Questions about Hyperinsulinemia/Diabetes

[Mojo]

You cling desperately to even the most silly notions forever, never really abandoning them even after people have been lecturing you endlessly on why you are wrong.

And, Kumar, please note that the important word in this sentence of Hans' is "why." It's not as if people just reject your ideas without giving reasons. You are given explanations, if only you'd understand them, of why your notions do not fit the observed facts.

 

[Kumar]

It tells me two conditions. The two major pathogeneses of type 2 diabetes mellitus (T2DM) are insulin resistance and insulin secretion deficiency.


Well, cut and paste does not show understanding. We already know you can cut and paste .

I already mentioned, it tells me.

This is not incorrect, since not all type 2 patients are obese, but that is not what the text says.

Relation of obesity with IR/type2 is bit contradictary. Mojo's link tells these are not related.

Kumar tries to reassemble the words in the text to support his pet theory. Kumar, I have news for you: In English, the sequence of the words have an impact on the meaning, so you can't just shuffle them about at will.

I meant insulin defficient (unless medicated) can't become hyperinsulinemic. So they may not be obese.

Insulin resistant can be obese--naturally & medicated.

How can you be medicated obese?

Insulin resistasnt can become obese either due to natural secretion of excess insulin or promoted by medications.

Rest just TTTT, so deleted/ignored.

 

[Kumar]

What is incomplete about that? What more do you want to know?

Rolfe.

About decreased renal threshold for sugar. What can do that?

 

[MRC_Hans]

*snip*

Rest just TTTT, so deleted/ignored.

[/B]

All just TTTT, so ignored.

Hans

 

[Kumar]

....Nonsense. Normally, I encourage people to think, but in your case, I'll make an exception: Don't think too much Kumar. Nothin good seems t ocome out of it.



Mr. Hans, you may restrict/resist or request me not to think buy you people just Think about "Insulin secretion still remain normal in many resistant cases". How then it can be a beta cells disorder/diabetes? Persistent hammer of Excess glucose can impair insulin secretion & create insulin defficient or type2/1 patients. How hammering of glucose can become possible?? Just think deeply.

Rest bit TTTT, which I can't entertain as bit over-loaded...Sorry.

 

[Mojo]

Relation of obesity with IR/type2 is bit contradictary. Mojo's link tells these are not related.

No it doesn't. It says that insulin resistance is not caused by insufficient fat storage capacity.

 

[Kumar]

No, type 1 diabetes does not encourage glucose conversion to fat. This is because the high blood glucose level in diabetics is caused by their cells being unable to take up and metabolise glucose.

Why type1 can't encourage glucose conversion into fats when excess glucose/insulin is present to do that? I think type1 are not considered as resistant.

I don't think Rolfe has said this. In fact, she's indicated that glycosuria is caused by hyperglycaemia, not hypoinsulinaemia:

Are you making fun of me? Are hyperglycaemia & hypoinsulinaemia not related to each other?

Anyway, I am more interested to understand about "decreased renal threshold for sugar" in IR/type2 conditions who are medicated or not/insufficient medicated.

 

[Kumar]

And, Kumar, please note that the important word in this sentence of Hans' is "why." It's not as if people just reject your ideas without giving reasons. You are given explanations, if only you'd understand them, of why your notions do not fit the observed facts.

This thread is going pretty well to my satisfaction. Thanks to all for their contributions & efforts. Even 1% gain will be real gain.

 

[Mojo]

This thread is going pretty well to my satisfaction. Thanks to all for their contributions & efforts. Even 1% gain will be real gain.

There seem to be important things going on in the real world today, so excuse me if I don't deal with your nonsense for a while.

 

[Rolfe]

I note that some pretty high-glucose samples are still low-SG. Which makes me conclude that the amount of diuresis must be pretty spectacular. But even though it's a significant calorie loss to the body, it never makes any difference to the blood glucose.

Excessive excretion of sugar in the urine will decrease the blood sugar level....

Kumar, HAVE YOU A PROBLEM WITH READING????

Rolfe.

