Questions about Hyperinsulinemia/Diabetes

[Kumar]

Hello all,

It ia better to discuss specific subject on diabetes here.



I am just trying to understand effects of hyperinsulinemia--natural, induced or medicated esp. in type2 with IR patients. In this respect I want to know:-

1. Whether we have yet studied, progression of diabetes in untreated Insulin resistant patients who have gain weight or not yet lost weight(for no other reason)?

2. Whether we have yet clinically tried & researched, what happens on reducing/discontinuing normal medication programme to Insulin resistant patients who have gain weight or not yet lost weight(for no other reason)?

Do we have some data on these studies & clinical trials if already done? Can you provide some referances to this effect?

3. Furthur, can insulin resistance also be possible in type1/IDDM patients, suppose if they are taking excess injected insulin? If not, WHY?

"Type 2 diabetes commonly occurs in adults who are obese. There are many underlying factors that contribute to the high blood glucose levels in these individuals. An important factor is the body's resistance to insulin in the body, essentially ignoring its insulin secretions. A second factor is the falling production of insulin by the beta cells of the pancreas. Therefore, an individual with type 2 diabetes may have a combination of deficient secretion and deficient action of insulin."
http://www.ncbi.nlm.nih.gov/boÂ_oks/bv.fcgi?rid=diabetes.sectiÂ_on.4

Now my doubts are:-


Whether obesity is a reason/cause of getting Type 2 diabetes OR Type 2 diabetes with deficient action of insulin is the cause/reson of making a person obese(central obesity)--may be due to conversion of excess glucose into fats?


How a type2 patient can get deficient secretion of insulin in early
stages? Can excess BG level cause low secretion of insulin?

Can't expression of excess insulin present due to IR or
induced/medicated discourage more insulin secretion from pancreas?

Can't this persistant long term expression of excess insulin cause
inactivity or damage to beta cells or trigger autoimmunity?

Best wishes.

 

[Kumar]

I got awnser to my question no 3 from Mojo in other topic & posting for referance here:-


Kumar: 3. Furthur, can insulin resistance also be possible in type1/IDDM patients, suppose if they are taking excess injected insulin? If not, WHY?

Mojo: Type 1 diabetics cannot be treated with diet and excercise because they do have significantly impaired beta cells.
Type 1 diabetics don't generally suffer from insulin resistance, because they don't exhibit the hyperinsulinaemia that leads to it.

Kumar: Does it not indicates that, insulin secretion from pancreas is ONLY related to IR and its imbalanced excess secretion is a cause to IR?

Furthur, how can we differenciate between "insulin tollerance" & "insulin resistance" as Mojo indicated there?

I am bit worried due to:-

More than 80% of DM population die of some form of cardiovascular disease; 20% of deaths in diabetics are due to myocardial infarctions.

3 Risk Factors for Diabetic Heart Disease:

Hyperinsulinemia, very high blood insulin levels present in most pre-diabetics and all NIDDM sufferers, increases the risk of heart attack and/or other factors, such as high blood levels of low-density lipoprotein (LDL), cholesterol and lipoprotein apo B, which are also strong independent risk factors. The typical individual with diabetes experiences all three conditions, each of which increases the harmful effects of the other two.


http://www.musc.edu/bmt737/Spr_1999/valerie/DMCardiac.html

What lead to it? Nature, we, wrong theories & practices or otherwise?

 

[Kumar]

I do understand egoistic adaptations & bad luck to humanity may be due to "current age entitlements", for not posting here. Anyway, I don't got effected by sentiments or useless EGO--so do & continue my duties.

MORE DYNAMIC/DIFFERENT THOUGHTS/QUESTIONS:-

1.What can cause insulin resistance-- persistant gluco-toxicity or insulin-toxicity?

2.What IR can suggest--body don't want more glucose, excess glucose is there in body or body unable to take glucose?

3.Whether "no weight loss or gain body weight" with normal lipids levels can suggest that, reqiured metabolism of glucose is taking place, but its excesses or problem in its excretion is showing excess BG levels?

4.Type1 patients don't experiance IR conditions. They may have occasional excess BG levels, not excess insulin levels. Doet it suggests persistant excess insulin as a reason of getting IR?

5.Does it also suggests that persistant excess insulin discourage more insulin when it is excess in blood resulting in damage to beta cells in long term?

6.If yes, how induced excess insulin can help?

