Questions about Hyperinsulinemia/Diabetes

[Kumar]

You're probably right. We should go back to using natural pig insulin in people.

Can you suggest how synthetic human insulin is different from natural human insulin?

I am not suggesting but asking?

I have asked it many times, but couldn't yet get satisfactory reply about differences in structure & effects of natural & synthetic insilin? Can you tell? Forget C-peptide part.

 

[MRC_Hans]

*snip*
As I told price difference between animal & human synthetic insulin on poor countries is negligible on per day bases.
*snip*

The end-user price may be nearly the same, but modern insulin has to be mostly imported, whereas animal insulin can be produced locally. That makes a lot of difference for the economy in a poor country, but I don't suppose you understand economis, either.

Anyhow, your original point was that analogues was a bad alternative that was chosen for price reasons and that is nonsense. It is and remains the opposite: Animal insulin, while being the poor alternative, is still used in some third world countries, for reasons of economy.

Hans

 

[MRC_Hans]

I am not suggesting but asking?

I have asked it many times, but couldn't yet get satisfactory reply about differences in structure & effects in natural & synthetic insilin? Can you tell?

You were told: Animal insulin does not match the body perfectly and can give immune responses.

Do you ignore answers because:

a) Because you don't like them.

b) You are too lazy to read them.

c) You cannot really read English.

d) A combination of the above.

Hans

 

[Mojo]

How insulin secretion can be inactivated in case of hyperinsulinemia due to IR when glucose level can also be high?

It seems that there can be eventual damage to the beta cells in type 2 diabetes, but it is not a question of the beta cells being inactivated directly by high blood insulin levels, as you seem to be suggesting in another thread. If this were the case, an increase in blood insulin level would lead to reduced production of insulin by the pancreas, and hyperinsulinaemia would not develop.

 

[Mojo]

I have asked it many times, but couldn't yet get satisfactory reply about differences in structure & effects of natural & synthetic insilin? Can you tell? Forget C-peptide part.

There is no difference between them. That's why synthetic human insulin is preferable to non-synthetic non-human insulin.

 

[Kumar]

Y'know...I had several smart-arse responses to this question...but I'm afraid Kumar would take them seriously.


*sigh*


Not to knock on BSM, but just for humor's sake. Ah well.

I am one of the most serious person, bold but beautiful/good, logical & dynamic/different, do not like only reading, copying & repeating--so doing all this. You can do your duties rest leave on nature. Otherwise these will suffocate & die within you & you may get "suppression's bad effects".

Just for referance:-

The two major pathogeneses of type 2 diabetes mellitus (T2DM) are insulin resistance and insulin secretion deficiency....
...In conclusion, in IRS-2G1057D variation DD genotype apparently showed two phenotypes. The insulin sensitivity of non-obese subjects with DD genotype was increased; which indicated that DD genotype might be the protective factor of T2DM. The insulin sensitivity of obese (especially central obesity) subjects with DD genotype was decreased; which indicated that DD genotype might be the risk factor of T2DM occurrence. All of these results demonstrated that the IRS-2G1057D variation and obesity were connected to T2DM.
http://www.cmj.org/information/full.asp?pmid=20055415

 

[MRC_Hans]

Let's have a little fun. Kumar, please explain the snippet you just quoted. Show us how much of it you understand .

Hans

 

[Kumar]

Apologies for adding extra fuel to the fire.....

http://main.pslgroup.com/news/content.nsf/MedicalNews/8525697700573E188525702A006A981A

Use of an anti-CD3 monoclonal antibody seems to be very promising.
Now we need Kumar to incorporate this into his pathological models for auto-immunity and diabetes.
Enjoy.

This just tells about, what had already happened and immunosupression effect. But I am trying to know, how it(type1) can happen primarily?

Can it be a result of progressive effect of persistent high BG/Insulin-natural, induced or medicated, anytime during lifetime or inhereted? Can it be caused due persistent exposure of weak acid/lactic acid to pancreas?

 

[MRC_Hans]

This just tells about, what had already happened and immunosupression effect. But I am trying to know, how it(type1) can happen primarily?

You mean WHY it happens? We don't really know for sure. There seems to be several possible triggers.

