Unfortunatelty.....the OTHER ala thread was closed so......

[Drveejay11]

Exercise in Type II Diabetes Mellitus

Initial treatment of type II diabetes consists of weight reduction, dietary control, exercise, and oral hypoglycemic agents. Insulin replacement is seldom necessary but should be added to the treatment regimen when hyperglycemia remains unchecked by these methods. Exercise is a major contributor in controlling hyperglycemia through improved peripheral insulin sensitivity, enhanced insulin binding, and reduced obesity.

Exercise can aid glycemic control and in combination with proper diet help prevent type II diabetes from occurring in those persons at risk. Exercise does this by improving short-term insulin sensitivity and reducing insulin resistance, both of which begin to disappear a few days after exercise is discontinued. Althought the number of insulin receptors remains constant with exercise, the biding of insulin to adipocytes is increased with no increase noted in binding to myocytes. In both cell types, however, the number and activity of glucose transport proteins (particularly Glut-4-isoform) are increased with exercise. This results in an increase in insulin-stimulated glucose transport into these cells following exercise, which improves glycemic control.

With the onset of exercise, the type II patient, does not respont with a decrease in serum glucose concentration as in the nondiabetic. This is due to increased glucose uptake in the peripheral tissues. As a result, serum glucose is higher, and liver glucose production is halted to allow for normalization of the hyperglycemia by overall reduction in the glucose level. In constrast to the type I patient, type II diabetics do not usually suffer hypoglycemia because endogenous insulin levels can usually be maintained. Those athletes on oral hypoglycemic agents or insulin, however, may have problems with glucose homeostasis during exercise. The athlete may need to lower the medication dose or increase carbohydrate intake (or both) before exercise to prevent hypoglycemia. Severe hypoglycemia is unusual because individuals are still able to reduce endogenous insulin production as blood glucose levels decline.


Bibliography

1. Sports Medicine for Primary Care, Willian E. Moats
2. Goodman, The Pharmacological Basis of Therapheutics, Nineth Edition, Goodman & Gilman’s
3. The Medical Clinics of North America, Vol 78, Num 2 , Gray I. Wadler.
4. Cecil , Textbook of Medicine. twenth edition, Bennet & Plum
5. Exercise prescription fo Individuals with metabolic disorders (pratical considerations) John C. Young. SPORTS MED. 19(1) PAG 43 - 54 1995

 

[Animalkits]

Again, we aren't diabetic, most of us.

And you see exactly THEIR problem which is myocetes don't change.

 

[macro]

Again, we aren't diabetic, most of us.

.

actually upwards of 2/3's of the population has some form of insulin resistance.

Insulin resistance increases with age,in the absence of genetic abnormalities even with exercise and low body fat.

 

[macro]

And please, tell us how fat cells are sucking glucose out of the bloodstream over muscle during exercise? It ain't happening though I'm sure somebody will be amused by the story.

no its not, but most people, on these boards and in general, train for 1-2hrs per day or less. They are not endurance atheletes.

no one argued that point. so you won against yourself.

but if you are insulin resistant post exercise, due to spikes in insulin, you will uptake more glucose AND fatty acids into adipose tissue.

 

[Animalkits]

3/4 of the population is overweight or OBESE!

Insulin resistance EXACTLY occurs because you are overweight and DO NOT exercise. Just because YOU caused YOUR own condition by being fat and lazy doesn't change anything!

Your body is telling YOU something. Stop eating cause we don't want anymore glucose!

So sell it to them along with leptotrim which is so strong you shouldn't use it if you just want to lose 5-10 'vanity' pounds.

 

[macro]

BAHHAA!

I guess my muscle can't use the glucose I take in.

muscle makes up less than 20% of the bodies glycogen stores.

 

[macro]

1. r-ala does NOT make you fatter
2. glucose is preferentially taken up into muscle cells
3. R-ala inhibits adipogenesis and adipocyte differentiation

this does not take into account the benefits of lowering plasma insulin on LPL and adipogenesis. Particularly decreasing fatty acid uptake into adipose tissue.

an r-ala system with 250micromoles/l will in face of carbohydrate excess will increase carbohydrate oxidation via MaPK and PPAR-y activity... essentially it will raise metabolic rate through the oxidation of carbs.

 

[Animalkits]

And the study for number 1 is where?

A study for number 2 DOES NOT exist.

 

[Animalkits]

Oh yea, and you never did explain why yohimbine, HGH, and your ALA friend cause water to be held in abdominal fat, did you?

(I bet you forgot while posting my picture, so I'll give you a pass)

 

[Animalkits]

I didn't know we need insulin for fatty acid uptake. Maybe you mean retention?

 

[Animalkits]

muscle makes up less than 20% of the bodies glycogen stores.

I bet when we exercise, blood glucose is generated from fat, now, right?

Fat is a glycogen storage unit, now?