 

[MRC_Hans]

I am just trying to understand effects of hyperinsulinemia--natural, induced or medicated esp. in type2 with IR patients. In this respect I want to know:-

1. Whether we have yet studied, progression of diabetes in untreated Insulin resistant patients who have gain weight or not yet lost weight(for no other reason)?

Yes, throughly studied. We have not always been able to treat diabetes, and often patients are found that have had diabetes for a long time before the diagnosis was made.

2. Whether we have yet clinically tried & researched, what happens on reducing/discontinuing normal medication programme to Insulin resistant patients who have gain weight or not yet lost weight(for no other reason)?

I don't suppose it would be ethical to make a clinical study, but since patients often, for various reasons, stop their medication, we are throughly aware of the results.

3. Furthur, can insulin resistance also be possible in type1/IDDM patients, suppose if they are taking excess injected insulin? If not, WHY?

This was already answered (but of course, so were all your other questions ).


Now my doubts are:-


Whether obesity is a reason/cause of getting Type 2 diabetes

Yes.

OR Type 2 diabetes with deficient action of insulin is the cause/reson of making a person obese(central obesity)--may be due to conversion of excess glucose into fats?

No.

... When there is deficient action of insulin, glucose is not metabolized. How often do you have to be told this?

How a type2 patient can get deficient secretion of insulin in early
stages? Can excess BG level cause low secretion of insulin?

Not directly. Quite the opposite.

Can't expression of excess insulin present due to IR or
induced/medicated discourage more insulin secretion from pancreas?

No.

Can't this persistant long term expression of excess insulin cause
inactivity or damage to beta cells or trigger autoimmunity?

Yes.

Hans

 

[MRC_Hans]

Does it not indicates that, insulin secretion from pancreas is ONLY related to IR and its imbalanced excess secretion is a cause to IR?


The secretion of insulin is regulated by the BG. High BG means high insulin secretion, it is a closed regulation loop.

Furthur, how can we differenciate between "insulin tollerance" & "insulin resistance" as Mojo indicated there?

He just explained very plainly. READ the answers.

Hans

 

[MRC_Hans]

1.What can cause insulin resistance-- persistant gluco-toxicity or insulin-toxicity?

Overweight, sedentary life-style, smoking.

2.What IR can suggest--body don't want more glucose, excess glucose is there in body or body unable to take glucose?

It does not suggest anything. It means that the body cells loose their ability to utilize insulin. Therefore the glucose stays in the blood-stream instead of being metabolized.

3.Whether "no weight loss or gain body weight" with normal lipids levels can suggest that, reqiured metabolism of glucose is taking place, but its excesses or problem in its excretion is showing excess BG levels?

What?

4.Type1 patients don't experiance IR conditions. They may have occasional excess BG levels, not excess insulin levels. Doet it suggests persistant excess insulin as a reason of getting IR?

It suggests nothing of the kind. There is no direct connection between diabetes 1 and 2. Type 1 patients have normal glucose metabolism, they just fail to produce the insulin needed.

5.Does it also suggests that persistant excess insulin discourage more insulin when it is excess in blood resulting in damage to beta cells in long term?

No, but it is assumed that high insulin levels dabage beta cells in the long run.

6.If yes, how induced excess insulin can help?

Do you mean injected? Excess injected insulin does not help for anything, except as an emergency measure to lower a dangerously high BG in a type 2 patient.

Hans

 

[Donks]

You couldn't resist, could you Hans?

 

[MRC_Hans]

You couldn't resist, could you Hans?

I have a policy of trying to answer any straight question I see, where I think I know the answer. Even from Kumar.

I'm aware that this is the umpthenth time he has gotten most of those answers, and that he will just go on ignoring, cherry-picking, and misrepresenting the answers, but I recon this is the best way to continuously demonstrate his total intellectual corruption to the world.

Hans

 

[Kumar]

Mr. Hans,

Thanks for many awnsers. I am diiferent on following points:-

1. Glucose conversion into fats still continue normally, even on prevalent IR condition till maximum limit of fat store(converted or direct) is reached as this is a different system & different cells are involved in it.

2. Whether type2/IR causes central obesity OR central obesity causes type2/IR condition OR both can result into each other is bit unclear in current understandings. But predisposed inherant initiation/urge of occasional & excess eating OR aquired habit of it due to modern lifestyle & environment, can result into obesity & type2/IR condition. So both "predisposed inherant initiation/urge of occasional & excess eating" and "aquired habits of it due to modern lifestyle & environment" can be thought as contributing factors of development of IR condition.