It's hopeless. I give up (again).

 

[Kumar]

No. As you have been repeatedly told, insulin resistance is caused by long-term hyperglycaemia, and obesity is a contributing factor.

How obbesity is a contributing factor? Can you tell some science behind it?
quote:

If a patient is taking "sufficient medications" their glucose metabolism should be more or less normal, and their weight will be dependent on diet and exercise, the same as anyone else's. Weight loss in the later stages of type 2 diabetes is caused by their not being able to take up and utilise glucose from the blood as a result of not having sufficient levels of insulin to overcome resistance.

I think Insulin resistants commonly not lose the weight uptill ther are IR.


The intestines have evolved to absorb as much sugar as possible. "Excess sugar," as you put it, will be absorbed if there is too much sugar in the diet. This is certainly not a defect in the gut itself.

Alike low side of renal threshold, this also looks to me "a big doubt, miss or weakness" in view of normal secretion of insulin in many cases but still they are said as diabetic/IR. I think modern foods, lifestyle, envirinment contribute to excess absorption. How? We should try to find out. Salt, fats, gastric acid or some other is to be checked. Excess intake of salt & excess gastric acid due to modern stresses/food can be thought. Modern lifestyle is an acepted contributing factor to modern epidemic type of spread of diabetes, hypertention etc. How??
quote:

No. The kidneys, as you have already been told, are not part of the body's system for regulating blood sugar levels.

Do you want to say that there can't be change in normal "renal threshold for sugar" during the progression of diabetes due to it?

Do you also want to say that there can't be change in normal " sugar absorption in intestines" during the progression of diabetes due to it?

 

[Rolfe]

[BI don't think Rolfe has said this. In fact, she's indicated that glycosuria is caused by hyperglycaemia, not hypoinsulinaemia:

Are you making fun of me? Are hyperglycaemia & hypoinsulinaemia not related to each other?

Anyway, I am more interested to understand about "decreased renal threshold for sugar" in IR/type2 conditions who are medicated or not/insufficient medicated. [/B]

This is pathetic.

Glycosuria is caused by hyperglycaemia. Or by a kidney defect. Full stop. Yes, hypoinsulinaemia is one cause of hyperglycaemia, but it is not the only one. It is hyperglycaemia which is the cause, not hypoinsulinaemia, which may or may not be present.

"Decreased renal glucose threshold" is another way of describing "renal glycosuria", which is purely a disease of the kidney, and has nothing to do with diabetes. If you want to know about that, Google for "renal glycosuria" (or "renal glucosuria"), and also try "Fanconi Syndrome". And I would strongly recomment you include the quote marks!

Poorly controlled type II diabetic patients do not have a decreased renal glucose threshold (unless the coincidentally develop something like Fanconi Syndrome, which I have neve heard of happening). What on earth gave you the idea that they did?

Rolfe. (still giving up)

 

[Kumar]

Originally posted by Rolfe

"Decreased renal glucose threshold" is another way of describing "renal glycosuria", which is purely a disease of the kidney, and has nothing to do with diabetes. If you want to know about that, Google for "renal glycosuria" (or "renal glucosuria"), and also try "Fanconi Syndrome". And I would strongly recomment you include the quote marks!

I am not thinking about "renal glycosuria" as it is another disorder. But I am thinking about lesser total loss of sugar in urine. It may be due to kidney is absorbing more OR sugar is in low concentration in urine OR there is less total secretion of urine. I mean if total loss of sugar is lesser than normal/needed per day? This may cause high level of glucose in blood.

Poorly controlled type II diabetic patients do not have a decreased renal glucose threshold (unless the coincidentally develop something like Fanconi Syndrome, which I have neve heard of happening). What on earth gave you the idea that they did?

Yes naturally, hyperglycemia can cause more urine secretion, concentrated urine for sugar & probably low absorption by kidneys per day. It will also encourage thirst( polydipsia) which can be needed for excess secretion of urine per day & avoid dehydration. Is it not a natural mechanism to control hyperglycemia? Btw, how do you calculate renal threshold for sugar.

