Re: CR reverses heart tendon glycation?

[Guest guest]

Heh, the THREE interesting pieces of data from this study are the following:

"Results. Mean and maximum longevities were similar in CON and TG mice....."

"In peripheral muscle, glycation and glycemic damage were generally higher in TG mice...."

"Conclusions. Lifetime overexpression of GLUT4 in muscle results in a small decrease in mean glycemia......"

Somebody help me understand this and integrate these three concepts. I sometimes need help due to the fact that my math/logic skills sometimes leave something to be desired, as I tend to work in a "inductive, subjective fuzz" that, much to the consternation of others, tends to be right with a annoyingly high frequency.

It would seem that this study confirms previous research indicating that glycemic changes have nothing to do with lifespan modifying interventions, sending this whole research front into the same conceptual rubbish heap that de Grey's tripe has already been relegated to. If one organism [ the transgenic ] is experiencing less glycemia, and yet it lives exactly the same length of time as the other *eating the same amount of food*, then we don't have a variable that is contributing to aging significantly, do we?

The only way you could argue that it still had an impact is if you suggest that the reduction in glycemia was perfectly negated by the increase in peripheral muscle glycation, but, that is a bit of stretch in my book.

I'm not saying that we shouldn't think about such influences "at all", but, in a world of stuff to worry about, I want to pick my fights intelligently and not go tilting at windmills.

=-=-=-=-=-=-=-=-=-

Exp Gerontol. 2005 Apr;40(4):303-14.

Related Articles,

Links

Hyperglycemia, impaired glucose tolerance and elevated glycated hemoglobin levels in a long-lived mouse stock.

"Taken together, these findings suggest that neither a reduction of blood glucose levels nor an increase in glucose tolerance is necessary for life span extension in mice." - PMID: 15820611 =-=-=-=-=-=-=-=-=-=

T.

pct35768@...__________________________________________________

[Guest guest]

On an intuitive basis, I feel that the glycation theory is more

compelling than the free radical theory of aging, particularly because

the shaping of DNA and proteins is determined by sugars. (Quiocho FA.

Carbohydrate-binding proteins: tertiary structures and protein-sugar

interactions. Annu Rev Biochem. 1986;55:287-315. PMID: 3527044 )

However, I think that glycation and percent of body fat have some

interaction that is not being taken into consideration in the

experiments.

Caloric Restriction reduces the average level of blood glucose thereby

reducing the potential of creating glycation products. However, blood

glucose levels are mediated by pancreatic hormones. A fat person

(>30% Body Fat) will have more available fat that can be converted to

glucose by the action of glucagon. A thin person (<14% Body Fat) will

have less fat available for conversion to glucose.

Caloric Restriction may be more effective at reducing glycation in

thin people than in fat people, but only if glucagon continues being

produced as a response to " hunger " or food deprivation in spite of the

lower percentage of body fat.

The reduction of glycation by the hormonal reaction to hunger may be

operative in CR and every-other-day fasting, whereas ad libitum

feeding does not create periods low in glucose that are long enough to

stimulate glucagon and prevent glycation.

There is a HUGE gap in our understanding of all the hormones that

become active as a result of CR to regulate metabolism.

Tony

--- In , T <pct35768@y...>

wrote:

> Heh, the THREE interesting pieces of data from this study are the

following:

>

> " Results. Mean and maximum longevities were similar in CON and TG

> mice..... "

>

> " In peripheral muscle, glycation and glycemic damage were generally

higher in TG mice.... "

>

> " Conclusions. Lifetime overexpression of GLUT4 in muscle results in

a small decrease in mean glycemia...... "

>

> Somebody help me understand this and integrate these three concepts.

I sometimes need help due to the fact that my math/logic skills

sometimes leave something to be desired, as I tend to work in a

" inductive, subjective fuzz " that, much to the consternation of

others, tends to be right with a annoyingly high frequency.

>

> It would seem that this study confirms previous research indicating

that glycemic changes have nothing to do with lifespan modifying

interventions, sending this whole research front into the same

conceptual rubbish heap that de Grey's tripe has already been

relegated to. If one organism [ the transgenic ] is experiencing less

glycemia, and yet it lives exactly the same length of time as the

other *eating the same amount of food*, then we don't have a variable

that is contributing to aging significantly, do we?

>

> The only way you could argue that it still had an impact is if you

suggest that the reduction in glycemia was perfectly negated by the

increase in peripheral muscle glycation, but, that is a bit of stretch

in my book.

>

> I'm not saying that we shouldn't think about such influences " at

all " , but, in a world of stuff to worry about, I want to pick my

fights intelligently and not go tilting at windmills.

>

> =-=-=-=-=-=-=-=-=-

>

> Exp Gerontol. 2005 Apr;40(4):303-14.Related Articles, Links

>

>

> Hyperglycemia, impaired glucose tolerance and elevated glycated

hemoglobin levels in a long-lived mouse stock.

>

>

> " Taken together, these findings suggest that neither a reduction of

blood glucose levels nor an increase in glucose tolerance is necessary

for life span extension in mice. " - PMID: 15820611

> =-=-=-=-=-=-=-=-=-=

> T.

> pct35768@y...