3. Excess insulin secretion due to gluco-toxicity or induced, may trigger into IR condition. Persistent hyperinsulinemea than the required insulin, due to IR, may inactivate beta cells & this persistent inactivation of beta cells may result into progressive damage & autoimmunity to beta cells instead of excess use or "wear off" of these. I think "wearing off" can only be possible, when IR/hyperinsulinemia is not there.

Now few more new thoughts:-

Whether IR can also be a genetically predisposed condition OR it is just an aquired condition due to modern lifestyle & environment?

Why we consider excess sugar in urine as a disorder? How excess BG, on excess intake of sugar will be excreted, when a maximum limit of its usages as glucose or in fat conversion is exhausted?

Can any disorder in excretion of excess glucose in urine be also a reason to getting gluco/Insulin-toxicity, IR or diabetes?

(I am just talikg about normal progression of disease not accidental/secondary considerations)

 

[MRC_Hans]

Thanks for many awnsers. I am diiferent on following points:-

1. Glucose conversion into fats still continue normally, even on prevalent IR condition till maximum limit of fat store(converted or direct) is reached as this is a different system & different cells are involved in it.

Do you have any documentation on this revolutionary claim? Or is it just in your fantasy?

2. Whether type2/IR causes central obesity OR central obesity causes type2/IR condition OR both can result into each other is bit unclear in current understandings. But predisposed inherant initiation/urge of occasional & excess eating OR aquired habit of it due to modern lifestyle & environment, can result into obesity & type2/IR condition. So both "predisposed inherant initiation/urge of occasional & excess eating" and "aquired habits of it due to modern lifestyle & environment" can be thought as contributing factors of development of IR condition.

The answer is both. Obesity leads to type 2 diabets, but type 2 diabetes can lead to or increase obesity because the body, lacking energy from glucose may compensate by craving more ot eat.

3. Excess insulin secretion due to gluco-toxicity or induced, may trigger into IR condition.

No, it may not. "Trigger" implies a short-term effect. The interacting of IR/hyperinsulinaemia is a long-term, effect.

Persistent hyperinsulinemea than the required insulin, due to IR, may inactivate beta cells & this persistent inactivation of beta cells may result into progressive damage & autoimmunity to beta cells instead of excess use or "wear off" of these. I think "wearing off" can only be possible, when IR/hyperinsulinemia is not there.

What makes you think that?

Now few more new thoughts:-

Whether IR can also be a genetically predisposed condition OR it is just an aquired condition due to modern lifestyle & environment?

It is also genetically predisposed (as you have already been told a dozen times). This means that your latent risk for developing typr 2 due to lifestyle is genetical. Som can sit on their ass and be grossly overweight for a whole lifetime and not get diabetes. Others get it when they're 30.

Why we consider excess sugar in urine as a disorder?

Kumar, this is getting ridiculous! You asked this question in another thread, and it was immidiately answered. I tell you what: let me se you blatantly ignore ONE more answer after this post, and you go permanently on my ignore list.

Sugar in the urine is not a disorder, it is a symptom, of diabetes. Since the body cannot metabolize the excess glucose, it is secreted through the kidneys. The body tries to speed up this process by making you extra thirsty, in order to get rid of as much glucose as possible through the urine.

How excess BG, on excess intake of sugar will be excreted, when a maximum limit of its usages as glucose or in fat conversion is exhausted?

See? Just told you. And there is no extracellular fat conversion.

Can any disorder in excretion of excess glucose in urine be also a reason to getting gluco/Insulin-toxicity, IR or diabetes?

No.

Hans

 

[Mojo]

Whether IR can also be a genetically predisposed condition OR it is just an aquired condition due to modern lifestyle & environment?

There certainly seems to be a genetic predisposition to diabetes, in that it seems to run in families and appears to be more prevalent in certain ethnic groups, but the lifestyle factors also need to be present if type 2 diabetes is to develop.

Why we consider excess sugar in urine as a disorder? How excess BG, on excess intake of sugar will be excreted, when a maximum limit of its usages as glucose or in fat conversion is exhausted?

Excess sugar in the urine is a sign that there is excess sugar in the blood. If the glucose cannot, for any reason, be taken up and metabolised by the body's cells, it is excreted in the urine, rather than, as you seem to be suggesting, converted into fat.

This is how diabetes was originally discovered. Do you know what "diabetes mellitus" is Latin for?

Can any disorder in excretion of excess glucose in urine be also a reason to getting gluco/Insulin-toxicity, IR or diabetes?

