Questions about Insulin?

[Mojo]

Awww, kitty!

 

[Mojo]

Whether unintentional weight loss/stay constant or gain is indicative diabetes type & stage? Really if, promoting/adding insulin is needed when no weight loss occured in diabetics???

In type 1 diabetes, weight is not really an issue, afaik. It's just a question of the pancreas not being able to produce the insulin. No insulin means that glucose is not taken up from the blood. If the pancreas is not producing insulin, insulin must be administered or the patient will die pretty quickly.

For type 2 diabetes, weight does seem to be an important issue. Type 2 diabetes can often (not always) be regulated by getting some weight off through diet and exercise, but if this is not possible (either because it doesn't work or because the patient is unable to follow this course) other treatments are going to be needed.

 

[Zep]

I suggest we provide any further answers to Kumar in French, German or Spanish. I would suggest that they are equally legible to him (i.e. not), and would be equally read (i.e. not).

Idea? Comments?

 

[Donks]

I suggest we provide any further answers to Kumar in French, German or Spanish. I would suggest that they are equally legible to him (i.e. not), and would be equally read (i.e. not).

Idea? Comments?

Can I do mine in Frenish? How about Spanch?

 

[Mojo]

Can I do mine in Frenish? How about Spanch?

How about spinach?

Mmmmmm, spinach![/homer]

 

[Donks]

How about spinach?

Mmmmmm, spinach![/homer]

Your computer must be very different from mine. This one doesn't have a spinach-web interface.

 

[Zep]

I'm up for it, Donks! It would be a change trying to riddle out some REAL information for a change.

 

[Kumar]

In type 2 diabetes, although insulin levels can be elevated, insulin resistance means that cells are unable to take up glucose from the blood and utilise it by, for example, converting it into energy or storing energy as glycogen or fat. This is what causes the elevated blood glucose. Lipid imbalances do seem to be associated with the condition, but this does not necessarily mean that one causes the other.

Do you have any evidence that hyperinsulinaemia causes (not "is correlated with", causes) increased lipid levels?

Mojo, good reply. But just complete it by thinking dynamically/really.

How lipids (esp. TG) levels can be increased other than this in diabetics (high fats intake not considered)?

Some indirect indications:-

Metabolic Syndrome is a clinical designation that is useful for identifying persons at high risk for ASCVD. The definition of Metabolic Syndrome recognizes the clustering of important risk factors for cardiac and vascular disease. The core abnormality of Metabolic Syndrome is an increase in body fat, most commonly some form of central obesity. Having increased amounts of abdominal fat causes insulin resistance which may then lead to other abnormalities such as hypertension, elevated triglycerides and impaired glucose tolerance. Persons diagnosed with Metabolic Syndrome benefit from treatment of risk factors to prevent ASCVD.
http://www.netwellness.com/healthtopics/obesity/metabolicsyndrome.cfm

SUMMARY

From an initial perception that a disorder of glucose metabolism was the primary event in the pathogenesis of type 2 diabetes, there is now a growing appreciation that chronic elevation of FFA levels is an early event that contributes to the development of this disease. FFAs induce insulin resistance, which increases with FFA levels, and this can be a beneficial adaptive response during starvation and pregnancy. However, insulin resistance can become counterproductive when there is an excess of energy intake associated with physical inactivity. The extra fuel is stored in visceral and subcutaneous fat depots. As fat accumulates, there is an ongoing increase in the levels of plasma FFAs, which causes insulin resistance. In addition, the deficit of another product of adipose tissue (e.g., adiponectin) may contribute to increased insulin resistance. To counter insulin resistance and prevent hyperglycemia, insulin levels increase. In individuals with a genetic predisposition for diabetes, however, the pancreas cannot compensate for the increased secretory demands placed on it, resulting in type 2 diabetes.
http://care.diabetesjournals.org/cgi/content/full/27/9/2253

If this aspect will be clear, you can understand the effect.

 

[Kumar]

In type 1 diabetes, weight is not really an issue, afaik. It's just a question of the pancreas not being able to produce the insulin. No insulin means that glucose is not taken up from the blood. If the pancreas is not producing insulin, insulin must be administered or the patient will die pretty quickly.

Still weight can be relevant. Just check it: Weight gain/excess injected insulin, Stay Constant/right amount, loose/Insufficient insulin. I can't say if a T1 person taking excess insulin can develop IR/X Syndrome or not.