 

[ulter]

You want to argue out both sides of your mouth in opposite directions. Earlier physicians and pharmacists that approved Glucorell R as meeting the claims of the label were [incompetent]. NOW you want to read where doctors (I assume you have some in mind that meet your approval in a study) prove something (fat accumulation) doesn't exist in the presence of R+ALA. So you're asking that we prove something doesn't exist. But you said that no one can prove that something doesn't exist.
You just talk to talk sometimes.
NOTE: Not one of the 4000 repeat users of Glucorell R has reported fat gain. They have however reported fat LOSS. So maybe we'll just take their word for it instead of trying to prove something doesn't exist.

 

[Animalkits]

Please post their signed affidavits.

Researchers are the same as doctors?

Others have reported no change or what appears to be fat/water gain. See above to answer the question.

The glucose in the fat cell does what and turns into what?

Evidently YOU are claiming it DOES NOT change into fat and you have signed affidavits from people as well, but since your theory would dictate something extraordinary, you DO have to prove YOUR mechanism exists.

 

[Animalkits]

BTW, I was going along with ya, but you had to jack it up again.

Go ahead!

 

[Animalkits]

Did he answer any of the above questions?

Hmmm? I ask a question and we going into a sales pitch and customer testimonials.

 

[Animalkits]

but if you are insulin resistant post exercise, due to spikes in insulin, you will uptake more glucose AND fatty acids into adipose tissue.

Wait, how can I take in more than what's there? I don't get it.

Insulin gets FA's into the cell as opposed to where?

NEW YORK - (Reuters Health) - Scientists in Massachusetts have discovered that the sugar-regulating hormone insulin plays a crucial role in moving fatty acids from the blood to fat-storage cells after a meal.

Although the research was conducted on the cellular level, eventually it may lead to a better understanding of how fat is metabolized in the body, the study's lead author told Reuters Health.

After a meal, levels of both sugar, or glucose, and fatty acids rise in the blood. Scientists knew already that insulin reduces glucose in the blood in two ways. First, the hormone signals the liver to slow its production of glucose. Second, insulin increases the uptake of sugar into tissues by causing glucose transporters within each cell to move to the surface where they draw sugar into the cell.

How the body lowers levels of fatty acids in the blood has been uncertain, however.

Now Dr. Harvey F. Lodish and colleagues at the Whitehead Institute for Biomedical Research at the Massachusetts Institute of Technology in Cambridge report that insulin is also involved in regulating levels of fatty acids in the blood. A report on the findings appears in the April issue of the journal Developmental Cell.

``Insulin causes cells to take up fatty acids from the blood,'' Lodish said in an interview. ``It does so by a fundamentally similar mechanism'' to how it handles sugar, he explained.

When the researchers added insulin to cells called adipocytes--which store most of the body's fat--fatty acid transporters moved to the surface of the cells from other parts of the cells. These transporters, FATP1 and FATP4, seem to promote the uptake of fatty acids into cells, because as the transporters congregated at the cell membrane, levels of fatty acids in the blood dropped.

Now that researchers understand how fatty acid transporters affect the uptake of fat on the cellular level, the next step, according to Lodish, is to measure the impact the transporters have on overall levels of fat in the body.

Genetically altering mice to have more or fewer fatty acid transporters may reveal the role these transporters have in the metabolism of fat by the whole body, he said. Such research could also lead to a better understanding of diseases that affect metabolism, including type 2 diabetes, Lodish and his colleagues note in their report.

 

[Animalkits]

Here is how you induce insulin resistance!

"If you have high fuel levels in a muscle exposed to high glucose levels, one gets resistance to insulin," said Ruderman. "The second thing that produces insulin resistance is inactivity, the one thing known to increase insulin sensitivity. This is one of the bases for using physical activity to treat people with metabolic syndrome and type II diabetes in its early stages." Diet is also used to good effect to sensitize diabetes patients and others to insulin. Insulin-resistant rodents follow this pattern. Even lean rats have a dampened response to insulin when given excess glucose for a day.

 

[macro]

if you want to actually learn about the insulin/fat connection read up on insulin's effects on Lipoprotein lipase as well as its inhibition of GH related lipolysis. There is more to it than that, but those are among the basic concepts.

 

[macro]

agree that exercise is essential to getting good insulin sensitivity

its essential for a whole host of health benefits.

 

[Animalkits]

I know that insulin inhibits lipase which is a real tough one.

Again, that's not the problem. The problem is the glucose goes into the fat cell anyhow and it's metabolized into WHAT?

IGF works by keeping glucose OUT of the cell which is exactly what we want!

Basal and insulin-stimulated glucose incorporation into lipids was reduced in adipose tissue segments and isolated adipocytes from the IGF-I-treated rats IGF-I has opposite effects on glucose uptake in adipose tissue and skeletal muscle, findings which at least partly explain previous reports of reduced body fat mass, increased body cell mass, and increased insulin responsiveness after IGF-I treatment..

IGF keeps it out while increasing sensitivity in muscle.