity Gene Keeps Mice And Worms Lean

Science Daily — Researchers have revealed an antiobesity gene that has
apparently been keeping critters lean during times of plenty since
ancient times. The gene, first discovered by another team in flies,
also keeps worms and mice trim, according to the new report in the
September issue of Cell Metabolism. If the gene works similarly in
humans, the findings could lead to a new weapon against our burgeoning
waistlines, according to the researchers.

Animals without a working copy of the gene, known as Adipose (Adp),
become obese and resistant to insulin, while those with increased Adp
activity in fat tissue become slimmer, the researchers
found. Moreover, the gene's "dose" seems to determine how slender an
animal turns out to be.

"Maybe if you could affect this gene, even just a little bit, you
might have a beneficial effect on fat," said Jonathan Graff of the
University of Texas Southwestern Medical Center, noting that people
often become overweight very gradually--adding just one or two pounds
a year. "After 30 years, that's a lot."

While worms and flies are routinely studied as models of human health
and disease, that trend has been less true in fat biology, Graff
said. That's because unlike mammals, worms and flies store their fat
in multifunctional cells rather than in dedicated fat cells known as
adipocytes. However, those differences didn't preclude the possibility
that the animals might use similar genes to accomplish their fat
storage goals, he added.

In the new study, Graff's team found that worms lacking Adp activity
became fat, although they appeared to be otherwise healthy and
fertile. The researchers scoured the genetic database in search of
related genes and found one with "tremendous" similarity in flies.

Indeed, another scientist, Winifred Doane, had found a naturally
occurring strain of plump flies in Nigeria almost 50 years ago that
carried a mutation in their Adp gene. The flies lived in a climate
marked by cycles of famine, where they may have benefited from being
highly efficient at fat storage, Doane had suggested.

To explore Adp's function even further, Graff and his colleagues
produced a strain of mutant flies like those that Doane had found
years earlier. They found that the mutant flies were indeed fat and
also had trouble getting around. Flies with only one copy of the Adp
mutation fell somewhere in between the fat and normal flies, evidence
that the gene's effects are "dose dependent," they reported.

Treatments that increased Adp in the insects' fat tissue led them to
lose weight, evidence that the gene operates within fat cells
themselves. In mice that expressed the gene in fat-storing tissues,
the same patterns emerged.

"We made mice that expressed Adp in fat-storing tissues, and lo and
behold, what happened"" Graff said. "They were skinny--weighed less
with markedly less fat--and their fat cells were smaller." Smaller fat
cells usually translate into better metabolic function, he said,
including better blood sugar control.

"It's a striking conservation of genes that restrain fat," he
said. While fat storage is an important mechanism for getting through
lean times, "too much fat in times of plenty has deleterious
consequences."

The search for molecules underlying weight gain and poor blood sugar
control "has taken on additional urgency due to the recent dramatic
increase in obesity and diabetes," Graff said. But in a modern world
where many people have essentially unlimited access to food, it's a
wonder that even more people aren't overweight, he added. If this gene
plays a similar role in humans, "it may be that some people's Adp
works very well."

The researchers include Jae Myoung Suh, Daniel Zeve, Renee McKay, Jin
Seo, Zack Salo, Robert Li, Michael [censored], and Jonathan M. Graff of
University of Texas Southwestern Medical Center in Dallas.

This work was supported by awards to JMG from the NIH and the NIDDK.

Reference: Suh et al.: "Adipose is a conserved dosage-sensitive
anti-obesity gene." Publishing in Cell Metabolism 6, 195--207,
September 2007 DOI 10.1016/j.cmet.2007.08.001.

--
Aaron -- 285/254/200 -- aaron.baugher.biz

Your criticisms of my reaction are well taken.

My reaction was based on an intuitive sense that the story was bogus. I
found it odd that they would use the word "Adipose" as a name for the gene.
It is related, but too related. Shouldn't it be anti-adipose, or something
more Latin/Greek?

"Jim" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

Cubit said:

I'm not sure if this is real, or a story from The Onion.

Obviously, you failed to see the link to the press release from Science
Daily which I went to lengths to include.

http://www.sciencedaily.com/releases/2007/09/070904122443.htm

There is also the journal reference to the journal "Cell Metabolism"

You probably misunderstand a lot, don't you.

Actually, it seems more likely that you don't like to read long stuff and
make snap trivializing judgements -- which happens here sometimes.

Jim

Quoted message said:

So, before eating earthworms, do you wait until they pass all the soil
from their body?

"Jim" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

Ever wish you were like some "intrinsically thin" people, who seem never
to put on fat? Maybe there is a genetic reason they are thin, a "Thin
Gene". New research may have discovered the "Thin Gene" in animals.

Reference: Suh et al.: "Adipose is a conserved dosage-sensitive
anti-obesity gene." Publishing in Cell Metabolism 6, 195--207, September
2007 DOI 10.1016/j.cmet.2007.08.001.

--- sprinkled quotes from news release -----

The gene involved is known a Adipose (Adp).

Animals without a working copy of the gene, known as Adipose (Adp),
become obese and resistant to insulin, while those with increased Adp
activity in fat tissue become slimmer, the researchers found. Moreover,
the gene's "dose" seems to determine how slender an animal turns out to
be.

