Re: Percent Body Fat and CR (thermogenic UCP2 gene)

[Guest guest]

Rodney said:

> First, as we have discussed before, if it is a GENE that is

> responsible for obesity where [snip] did these obese people

> get this gene from? Three times as many people are obese now

> as were in their parents' generation thirty years ago. So their

> PARENTS clearly didn't have the gene. So where did they get it?

> ET?

Rodney,

Some genes only get triggered under special circumstances. The UPC2

gene may reduce obesity by converting calories to heat, but another

function may be to produce a fever to improve circulation and kill

bacteria during infections. Evolution would tend to preserve

thermogenic genes that improve our survival by keeping us from

freezing or by combatting infections. So, yes, we got UPC2 from our

parents who survived the ice age and many infections.

Tony

====

Biochem Biophys Res Commun. 1998 Mar 6;244(1):75-8.

Induction of UCP2 gene expression by LPS: a potential mechanism for

increased thermogenesis during infection.

Faggioni R, Shigenaga J, Moser A, Feingold KR, Grunfeld C.

Department of Medicine, University of California, San Francisco, USA.

UCP2 has been proposed to regulate thermogenesis and energy

expenditure. To identify potential mechanisms underlying the increased

energy expenditure and heat production during infection, we

investigated whether LPS and cytokines might increase UCP2 mRNA levels

in mice. LPS (100 micrograms, i.p.) increased the expression of UCP2

mRNA in liver (28-fold) and muscle and white adipose tissue (5-fold).

In liver, both IL-1 beta (1 microgram, i.p.) and TNF (5 micrograms,

i.p.) increased UCP2 mRNA levels, 4- and 3-fold respectively, whereas

in muscle and fat tissue, an increase was detectable after TNF, but

not IL-1 beta. Indomethacin (10 mg/kg, i.p.) administered immediately

before LPS markedly reduced (70%) the ability of LPS to increase UCP2

mRNA in liver, but not in muscle or adipose tissue. These results

suggest a role for UCP2 in the heat production and increased energy

expenditure that occurs during infection.

PMID: 9514886

[Guest guest]

Rodney said:

> First, as we have discussed before, if it is a GENE that is

> responsible for obesity where [snip] did these obese people

> get this gene from? Three times as many people are obese now

> as were in their parents' generation thirty years ago. So their

> PARENTS clearly didn't have the gene. So where did they get it?

> ET?

Rodney,

Some genes only get triggered under special circumstances. The UPC2

gene may reduce obesity by converting calories to heat, but another

function may be to produce a fever to improve circulation and kill

bacteria during infections. Evolution would tend to preserve

thermogenic genes that improve our survival by keeping us from

freezing or by combatting infections. So, yes, we got UPC2 from our

parents who survived the ice age and many infections.

Tony

====

Biochem Biophys Res Commun. 1998 Mar 6;244(1):75-8.

Induction of UCP2 gene expression by LPS: a potential mechanism for

increased thermogenesis during infection.

Faggioni R, Shigenaga J, Moser A, Feingold KR, Grunfeld C.

Department of Medicine, University of California, San Francisco, USA.

UCP2 has been proposed to regulate thermogenesis and energy

expenditure. To identify potential mechanisms underlying the increased

energy expenditure and heat production during infection, we

investigated whether LPS and cytokines might increase UCP2 mRNA levels

in mice. LPS (100 micrograms, i.p.) increased the expression of UCP2

mRNA in liver (28-fold) and muscle and white adipose tissue (5-fold).

In liver, both IL-1 beta (1 microgram, i.p.) and TNF (5 micrograms,

i.p.) increased UCP2 mRNA levels, 4- and 3-fold respectively, whereas

in muscle and fat tissue, an increase was detectable after TNF, but

not IL-1 beta. Indomethacin (10 mg/kg, i.p.) administered immediately

before LPS markedly reduced (70%) the ability of LPS to increase UCP2

mRNA in liver, but not in muscle or adipose tissue. These results

suggest a role for UCP2 in the heat production and increased energy

expenditure that occurs during infection.

PMID: 9514886

[Guest guest]

Hi Tony:

Valid point about genes getting triggered. So do we know why this

gene would, according to this hypothesis, be triggered in some people

today but not in their parents thirty years ago?

Of course I do not dispute that there is a mechanism, favored by

evolution, to ward off infection by raising body temperature

(fever). The rationale perhaps being to increase blood flow and

thereby circulation of white cells to the affected area to mop up the

infectious agent.

But that, imo, is a long way from attributing blame for obesity to

this particular gene. Especially in the light of the sizeably below-

normal body temperatures of people on CRON.

Rodney.

>

>

> Rodney,

>

> Some genes only get triggered under special circumstances. The UPC2

> gene may reduce obesity by converting calories to heat, but another

> function may be to produce a fever to improve circulation and kill

> bacteria during infections. Evolution would tend to preserve

> thermogenic genes that improve our survival by keeping us from

> freezing or by combatting infections. So, yes, we got UPC2 from our

> parents who survived the ice age and many infections.

>

> Tony

>

> ====

>

> Biochem Biophys Res Commun. 1998 Mar 6;244(1):75-8.

> Induction of UCP2 gene expression by LPS: a potential mechanism for

> increased thermogenesis during infection.