I am also thinking about relation of hyperinsulinemia+ hyperglycemia due to IR with total sugar loss in urine. Can hyperinsulinemia effect renal re-absorption, amount of total urine or sugar concentration in urine resulting in lesser total loss of sugar per day and hyperglycemia?

Insulin
When you eat a candy bar or a meal, the presence of glucose, amino acids or fatty acids in the intestine stimulates the pancreas to secrete a hormone called insulin. Insulin acts on many cells in your body, especially those in the liver, muscle and fat tissue. Insulin tells the cells to do the following:
Absorb glucose, fatty acids and amino acids
Stop breaking down:
glucose, fatty acids and amino acids
glycogen into glucose
fats into fatty acids and glycerol
proteins into amino acids
Start building:
glycogen from glucose
fats (triglycerides) from glycerol and fatty acids
proteins from amino acids
http://home.howstuffworks.com/fat-cell3.htm

Whether these roles of insulin indicate, hyperinsulinemia causes more absorption of glucose, fatty acids and amino acids in intestines and lesser loss of sugar in urine?

 

[Kumar]

The following image (just posting url/not image)/link clears one thing to me that, convertion of glucose to fats starts from "acetyl CO A", so IR can effect it as Mr.Hans/Mojo..insisted. So this theory of hyperinsulinemia effect due to glucose conversion can't work. Sorry.
IMG: http://www.elmhurst.edu/~chm/vchembook/images/590metabolism.gif

Lipids or fats are stored in cells throughout the body principle in special kinds of connective tissue called adipose tissue or depot fat. Whereas many cells contain phospholipids in the bilayer cell membranes, adipose tissue cells consist of fat globules of triglycerides which may occupy as much as 90% of the cell volume.

Fat insulates the body from heat loss and extreme temperature changes. At the same time, fat deposits under the skin may be metabolized to generate heat in response to lower skin temperatures.
http://www.elmhurst.edu/~chm/vchembook/620fattyacid.html

We may now check relation of obesity with IR, by lipids in muscle cell's membrane as phospholipids.

Chylomicrons do not last long in the bloodstream -- only about eight minutes -- because enzymes called lipoprotein lipases break the fats into fatty acids. Lipoprotein lipases are found in the walls of blood vessels in fat tissue, muscle tissue and heart muscle. The activity of lipoprotein lipases depends upon the levels of insulin in the body. If insulin is high, then the lipases are highly active; if insulin is low, the lipases are inactive.
http://home.howstuffworks.com/fat-cell3.htm

What Hyperinsulinemia can do in view of above quotes?

 

[Rolfe]

I am not thinking about "renal glycosuria" as it is another disorder.

Good, good, something seems to have been understood....

But I am thinking about lesser total loss of sugar in urine. It may be due to kidney is absorbing more OR sugar is in low concentration in urine OR there is less total secretion of urine. I mean if total loss of sugar is lesser than normal/needed per day? This may cause high level of glucose in blood.

Think a bit harder. It is not a decrease in the renal glucose threshold which will cause a decrease in the total loss of glucose on the urine, it is an increase. And yes, I believe this sometimes happens in long-term diabetics, but as I said it's not something I know much detail about.

There is no apparent effect on the blood glucose concentration. All the experience we have in dealing with diabetic patients indicates that blood glucose concentration is in practical terms unaffected by the amount of glucose lost in the urine. However, it does mean that the body is losing less energy, the patient is not dehydrated or polydipsic, and the risk of urinary tract infection is less.

Get over it, Kumar. Glycosuria is an incidental finding in diabetes, and of no metabolic consequence. Handy for diagnostic purposes (or it once was), and a nuisance because of causing the thirst and the cystitis, but not important otherwise.

Remember, normal urine glucose is (in practical terms) zero. So you can't possibly decrease urine glucose in a normal individual. When blood glucose concentration increases to greater than the renal threshold, glycosuria will occur. The only way to alter this is by getting the blood glucose back down, or if the renal glucose threshold happens to rise. But it's only important because of the side effects. In terms of the main issue of diabetic control, it's the
blood glucose that matters, and the only way you will decrease that is by the usual methods of treating diabetes. How much glucose you might (or might not) lose in the urine doesn't affect it.