For type 2 diabetes, weight does seem to be an important issue. Type 2 diabetes can often (not always) be regulated by getting some weight off through diet and exercise, but if this is not possible (either because it doesn't work or because the patient is unable to follow this course) other treatments are going to be needed.

I read somewhere on 300+ BG level excercise is not indicated. Anyway above reply can be thought in T2 case by adding own insulin to that.

I am not sure, what insulin test can tell in case of: diabetic patient not on medication, on just oral medicines, on medicines+injected insulin & just on injected insulin?

 

[Mojo]

Mojo, good reply. But just complete it by thinking dynamically/really.

How lipids (esp. TG) levels can be increased other than this in diabetics (high fats intake not considered)?

Some indirect indications:-

If this aspect will be clear, you can understand the effect.

Let's have a look at the link you posted here:

It has long been known that cardiovascular risk factors are not distributed randomly among members in a population but seem to cluster together in the same individuals. That is to say, people at risk to get diabetes are also more likely to have problems with high blood pressure and abnormalities in their blood triglyceride and cholesterol levels.

...

The clustering of risk factors in some individuals and complete sparing in others suggests that a common abnormality is involved in causing these problems.

Again, there is no indication here that diabetes causes abnormalities in blood triglyceride levels. The conditions are associated, but this does not necessarily mean that one causes the other.

 

[Kumar]

Mojo,

Pls re-read my previous two posts as I edited & added.

 

[Mojo]

In type 1 diabetes, weight is not really an issue, afaik. It's just a question of the pancreas not being able to produce the insulin. No insulin means that glucose is not taken up from the blood. If the pancreas is not producing insulin, insulin must be administered or the patient will die pretty quickly.

Still weight can be relevant. Just check it: Weight gain/excess injected insulin, Stay Constant/right amount, loose/Insufficient insulin.

In type 1, the vital thing to consider when deciding how much insulin to administer is the blood glucose level. Anything else is secondary to this.

I can't say if a T1 person taking excess insulin can develop IR/X Syndrome or not.

Agreed. I'm sure you can't.

 

[Mojo]

Mojo,

Pls re-read my previous two posts as I edited & added.

The quotation you added indicates that there are abnormalities in fatty acid levels associated with the development of diabetes, but note that it also says that this

is an early event that contributes to the development of this disease.

They are suggesting that this is a condition predisposing to type 2 diabetes, not that the elevated fat levels are caused by hyperglycaemia or hyperinsulinaemia. So your contention that the increased fat levels are caused by hyperinsulaemia or by the excess blood glucose in diabetes being converted to fat are not supported by what you have quoted.

As usual, you haven't bothered to read what you're posting.

 

[Zep]

Mojo, doesn't it seem "normal" now that we can presume Kumar doesn't read his own sources? I think we long ago cottoned on to the fact he simply Googles on buzz-phrases, and then cut-and-pastes the links. The fact that most of the matches he finds are in articles that actually refute his inane notions has yet to sink in.

I have noticed that lately we on JREF spend a great deal more effort researching Kumar's own sources for him than actually refuting his ideas directly ourselves. In effect, he's getting us to do his own work for him still. I, for one, don't intend to waste my time doing that any more. I can find kitties and recipes much faster.

Research, analysis and comprehension are just big words to Kumar, not anything he actually does.

 

[Mojo]

Well, yes, and as usual he's asking for explanations for phenomena that don't exist, even after it's been explained that they don't.

 

[Donks]

I can find kitties and recipes much faster.

Tu peux tambien faire las deux búsquedas au mismo temps.


Edited to test my Spanch.

 

[Kumar]

In type 1, the vital thing to consider when deciding how much insulin to administer is the blood glucose level. Anything else is secondary to this.

Yes, it should match exactly with BG level. How it is possible? How much insulin is required say for 100 excess sugar?

Mojo, I think that link tells:-

"FFAs induce insulin resistance, which increases with FFA levels...The extra fuel is stored in visceral and subcutaneous fat depots. As fat accumulates, there is an ongoing increase in the levels of plasma FFAs, which causes insulin resistance. "

The extra fuel here can be carbohydrates. FFAs can be converted from excess glucose in presence of insulin/extra insulin. It looks like visious circle but I think, it start with glucose conversion into fats(by How stuf works link provided by me in this topic).