Can it be a result of progressive effect of persistent high BG/Insulin-natural, induced or medicated, anytime during lifetime or inhereted?

That is the type 2 situation. Kumar, it is highly embarrassing for you that you STILL haven't grasped the difference between type 1 and type 2.

Can it be caused due persistent exposure of weak acid/lactic acid to pancreas?

Whatever gave you THAT idea?

Hans

 

[Mojo]

But I am trying to know, how it(type1) can happen primarily?

If you're trying to understand type 1 diabetes in this thread, why do you keep asking about insulin resistance? It has been repeatedly been pointed out to you that this occurs in type 2 diabetes, not type 1, and why type 1 diabetics do not develop insulin resistance.

 

[Donks]

Just for this I mention GOD/NATURE.

You mention god because it's a completely unscientific explanation? Good to know. Now every time you ask for a scientific explanation, I can justly tell you to piss off.

He has indicated "mainly from collection process" which can also be different in poor countries. As I told price difference between animal & human synthetic insulin on poor countries is negligible on per day bases.

Care to back up you asseretion? Let's see what I can find... hmmm, article from 2002, Madras Diabetes Research Foundation in India, conclusion:

Currently human insulins are almost twice as expensive as porcine insulin. Hence in developing countries like India, animal insulin should continue to be available.
source

.
Ok, it's 2005. Please present your evidence that the price of human insulin is now "negligible" as opposed to twice as much 3 years ago.

No, or other words can be common in dynamic/different thoughts.

Meaningless sentence. I'll skip it.

Who may be earing more & adding to diseases...probably. Money adiction can also be thoght, and more money may cause craving of getting more money--alike alcohol/durgs addictions & cravings. Can an addicted person do more advesities due to his craving?

Are you accusing health care profesionals of avoiding your grandious ideas because they are addicted to money, patient health be dammed?

 

[Kumar]

I think this concept is bit confusing and is alike ' which out of egg
and hen came first'. It can also be a visious circle. Genetic
predispostion is said to be there in every diabetic patient unless we seprate insulin resistance from diabetes. Modern lifestyle &
environment said to cause epidemic type of diabetes spread only in predisposed people.


I suspect genetic predisposed condition causes a person to eat more & irregularly--may be due to more & occasional insulin/gastric acid secretions resulted from this predisposed inharent effect or aquired/added due to modern lifestyle/environment.


This may make a person obese(not centrally at this stage). The fat storage capacity due to it is exhaused & body may then stop
metabolising glucose, glucose conversion into fats and storing more fats. This then may result into insulin resistance indicating all body capacity to accept glucose is full. However when mucsle cells are enable to take glucose body may get signals of less glucose & may store these as fats centrally for the emergency need of fuel(visceral fats may be used immidiately). But already excess fats in body don't leave any room for furthur store of fats, so IR can starts.

The question here can be, when glucose can't be used due to IR and as Mr. Hans is insisting--it can't be converted into fats and stored--what is the meaning of central obesity & why IR person don't lose the weight, commonly?


Anyway, I have some other thoughts:-


1. Can traped water in partly metabolized sugar (lactic acid or
purvrate) be also a reason of central obesity/blotting of abdomen & weight gain? This may be modality of immediate 5-10% weight loss(water not fats) as claimed by some health providers. More
O2/breathing/aerobic excercises may also do this.


2.Can diabetes/elevated BG levels with IR, be due to some disorder in intestinal absorption of sugar? Can excess intake of salt/sodium/fats, imbalances in gastric acid due to stesses & modern ltfestyle, bile and bicarbonate leading to changes in intestinal mucus lining, costipation or delayed motions etc. cause diabetes/elevated BG levels or IR, primarily? I have noted craving for taking more sugar sufficiently decreased even in chronic type2 with IR parient, when one discontinue or reduce salt intake for some time. HOW??


3. Can diabetes/elevated BG levels with IR be due to some disorder in excretion of excess sugar in urine?


4. Can 2 & 3 be possible or aggravated due to high BG or high insulin levels--natural, induced or medicated?

 

[Mojo]

Are you accusing health care profesionals of avoiding your grandious ideas because they are addicted to money, patient health be dammed?