Yes naturally, hyperglycemia can cause more urine secretion, concentrated urine for sugar & probably low absorption by kidneys per day. It will also encourage thirst( polydipsia) which can be needed for excess secretion of urine per day & avoid dehydration.

Good, so far somebody might even have been listening.....

Is it not a natural mechanism to control hyperglycemia?

NO!!!! How many times do I have to tell you? It doesn't make a blind bit of difference to hyperglycaemia. It's an unavoidable side-effect of the way the kidney works, that's all.

Btw, how do you calculate renal threshold for sugar.

You perform a glucose tolerance test, collecting urine samples every 30 minutes or so during the test.

I am also thinking about relation of hyperinsulinemia+ hyperglycemia due to IR with total sugar loss in urine. Can hyperinsulinemia effect renal re-absorption, amount of total urine or sugar concentration in urine resulting in lesser total loss of sugar per day and hyperglycemia?

Whether these roles of insulin indicate, hyperinsulinemia causes more absorption of glucose, fatty acids and amino acids in intestines and lesser loss of sugar in urine?

I'm going home.

Rolfe.

 

[Kumar]

You perform a glucose tolerance test, collecting urine samples every 30 minutes or so during the test.

Rolfe, I started understanding & learning from you. Thanks.

Does it make some difference, if collection of urine in on per day basis instead of random or 2-3 times?

Your subject.

Do animals also get diabetes & IR conditions? Could you be able to differenciate it in city & wild animals?

 

[Kumar]

You have been repeatedly told that type 1 and type 2 diabetes are diffrerent conditions, with different causes. You have been repeatedly told that insulin resistance is not caused by hyperinsulinaemia; it's the other way round. You have even posted an abstract indicating this yourself! Why can't you grasp these simple facts?

Try to get it straight: Both type 1 and type 2 diabetics have elevated blood sugar levels. In type 1 diabetes is this is caused by the pancreas not producing enough insulin; in type 2 it is caused by the body's cells not responding properly to insulin. The end result is similar, but the causes are different.

I know the difference, better. Type2 can also be IDDM and IR.

I am only trying to understand & differenciate;" pancreas not producing enough insulin" AND "pancreas still producing enough insulin" and if should both be covered under diabetes, genetic predisposition(or genetic adaption/impression to changed environment) or not?

For this;

Modern lifestyle/environment is a contributing factor to current epidemic type spread of diabetes....means to most of diabetes cases. What by Modern lifestyle/environment can contribue to getting this much diabetes? These may be some;

1.Oxygen levels/Intake & its normal use, if effected due to suspended particles, O2 levels, pollution etc.

2. Modern foods-if acid producing.

3. Modern stresses(by electronics, travels, tensions, manipulations, posting on forums on on iernet, addictions (can't say about belief/skepticism related) etc.-- mostly mental--if can cause excess gastric acid secretions or pH/bile/mucus imbalances.

4. Intake of Excess Salt, fried snacks, choclates, new fats, outside foods, white sugar etc. Sodium, white sugar & fried snacks can be of great importance.

5. Concrete jungles, lesser green covers, lesser outdoor activities & mass air conditioning, clothings..

6. Excess sex?.

You can tell other contributing factors.

 

[Donks]

I am only trying to understand & differenciate;" pancreas not producing enough insulin" AND "pancreas still producing enough insulin" and if should both be covered under diabetes

Yes.

genetic predisposition

They are both related to genetic predispositions, but different ones. Type 1 is related to a predisposition to autoimune disorders. Type 2 is related to a predisposition to IR.

1.Oxygen levels/Intake & its normal use, if effected due to suspended particles, O2 levels, pollution etc.

Unless you have evidence for this, I'll dimiss it as an idiotic assertion. Where did you see that Oxygen intake was a risk factor for diabetes?