In summary, insulin resistance appears to be a syndrome that is associated with a clustering of metabolic disorders, including non-insulin-dependent diabetes mellitus, obesity, hypertension, lipid abnormalities, and atherosclerotic cardiovascular disease.

www.nutritionandmetabolism.com/pubmed/2044434

High blood glucose levels trigger the pancreas to produce insulin — the body’s hormone messenger for telling the energy storage cells to start taking in the glucose for storage because an elevated glucose level in the blood is dangerous to health. The priority storage areas are muscle and liver cells, where that excess glucose is converted into quick release glycogen. Once the quick release energy reserves are topped up, glucose is converted into fat in our fat cells for longer-term storage. However, a combination of high levels of sugar and a sedentary lifestyle means that all these storage areas are usually full — so full that the fat cells have become bloated (we get fatter) and cannot soak up any more glucose. This means that the excess glucose starts to circulate in the blood, where it can potentially damage blood vessels, kidney function, the retina and general metabolic efficiency.

Doctors estimate that as many as 1 in 5 of us have a metabolism which cannot cope with this chronic exposure to high insulin levels caused by this excess glucose in the blood: the storage cells are full and so they can no longer respond to insulin's message to store more glucose — they become insulin resistant. This means that the cells exposed to chronically high levels of insulin have become conditioned to ignore insulin’s message to take out the excess glucose in the blood. The result is that glucose levels start to rise as less can stored which triggers the pancreas to flood the body with even more insulin to try to control it. This creates a dangerous metabolic imbalance which can lead to serious health problems such as excessive free radical damage, hypertension, high blood pressure, unhealthy blood-fat profiles and Type II diabetes. (This insulin resistance is also compounded by stress, which naturally signals the body to release even more glucose and fatty acids into the bloodstream so that we are ready for action. It also causes the brain to release stress hormones which causes the fat storage cells to be even less insulin-sensitive.)http://www.weightlosscenter.co.uk/syndrome-x.asp

Indications of hyperinsulinemia include weight gain (especially around the waist, producing the apple shape, not the pear shape), increased blood pressure and cholesterol. Testing for elevated insulin levels can be an important step toward better health, and the prevention of diabetes and chronic disease processes later in life.
http://www.diagnose-me.com/cond/C312817.html

Over 80 million Americans suffer from insulin resistance, and it appears to sit at the center of a web of related health problems. Women who are insulin resistant are at much greater risk of obesity, diabetes, hypertension (high blood pressure), heart disease, high cholesterol, breast cancer and polycystic ovarian syndrome (PCOS). There is some evidence that insulin resistance may contribute to endometrial cancer. It's also been implicated in Alzheimer's disease.
http://www.womentowomen.com/LIBinsulinresistance.asp

Insulin resistance
When your cells are exposed to insulin at all, they get a little bit more resistant to it. So the pancreas just puts out more insulin. Cells become insulin resistant because they are trying to protect themselves from the toxic effects of high insulin. They down-regulate their receptor activity and number of receptors so that they don't have to be subjected to all that stimuli all the time.

Different cells respond to insulin differently. Some cells are more resistant than others, as some cells are incapable of becoming very resistant. The liver becomes resistant first, followed by the muscle tissue and lastly the fats. As all these major tissues, become insulin resistant your pancreas is putting out more insulin to compensate. Any time your cell is exposed to insulin it is going to become more insulin resistant. That is inevitable, we cannot stop this process, but the rate we can control.

http://www.healingdaily.com/detoxification-diet/insulin.htm

You can find many links.

 

[Mojo]

Mojo, I think that link tells:-

"FFAs induce insulin resistance, which increases with FFA levels...The extra fuel is stored in visceral and subcutaneous fat depots. As fat accumulates, there is an ongoing increase in the levels of plasma FFAs, which causes insulin resistance. "

The extra fuel here can be carbohydrates. FFAs can be converted from excess glucose in presence of insulin/extra insulin.

Are you talking about excess glucose in the blood or too much sugar in the diet here?

 

[Eos of the Eons]

 

[Kumar]

Are you talking about excess glucose in the blood or too much sugar in the diet here?

Both are related in diabetics.

Btw, what do your understanding tell now, can hyperinsulinemia cause excess lipids in blood & possible CV problems or not? If you say not, how diabetes patients commonly get high TG/lipid levels?