>

> Faggioni R, Shigenaga J, Moser A, Feingold KR, Grunfeld C.

> Department of Medicine, University of California, San

Francisco, USA.

> UCP2 has been proposed to regulate thermogenesis and energy

> expenditure. To identify potential mechanisms underlying the

increased

> energy expenditure and heat production during infection, we

> investigated whether LPS and cytokines might increase UCP2 mRNA

levels

> in mice. LPS (100 micrograms, i.p.) increased the expression of UCP2

> mRNA in liver (28-fold) and muscle and white adipose tissue (5-

fold).

> In liver, both IL-1 beta (1 microgram, i.p.) and TNF (5 micrograms,

> i.p.) increased UCP2 mRNA levels, 4- and 3-fold respectively,

whereas

> in muscle and fat tissue, an increase was detectable after TNF, but

> not IL-1 beta. Indomethacin (10 mg/kg, i.p.) administered

immediately

> before LPS markedly reduced (70%) the ability of LPS to increase

UCP2

> mRNA in liver, but not in muscle or adipose tissue. These results

> suggest a role for UCP2 in the heat production and increased energy

> expenditure that occurs during infection.

>

> PMID: 9514886

>

[Guest guest]

Hi Tony:

Valid point about genes getting triggered. So do we know why this

gene would, according to this hypothesis, be triggered in some people

today but not in their parents thirty years ago?

Of course I do not dispute that there is a mechanism, favored by

evolution, to ward off infection by raising body temperature

(fever). The rationale perhaps being to increase blood flow and

thereby circulation of white cells to the affected area to mop up the

infectious agent.

But that, imo, is a long way from attributing blame for obesity to

this particular gene. Especially in the light of the sizeably below-

normal body temperatures of people on CRON.

Rodney.

>

>

> Rodney,

>

> Some genes only get triggered under special circumstances. The UPC2

> gene may reduce obesity by converting calories to heat, but another

> function may be to produce a fever to improve circulation and kill

> bacteria during infections. Evolution would tend to preserve

> thermogenic genes that improve our survival by keeping us from

> freezing or by combatting infections. So, yes, we got UPC2 from our

> parents who survived the ice age and many infections.

>

> Tony

>

> ====

>

> Biochem Biophys Res Commun. 1998 Mar 6;244(1):75-8.

> Induction of UCP2 gene expression by LPS: a potential mechanism for

> increased thermogenesis during infection.

>

> Faggioni R, Shigenaga J, Moser A, Feingold KR, Grunfeld C.

> Department of Medicine, University of California, San

Francisco, USA.

> UCP2 has been proposed to regulate thermogenesis and energy

> expenditure. To identify potential mechanisms underlying the

increased

> energy expenditure and heat production during infection, we

> investigated whether LPS and cytokines might increase UCP2 mRNA

levels

> in mice. LPS (100 micrograms, i.p.) increased the expression of UCP2

> mRNA in liver (28-fold) and muscle and white adipose tissue (5-

fold).

> In liver, both IL-1 beta (1 microgram, i.p.) and TNF (5 micrograms,

> i.p.) increased UCP2 mRNA levels, 4- and 3-fold respectively,

whereas

> in muscle and fat tissue, an increase was detectable after TNF, but

> not IL-1 beta. Indomethacin (10 mg/kg, i.p.) administered

immediately

> before LPS markedly reduced (70%) the ability of LPS to increase

UCP2

> mRNA in liver, but not in muscle or adipose tissue. These results

> suggest a role for UCP2 in the heat production and increased energy

> expenditure that occurs during infection.

>

> PMID: 9514886

>

[Guest guest]

> Some genes only get triggered under special

> circumstances. The UPC2 gene may reduce obesity by

> converting calories to heat, but another function

> may be to produce a fever to improve circulation and

> kill bacteria during infections.

There are three types of uncoupling proteins: UPC1,

UPC2 and UPC3. UPC1, also called thermogenin, is in

brown adipose tissue and allows the fat to be burned

as heat instead of as energy. It is not unexpected

that the two other proteins may have similar roles.

Nonetheless, it's been found that obese individuals

have low sympathetic activity, e.g. they do not

release enough noradrenaline to stimulate thermogensis

in the first place. So any blame at the uncoupling

proteins may be putting the cart before the horse.

Such a " fix " works when being overweight too, but it

may not be proper to ascribe being overweight as a

genetic defect.

Logan

__________________________________________________

[Guest guest]

> Some genes only get triggered under special

> circumstances. The UPC2 gene may reduce obesity by

> converting calories to heat, but another function

> may be to produce a fever to improve circulation and

> kill bacteria during infections.

There are three types of uncoupling proteins: UPC1,

UPC2 and UPC3. UPC1, also called thermogenin, is in

brown adipose tissue and allows the fat to be burned

as heat instead of as energy. It is not unexpected

that the two other proteins may have similar roles.

Nonetheless, it's been found that obese individuals

have low sympathetic activity, e.g. they do not

release enough noradrenaline to stimulate thermogensis

in the first place. So any blame at the uncoupling

proteins may be putting the cart before the horse.

Such a " fix " works when being overweight too, but it

may not be proper to ascribe being overweight as a

genetic defect.

Logan

__________________________________________________