2. Modern foods-if acid producing.

Unless you have evidence for this, I'll dimiss it as an idiotic assertion. Where did you see that acidic foods, or foods that produce an acid environment in the disgestive tract are a risk factor for diabetes?

3. Modern stresses(by electronics, travels, tensions, manipulations, posting on forums on on iernet, addictions (can't say about belief/skepticism related) etc.-- mostly mental--if can cause excess gastric acid secretions or pH/bile/mucus imbalances.

Unless you have evidence for this, I'll dimiss it as an idiotic assertion. Where did you see that... any of this idiotic gibberish is a risk factor for diabetes?

4. Intake of Excess Salt, fried snacks, choclates, new fats, outside foods, white sugar etc. Sodium, white sugar & fried snacks can be of great importance.

Now you're getting somewhere.

5. Concrete jungles, lesser green covers, lesser outdoor activities & mass air conditioning, clothings..

Lesser outdoor activities. Close enough. The other are just inane gibberish, unless you have evidence.

6. Excess sex?..

No such thing. And if it has any effect on diabetes, it's the opposite. It's physical excercise, which is good.

You can tell other contributing factors.

The major risk factors for type 2 diabetes mellitus are the following:

* Age - Older than 45 years

* Obesity - Weight greater than 120% of desirable body weight (true for approximately 90% of patients with type 2 diabetes)

* Family history of type 2 diabetes in a first-degree relative (parent or sibling)

* Hispanic, Native American, African American, Asian American, or Pacific Islander descent

* History of prior impaired glucose tolerance (IGT) or impaired fasting glucose (IFG)

* Hypertension (>140/90 mm Hg) or dyslipidemia (high-density lipoprotein [HDL] cholesterol <35 mg/dL or triglyceride level >250 mg/dL)

* History of GDM or delivering a baby who weighed more than 9 pounds, which suggests GDM (source)

You could have found out in a 20 second google, and it would have saved a lot of people a lot of time.

 

[Mojo]

Excess sex?

Well, maybe, but I don't think I want you to be involved.

It was nice of you to ask though.

 

[Kumar]

Yes.

They are both related to genetic predispositions, but different ones. Type 1 is related to a predisposition to autoimune disorders. Type 2 is related to a predisposition to IR.

Yes that is ok but when pancreas is secretinf enough insulin, how can it can be a genetically predisposed pancreas defect? Can't it be a temporary inherant or aqired expression of that, more sugar/insulin was/is needed as in gest. diabetes:-

What is gestational diabetes?

Pregnant women who have never had diabetes before but who have high blood sugar (glucose) levels during pregnancy are said to have gestational diabetes...

We don't know what causes gestational diabetes, but we have some clues. The placenta supports the baby as it grows. Hormones from the placenta help the baby develop. But these hormones also block the action of the mother's insulin in her body. This problem is called insulin resistance. Insulin resistance makes it hard for the mother's body to use insulin. She may need up to three times as much insulin.

Gestational diabetes starts when your body is not able to make and use all the insulin it needs for pregnancy. Without enough insulin, glucose cannot leave the blood and be changed to energy. Glucose builds up in the blood to high levels.
http://www.diabetes.org/gestational-diabetes.jsp

I think pollutions as air, sound etc. O2 intake*, mental stresses, higher gastric acid(better digestion of carbs so more absorption), modern foods(more carbs, fried & acidic foods, more salt--can also lead to obesity), modern travels(mat add to mental stresses), air-conditioning, indoor livings/activities etc. all can effect BG. Persistant exposure of all these can create an impression to our genetic system that "more sugar in needed"--which can just be an inharent or aquired impression.

*(Hyperbaric oxygen doubles the mean healing rate of nonischemic chronic foot ulcers in selected diabetic patients.http://www.diabetesincontrol.com/modules.php?name=News&file=article&sid=1471

http://www.google.com/search?hl=en&q=oxygen+diabetes&btnG=Google+Search

There is a specific condition related to 'blood supply near lungs & in extremeties related to O2 levels/pressure(I previously mentioned but just forget).