Mechanism - High Fat Diet >>> Diabetes???

[Guest guest]

http://news.bbc.co.uk/2/hi/health/4563604.stm

Rodney.

[Guest guest]

A few months ago I posted the following article:

http://jp.physoc.org/cgi/content/full/554/3/595

Its relevance to CR, not immediately obvious because it is hidden

under a few layers of chronocentric assumptions which the article

tries to gently put aside by establishing a more plausible

evolutionary hintergrund to modern ills such as obesity and diabetes

than can be accounted for by the role assigned to thrifty genes, was

at that time called into question.

" The continuum between adiposity and impaired carbohydrate metabolism

has led to the belief that the extra energy stored by the body as fat

is causative in the development of insulin resistance. "

Not so. It seems that it isn't the extra glucose mediated energy which

is directly responsible for IR but rather the chronically elevated

blood lipids caused by adiposity and lack of exercise.

" Obesity results in a chronically elevated blood lipid profile,

largely because of the mass action effect of excessive adipose tissues

stores. Therefore in obesity, an `unnatural' situation for the

hunter–gatherer, the elevated blood lipid profile, akin to the

circulatory environment experienced in fasting or carbohydrate

restriction, acts to trigger the physiological responses for such

conditions (Fig. 2). The `misguided' response is to protect

circulating glucose via inhibition of muscle glucose transport whilst

accumulating IMTG to ensure a readily available substrate for

subsequent contractile activity. "

Essentially, drawing from much research, the authors postulate that

because " Insulin sensitivity is decreased in response to a short-term

(3 day) high fat diet (Bachmann et al. 2001) or calorie restriction

(Webber et al. 1994; Gazdag et al. 2000). The latter effect is evident

as little as 14 h after the last meal (Horowitz et al. 2001) " it could

play a significant part in a very dynamic process whereby glucose is

spared in order to insure that the brain's needs are met in periods of

caloric/nutrient restriction while plasma lipids provide a very

effective energy substrate for the glucose deprived skeletal muscles

as well as assist in their recovery following exertion.

" The survival advantage of elevated IMTG in prehistoric man may have

been to provide muscle with an alternative to muscle glycogen as a

readily available substrate to support muscle metabolism at the onset

of exercise or cold exposure during early starvation or carbohydrate

restriction. The recent finding that 72 h of complete food restriction

results in a nearly three-fold increase in IMTG in physically trained

men (Stannard et al. 2002) is salient evidence that under such

conditions FFAs from adipose tissue may be re-distributed to skeletal

muscle for storage in the form of IMTG. "

Obviously useful when trying to survive on an empty stomach while

looking for food.

Not surprising if elevated level of plasma lipids cause type 2

diabetes in a context made up of calorie abundant foods and sedentary

lifestyle.

BY IMPLICATION it seems that a diet high in carbohydrates, but not

over abundant in calories, is the best way to avoid the viscious cycle

caused by this glucose sparing effect brought about by the mediation

of insulin resistance, WHEN NOT REGURLARLY EXERCISING or otherwise

approaching the levels of physical activity of paleolithic humans

where extra fat intake would have represented great advantages given

the paucity of glucose sources.

" The whole-body effects of impaired muscle glucose disposal and

insulin resistance during starvation or carbohydrate restriction would

be relatively greater in the athlete/hunter–gatherer than in sedentary

modern man because of their greater relative muscle mass and thus

greater sink for glucose disposal. "

>

> http://news.bbc.co.uk/2/hi/health/4563604.stm

>

> Rodney.

>

[Guest guest]

A few months ago I posted the following article:

http://jp.physoc.org/cgi/content/full/554/3/595

Its relevance to CR, not immediately obvious because it is hidden

under a few layers of chronocentric assumptions which the article

tries to gently put aside by establishing a more plausible

evolutionary hintergrund to modern ills such as obesity and diabetes

than can be accounted for by the role assigned to thrifty genes, was

at that time called into question.

" The continuum between adiposity and impaired carbohydrate metabolism

has led to the belief that the extra energy stored by the body as fat

is causative in the development of insulin resistance. "

Not so. It seems that it isn't the extra glucose mediated energy which

is directly responsible for IR but rather the chronically elevated

blood lipids caused by adiposity and lack of exercise.