No, he is accusing doctors of actually causing or worsening illnesses to feed their alleged "addictions."

Originally posted by Kumar
Can an addicted person do more advesities due to his craving?

He is thereby revealing his devious, dishonest, half-baked quackery-based agenda.

 

[Kumar]

How insulin secretion can be inactivated in case of hyperinsulinemia due to IR when glucose level can also be high?

Rephrase to make sense.

Can't pacreas be sensed from insulin levels in blood instead of glucose levels & if sufficient, can't it inactivate the secretion of more insulin?

There can be some limit of sugar usage.

Rephrase to make sense. (I expect t ouse this sentence a lot )

Means: there can be some limit of body to use the glucose in muscle & in fat conversion(if possible). can this limit of glucose use be decided by the quantity of insulin present in blood?

If extra is excreted in urine, what is problem in it.

It is a symptom of high BG, and high BG is a problem.

Can excess sugar in urine cause direct damages?

 

[MRC_Hans]

I think this concept is bit confusing and is alike ' which out of egg
and hen came first'.

I may be confusing to you. The rest of us have no problems with it.

It can also be a visious circle. Genetic
predispostion is said to be there in every diabetic patient unless we seprate insulin resistance from diabetes. Modern lifestyle &
environment said to cause epidemic type of diabetes spread only in predisposed people.

No, it is not said so. It is just your binary thinking mode. Genetic predisposition just increases your risk. Oh, and we can't separate insulin resistance from diabetes. Insulin resistance is, basically, diabetes (type 2).

I suspect genetic predisposed condition causes a person to eat more & irregularly--may be due to more & occasional insulin/gastric acid secretions resulted from this predisposed inharent effect or aquired/added due to modern lifestyle/environment.

Total raving nonsense.


This may make a person obese(not centrally at this stage). The fat storage capacity due to it is exhaused & body may then stop
metabolising glucose, glucose conversion into fats and storing more fats.

Total nonsense.

This then may result into insulin resistance indicating all body capacity to accept glucose is full.




However when mucsle cells are enable to take glucose body may get signals of less glucose & may store these as fats centrally for the emergency need of fuel(visceral fats may be used immidiately). But already excess fats in body don't leave any room for furthur store of fats, so IR can starts.

Kumar, there is virtually no limits to the body's capacity for storing fat.

The question here can be, when glucose can't be used due to IR and as Mr. Hans is insisting--it can't be converted into fats and stored--what is the meaning of central obesity & why IR person don't lose the weight, commonly?

The meaning is that you are wrong. W. R. O. N. G. Your entire "theory" is gibberish, grabbed out of thin air. It is contrary to known facts, it lacks inner logic, and, to top it, it is useless.


Anyway, I have some other thoughts:-


1. Can traped water in partly metabolized sugar (lactic acid or
purvrate) be also a reason of central obesity/blotting of abdomen & weight gain?

No.

This may be modality of immediate 5-10% weight loss(water not fats) as claimed by some health providers.

Loosing 5-10% as water is possible, but will leave you dehydrated.

More
O2/breathing/aerobic excercises may also do this.

Well, yes, if you sweat enough .


2.Can diabetes/elevated BG levels with IR, be due to some disorder in intestinal absorption of sugar?

No.

Can excess intake of salt/sodium/fats, imbalances in gastric acid due to stesses & modern ltfestyle, bile and bicarbonate leading to changes in intestinal mucus lining, costipation or delayed motions etc. cause diabetes/elevated BG levels or IR, primarily?

No.


I have noted craving for taking more sugar sufficiently decreased even in chronic type2 with IR parient, when one discontinue or reduce salt intake for some time. HOW??

No special connection, except when you change your eating habits, your eating habits ... change.


3. Can diabetes/elevated BG levels with IR be due to some disorder in excretion of excess sugar in urine?

Already explained. Read Rolfe's excellent and comprehensive explanation on how glucose is excreted in urine. And, of course, as usual you put the cart before the horse. Glucose in the urine is CAUSED by diabetes, not the other way around .