No. Excess glucose in the urine is a symptom of hyperglycaemia, not a cause. If for some reason excessive amounts of glucose were to be excreted by someone with normal blood sugar levels, they would tend to become hypoglycaemic.

 

[Rolfe]

Since the body cannot metabolize the excess glucose, it is secreted through the kidneys. The body tries to speed up this process by making you extra thirsty, in order to get rid of as much glucose as possible through the urine.

This is a nitpick, but I don't look at it that way.

Since the glucose cannot get into the cells (due to the lack of insulin or insulin resistance), blood glucose concentration increases. The way the kdney works is that all the glucose presented to the proximal tubule is filtered, but then it all ought to be reabsorbed further down the system. However, the reabsorption system can only handle up to about 10mmol/l glucose in the blood (the renal glucose threshold). If blood glucose is higher than this, the capacity of the reabsorption is exceeded and the excess glucose spills oven into the urine. The kidney isn't trying to excrete the glucose, it simply can't help it.

Then, the presence of all that glucose in the urine increases the osmolarity of the fluid. This interferes with the ability of the kidney to conserve water. Osmotic pressure created by the glucose pulls the water into the urine - osmotic diuresis. This tends to dehydrate the body, and of course the result is that the person feels thirsty and drinks to compensate.

This has always seemed to me to be the inevitable consequence of the fact that the system of filtration and reabsorption used by the kidney only works properly at fairly normal blood glucose concentrations. Concentrations above the renal glucose threshold lead to glycosuria and osmotic diuresis as an inevitable result of the way the kidney works. I don't think that either the glycosuria or the polyuria/polydipsia are really beneficial to the patient, and I don't think they're a deliberate mechanism evolved by the body to cope with hyperglycaemia. (Indeed, experience shows that long-term diabetics often have an increased renal glucose threshold, apparently an adaptive response to avoid losing so much glucose in the urine, which would suggest that it isn't beneficial.) I think it just happens, because that's the way the kidney works.

Rolfe.

 

[Rolfe]

If for some reason excessive amounts of glucose were to be excreted by someone with normal blood sugar levels, they would tend to become hypoglycaemic.

Renal glycosuria, e.g. Fanconi syndrome. In my experience such patients are normoglycaemic, because the hormonal systems in place to prevent hypoglycaemia are multiply redundant, and all working. They probably just eat more.

Rolfe.

 

[Kumar]

Do you have any documentation on this revolutionary claim? Or is it just in your fantasy?

How then "weight stay constant or gain weight" can happen in many IR/T2 patients? Can it happen without fat stores?

The answer is both. Obesity leads to type 2 diabets, but type 2 diabetes can lead to or increase obesity because the body, lacking energy from glucose may compensate by craving more ot eat.

Central obesity is more related to IR condition.

3. Excess insulin secretion due to gluco-toxicity or induced, may trigger into IR condition.

No, it may not. "Trigger" implies a short-term effect. The interacting of IR/hyperinsulinaemia is a long-term, effect.

You may take it as "Excess insulin secretion due to gluco-toxicity or induced, may trigger IR condition & its persistence may result into pesistent of IR condition".

Persistent hyperinsulinemea than the required insulin, due to IR, may inactivate beta cells & this persistent inactivation of beta cells may result into progressive damage & autoimmunity to beta cells instead of excess use or "wear off" of these. I think "wearing off" can only be possible, when IR/hyperinsulinemia is not there.

What makes you think that?

Is it not in physiology that secretion of any harmone, enzyme or body's fluid will stop when it is in sufficient/excess quantity at the target sites? In IR patients, is insulin not remain in excess/sufficient quantity?

It is also genetically predisposed (as you have already been told a dozen times). This means that your latent risk for developing typr 2 due to lifestyle is genetical. Som can sit on their ass and be grossly overweight for a whole lifetime and not get diabetes. Others get it when they're 30.

I think you are just talking about diabetes. IR can be one condition related to diabetic patients, not whole diabetes.


Kumar, this is getting ridiculous! You asked this question in another thread, and it was immidiately answered. I tell you what: let me se you blatantly ignore ONE more answer after this post, and you go permanently on my ignore list.

Sorry, I think I haven't yet read it.

Sugar in the urine is not a disorder, it is a symptom, of diabetes. Since the body cannot metabolize the excess glucose, it is secreted through the kidneys. The body tries to speed up this process by making you extra thirsty, in order to get rid of as much glucose as possible through the urine.

Thanks, but then why a diabetic patient don't get controlled BG levels when excess sugar can be excreted in urine?