" Obesity results in a chronically elevated blood lipid profile,

largely because of the mass action effect of excessive adipose tissues

stores. Therefore in obesity, an `unnatural' situation for the

hunter–gatherer, the elevated blood lipid profile, akin to the

circulatory environment experienced in fasting or carbohydrate

restriction, acts to trigger the physiological responses for such

conditions (Fig. 2). The `misguided' response is to protect

circulating glucose via inhibition of muscle glucose transport whilst

accumulating IMTG to ensure a readily available substrate for

subsequent contractile activity. "

Essentially, drawing from much research, the authors postulate that

because " Insulin sensitivity is decreased in response to a short-term

(3 day) high fat diet (Bachmann et al. 2001) or calorie restriction

(Webber et al. 1994; Gazdag et al. 2000). The latter effect is evident

as little as 14 h after the last meal (Horowitz et al. 2001) " it could

play a significant part in a very dynamic process whereby glucose is

spared in order to insure that the brain's needs are met in periods of

caloric/nutrient restriction while plasma lipids provide a very

effective energy substrate for the glucose deprived skeletal muscles

as well as assist in their recovery following exertion.

" The survival advantage of elevated IMTG in prehistoric man may have

been to provide muscle with an alternative to muscle glycogen as a

readily available substrate to support muscle metabolism at the onset

of exercise or cold exposure during early starvation or carbohydrate

restriction. The recent finding that 72 h of complete food restriction

results in a nearly three-fold increase in IMTG in physically trained

men (Stannard et al. 2002) is salient evidence that under such

conditions FFAs from adipose tissue may be re-distributed to skeletal

muscle for storage in the form of IMTG. "

Obviously useful when trying to survive on an empty stomach while

looking for food.

Not surprising if elevated level of plasma lipids cause type 2

diabetes in a context made up of calorie abundant foods and sedentary

lifestyle.

BY IMPLICATION it seems that a diet high in carbohydrates, but not

over abundant in calories, is the best way to avoid the viscious cycle

caused by this glucose sparing effect brought about by the mediation

of insulin resistance, WHEN NOT REGURLARLY EXERCISING or otherwise

approaching the levels of physical activity of paleolithic humans

where extra fat intake would have represented great advantages given

the paucity of glucose sources.

" The whole-body effects of impaired muscle glucose disposal and

insulin resistance during starvation or carbohydrate restriction would

be relatively greater in the athlete/hunter–gatherer than in sedentary

modern man because of their greater relative muscle mass and thus

greater sink for glucose disposal. "

>

> http://news.bbc.co.uk/2/hi/health/4563604.stm

>

> Rodney.

>

[Guest guest]

Hi all, see this link,it seem´s to me like a good resume of the actual knowledge. Question: if pancreas is not enough insulin production what about obesity and insulin resistance? what is first? http://mp.medscape.com/cgi-bin1/DM/y/hwsJ0Fs5jj0Dzr0HAuL0Eh

1GB gratis, Antivirus y Antispam Correo , el mejor correo web del mundo Abrí tu cuenta aquí

[Guest guest]

Hi all, see this link,it seem´s to me like a good resume of the actual knowledge. Question: if pancreas is not enough insulin production what about obesity and insulin resistance? what is first? http://mp.medscape.com/cgi-bin1/DM/y/hwsJ0Fs5jj0Dzr0HAuL0Eh

1GB gratis, Antivirus y Antispam Correo , el mejor correo web del mundo Abrí tu cuenta aquí

[Guest guest]

>>>if pancreas is not enough insulin production what about obesity and insulin

resistance? what is first?

In most all cases.... Obesity

Insulin resistance, (IR) if you think about it, should cause thinness, not

fatness.

In type I diabetics, (no insulin) which could be thought of as the epitomy of

IR, they are thin, not fat.

Jeff

[Guest guest]

>>>if pancreas is not enough insulin production what about obesity and insulin

resistance? what is first?

In most all cases.... Obesity

Insulin resistance, (IR) if you think about it, should cause thinness, not

fatness.

In type I diabetics, (no insulin) which could be thought of as the epitomy of

IR, they are thin, not fat.

Jeff