4. Can 2 & 3 be possible or aggravated due to high BG or high insulin levels--natural, induced or medicated?

No.

Kumar, you have just (again) confirmed you are a total idiot. This is not a violation of rule 8, but a factual observation. You ask questions you don't understand the implications of, you get answers and ignore or misrepresent them. You keep developing silly, unnecessary theories that don't fit the facts you have been provided with.

Maybe you think we are all wrong and don't know what we are talking about, but then you are even more idiotic by commencing to build theories on what we tell you.

You are a total loss. Even at the homeopathic forums they laugh at you. Even they can see how silly you are.

Bye, Kumar.

Hans

 

[Mojo]

This may make a person obese(not centrally at this stage). The fat storage capacity due to it is exhaused & body may then stop metabolising glucose, glucose conversion into fats and storing more fats. This then may result into insulin resistance indicating all body capacity to accept glucose is full. However when mucsle cells are enable to take glucose body may get signals of less glucose & may store these as fats centrally for the emergency need of fuel(visceral fats may be used immidiately). But already excess fats in body don't leave any room for furthur store of fats, so IR can starts.

No. See here:

More importantly, we found no correlation between visceral fat, IMCL and the degree of postprandial glycemia or insulin resistance. Furthermore, there is no evidence to suggest that our SE Asian subjects had reached their maximum fat storage capacity.

Insulin resistance is a problem with sugar metabolism, not fat metabolism.

The question here can be, when glucose can't be used due to IR and as Mr. Hans is insisting--it can't be converted into fats and stored--what is the meaning of central obesity & why IR person don't lose the weight, commonly?

An insulin resistant patient is not totally unable to utilise blood sugar. This is characteristic of type 1 diabetics, not type 2 (I wish you would make up your mind which you are trying to discuss). Weight loss can be observed in insulin resistant patients, particularly in the later stages when the condition is more severe, but if they're not expending more calories than they are able to take in, they won't lose weight, just the same as anyone else.

1. Can traped water in partly metabolized sugar (lactic acid or
purvrate) be also a reason of central obesity/blotting of abdomen & weight gain? This may be modality of immediate 5-10% weight loss(water not fats) as claimed by some health providers. More
O2/breathing/aerobic excercises may also do this.

No.

2.Can diabetes/elevated BG levels with IR, be due to some disorder in intestinal absorption of sugar? Can excess intake of salt/sodium/fats, imbalances in gastric acid due to stesses & modern ltfestyle, bile and bicarbonate leading to changes in intestinal mucus lining, costipation or delayed motions etc. cause diabetes/elevated BG levels or IR, primarily?

No. Insulin resistance is caused by persistently elevated blood sugar levels. If there were a problem with absorbtion of sugar by the gut, it wouldn't lead to increased blood sugar levels, would it? Try to use a little common sense.

3. Can diabetes/elevated BG levels with IR be due to some disorder in excretion of excess sugar in urine?

No. This has already been explained to you. How could excessive excretion of sugar in the urine increase the blood sugar level? Try to use a little common sense.

4. Can 2 & 3 be possible or aggravated due to high BG or high insulin levels--natural, induced or medicated?

As 2 and 3 do not occur, they can't be aggravated. Try to use a little common sense.

 

[MRC_Hans]

*snip*
Try to use a little common sense.
*snip*
Try to use a little common sense.
*snip
Try to use a little common sense.[/B]

Kumar, common sense? Incompatible .

Hans

 

[Kumar]

Sorry, I am bit overinvolved & will awnser one by one. I can post some referances for future need--may not be related to any of post.

Insulin resistance in the first-degree relatives of persons with type 2 diabetes.