"We made mice that expressed Adp in fat-storing tissues, and lo and
behold, what happened"" Graff said. "They were skinny--weighed less with
markedly less fat--and their fat cells were smaller." Smaller fat cells
usually translate into better metabolic function, he said, including
better blood sugar control.

"It's a striking conservation of genes that restrain fat," he said. While
fat storage is an important mechanism for getting through lean times,
"too much fat in times of plenty has deleterious consequences."

The search for molecules underlying weight gain and poor blood sugar
control "has taken on additional urgency due to the recent dramatic
increase in obesity and diabetes," Graff said. But in a modern world
where many people have essentially unlimited access to food, it's a
wonder that even more people aren't overweight, he added. If this gene
plays a similar role in humans, "it may be that some people's Adp works
very well."
=============================== Full News Release Below ===============
http://www.sciencedaily.com/releases/2007/09/070904122443.htm

Gene Therapy, Genes, Mice, Life Sciences, Diet and Weight Loss, Genetics
Anti-obesity Gene Keeps Mice And Worms Lean

Science Daily — Researchers have revealed an antiobesity gene that has
apparently been keeping critters lean during times of plenty since
ancient times. The gene, first discovered by another team in flies, also
keeps worms and mice trim, according to the new report in the September
issue of Cell Metabolism. If the gene works similarly in humans, the
findings could lead to a new weapon against our burgeoning waistlines,
according to the researchers.

Animals without a working copy of the gene, known as Adipose (Adp),
become obese and resistant to insulin, while those with increased Adp
activity in fat tissue become slimmer, the researchers found. Moreover,
the gene's "dose" seems to determine how slender an animal turns out to
be.

"Maybe if you could affect this gene, even just a little bit, you might
have a beneficial effect on fat," said Jonathan Graff of the University
of Texas Southwestern Medical Center, noting that people often become
overweight very gradually--adding just one or two pounds a year. "After
30 years, that's a lot."

While worms and flies are routinely studied as models of human health and
disease, that trend has been less true in fat biology, Graff said. That's
because unlike mammals, worms and flies store their fat in
multifunctional cells rather than in dedicated fat cells known as
adipocytes. However, those differences didn't preclude the possibility
that the animals might use similar genes to accomplish their fat storage
goals, he added.

In the new study, Graff's team found that worms lacking Adp activity
became fat, although they appeared to be otherwise healthy and fertile.
The researchers scoured the genetic database in search of related genes
and found one with "tremendous" similarity in flies.

Indeed, another scientist, Winifred Doane, had found a naturally
occurring strain of plump flies in Nigeria almost 50 years ago that
carried a mutation in their Adp gene. The flies lived in a climate marked
by cycles of famine, where they may have benefited from being highly
efficient at fat storage, Doane had suggested.

To explore Adp's function even further, Graff and his colleagues produced
a strain of mutant flies like those that Doane had found years earlier.
They found that the mutant flies were indeed fat and also had trouble
getting around. Flies with only one copy of the Adp mutation fell
somewhere in between the fat and normal flies, evidence that the gene's
effects are "dose dependent," they reported.

Treatments that increased Adp in the insects' fat tissue led them to lose
weight, evidence that the gene operates within fat cells themselves. In
mice that expressed the gene in fat-storing tissues, the same patterns
emerged.

"We made mice that expressed Adp in fat-storing tissues, and lo and
behold, what happened"" Graff said. "They were skinny--weighed less with
markedly less fat--and their fat cells were smaller." Smaller fat cells
usually translate into better metabolic function, he said, including
better blood sugar control.

"It's a striking conservation of genes that restrain fat," he said. While
fat storage is an important mechanism for getting through lean times,
"too much fat in times of plenty has deleterious consequences."

The search for molecules underlying weight gain and poor blood sugar
control "has taken on additional urgency due to the recent dramatic
increase in obesity and diabetes," Graff said. But in a modern world
where many people have essentially unlimited access to food, it's a
wonder that even more people aren't overweight, he added. If this gene
plays a similar role in humans, "it may be that some people's Adp works
very well."

The researchers include Jae Myoung Suh, Daniel Zeve, Renee McKay, Jin
Seo, Zack Salo, Robert Li, Michael [censored], and Jonathan M. Graff of
University of Texas Southwestern Medical Center in Dallas.

This work was supported by awards to JMG from the NIH and the NIDDK.

Reference: Suh et al.: "Adipose is a conserved dosage-sensitive
anti-obesity gene." Publishing in Cell Metabolism 6, 195--207, September
2007 DOI 10.1016/j.cmet.2007.08.001.

Cubit said:

Your criticisms of my reaction are well taken.

My reaction was based on an intuitive sense that the story was bogus. I
found it odd that they would use the word "Adipose" as a name for the gene.
It is related, but too related. Shouldn't it be anti-adipose, or something
more Latin/Greek?

Why don't you take this issue up with the authors.

They will do what they find sits their publication purposes, no matter
how it looks to you.

Your basis for thinking it is bogus is quite lame.