BACKGROUND: Type 2 diabetes is characterized by impaired insulin secretion and insulin resistance. Both genetic and environmental factors are thought to play a role in the pathogenesis of this disease. Obesity is associated with increased risk of type 2 diabetes, but some metabolic abnormalities may also be present in lean, predisposed subjects. The aim of the present study was to assess insulin sensitivity in lean normoglycemic offspring of parents with type 2 diabetes. MATERIAL/METHODS: We examined 17 lean offspring (BMI<25 kg x m-2) whose parents had type 2 diabetes, and 17 age, sex and BMI-matched subjects without family history of diabetes as controls. Anthropometric and biochemical measurements, oral glucose tolerance test (OGTT), and euglycemic hyperinsulinemic clamp were performed. RESULTS: The subjects did not differ in anthropometric measurements, and all had normal glucose tolerance according to WHO criteria. Offspring of type 2 diabetic parents were markedly more hyperinsulinemic (p<0.05) and insulin resistant (p<0.005). The ratio of the increase in insulin to the increase in glucose during the first 30 minutes of the OGTT, a crude index of first-phase insulin secretion, did not differ between groups. Insulin sensitivity was negatively related to fasting plasma insulin (r=-0.67, p<0.001) and non-esterified fatty acids (r=-0.43, p<0.02). CONCLUSIONS: Insulin resistance is present even in young lean subjects at high risk to develop type 2 diabetes. Our data suggest that insulin resistance may be a primary abnormality in the pathogenesis of this disease... From pubmed.
http://tinyurl.com/ct4jc

There can be many possibilities.

 

[Kumar]

You simply don't have a clue. This is getting fun. Lactic acid is produced in anaerobic glucose metabolism. If you have increased lactic acid levels except short-term after exercise, you have serious respiratory problems.
But yes, water retention can lead to increased weight. Not relevant to this discussion, however.

Whether modern lifestyle, pollution/environment is making us more anaaerobic? Excess Lactic acid( i don't know about pyruvate) can be immediate toxic/fatal. Can't it then encourage water retention to keep it diluted? Can't modern lifestyle, pollution etc. cause more Lactic acid production & prevalence?

There is basically no limit to fat storage. Some people weigh over 300 kg.

Still there can be some different limit in different people. All can't become 100,200,300 Kgs.


WOW! Kumar discovers the reason for central obesity! Quick! Send your synopsis with documentation to the Lancet. Fame and fortune awaits you.

What for then Central obesity is meant for?


No, I may not. Excess insulin will result in hypoglycaemia if there is in insulin resistance. The two conditions go hand in hand, and it is a long-term process. No triggering.

Triggering means most basic stage. If excess insulin will always result in hypoglycaemia, then how it is excess in IR & what is IR?


It is said that excess insulin is always present in IR patients.

No, raised insulin levels. It is not excess because the patient needs the high level to be able to metabolize glucose at all.

Is is not persistant high/excess level in blood in case of IR patients? I think insulin tests tells it.

Doubt all you will. You remain wrong.


Anything can be wrong till.......

Read Rolfe's explanation. My wording made it look as if it was some regulation system, this is probably not the case. At any rate, it is not sufficient. It might keep the patient from going directly in ketosis, but it certainly cannot keep the BG t onormal levels.
so you don't think Rolfe's explanation is serious? You are incredibly arrogant.

I have replied Rolfe's post accordingly. Can't excess insulin(naturally secreted or induced by medication) put some hold in proper excretion of sugar in urine? Can excess insulin effect renal threshhold of sugar absorption? There can be an impression of sugar need or it can be used due to excess insulin?

Clucose is converted in cells. Insulin helps glucose to be absorbed by cells. Cells with IR have difficulty absorbing glucose. Insulin does not interact with glucose outside cells.

(Yes, I'm sure).

Does it not happen by involvement of different cells/liver?



Oh, but I can tell you that. We ARE going against the natural mechanisms. The natural mechanisms for diabetes are skyrocketing BG, ketosis, coma, and death. We go against it and enable patients to live an almost normal life. Feel free to follow nature, if you prefer.

Yes, you ARE going against the natural mechanisms--first creating it( bymodern lifestyle/environment/practices etc.) then treating it. Un-nature vs, un-nature..

 

[MRC_Hans]

Snippet from the source Kumar just quoted :

CONCLUSIONS: Insulin resistance is present even in young lean subjects at high risk to develop type 2 diabetes. Our data suggest that insulin resistance may be a primary abnormality in the pathogenesis of this disease... From pubmed.

I think we might have a record here. Correct me if I'm wrong, but I cannot remember any other poster posting sources that directly and explicitly contradicted their ideas.



Hans