How excess BG, on excess intake of sugar will be excreted, when a maximum limit of its usages as glucose or in fat conversion is exhausted?

See? Just told you. And there is no extracellular fat conversion.

What is then glucose conversion into fats & its store? Anyway this point is related to WHY all excesses of glucose couldn't be excreted in urine? When excretion is possible, why diabetic patients experiances high BG levels? Can it be resulted due to any disorder in system of this excretion OR hyperinsulinemia?

Can any disorder in excretion of excess glucose in urine be also a reason to getting gluco/Insulin-toxicity, IR or diabetes?

No.

This is a new point & deep understandings may be needed. can you bit satisfy me on this point otherwise I will check it properly.

 

[Mojo]

Furthur, how can we differenciate between "insulin tollerance" & "insulin resistance" as Mojo indicated there?

Maybe I didn't explain this clearly enough.

They are completely different conditions.

In insulin resistance, insulin is present, often at an elevated level, but the body's cell do not respond properly to it by taking up glucose from the blood. The problem is in the response of the cells to insulin.

Pig insulin used to be used to treat insulin-dependent diabetics. Because pig insulin is not quite the same as human insulin, the body's immune system would respond to repeated exposure to it by producing antibodies to the pig insulin, thus taking it out of circulation, so that larger doses were needed to produce the required level of insulin in the blood. The problem here was to do with acheiving an adequate level of insulin in the blood.

As another poster (I think it was Donks) has indicated, pig insulin is no longer used because synthetic human insulin is now available, so this is no longer an issue.

And before you get excited about this, Kumar, producing antibodies to pig insulin is NOT an autoimmune condition. It is part of the normal immune response to a foreign protein.

 

[Kumar]

This is a nitpick, but I don't look at it that way.

Since the glucose cannot get into the cells (due to the lack of insulin or insulin resistance), blood glucose concentration increases. The way the kdney works is that all the glucose presented to the proximal tubule is filtered, but then it all ought to be reabsorbed further down the system. However, the reabsorption system can only handle up to about 10mmol/l glucose in the blood (the renal glucose threshold). If blood glucose is higher than this, the capacity of the reabsorption is exceeded and the excess glucose spills oven into the urine. The kidney isn't trying to exvrete the glucose, it simply can't help it.

Then, the presence of all that glucose in the urine increases the osmolarity of the fluid. This interferes with the ability of the kidney to conserve water. Osmotic pressure created by the glucose pulls the water into the urine - osmotic diuresis. This tends to dehydrate the body, and of course the result is that the person feels thirsty and drinks to compensate.

This has always seemed to me to be the inevitable consequence of the fact that the system of filtration and reabsorption used by the kidney only works properly at fairly normal blood glucose concentrations. Concentrations above the renal glucose threshold lead to glycosuria and osmotic diuresis as an inevitable result of the way the kidney works. I don't think that either the glycosuria or the polyuria/polydipsia are really beneficial to the patient, and I don't think they're a deliberate mechanism evolved by the body to cope with hyperglycaemia. (Indeed, experience shows that long-term diabetics often have an increased renal glucose threshold, apparently an adaptive response to avoid losing so much glucose in the urine, which would suggest that it isn't beneficial.) I think it just happens, because that's the way the kidney works.

Rolfe.

Rolfe, even though not addressed to me, since giid information.

But my doubts are:-

When body can excrete excess glucose in urine, how it remains always higher in many patients? Can it be due to some defects in this excretion mechanism or persistant hyperinsulinemia due to IR? Does insulin in blood can put some hold on excretion of excess sugar?

 

[Mojo]

Is it not in physiology that secretion of any harmone, enzyme or body's fluid will stop when it is in sufficient/excess quantity at the target sites?

Yes, this is the case in a healthy person. In type 2 diabetics the system isn't working properly. That's why they have diabetes.

Thanks, but then why a diabetic patient don't get controlled BG levels when excess sugar can be excreted in urine?

Rolfe has just covered this above. Basically, the kidneys aren't really supposed to excrete glucose at all, but if the blood glucose level is sufficiently high, they are unable to cope and some of it ends up in the urine.

 

[MRC_Hans]

This is a nitpick, but I don't look at it that way.

*snip* and I don't think they're a deliberate mechanism evolved by the body to cope with hyperglycaemia. (Indeed, experience shows that long-term diabetics often have an increased renal glucose threshold, apparently an adaptive response to avoid losing so much glucose in the urine, which would suggest that it isn't beneficial.) I think it just happens, because that's the way the kidney works.

Rolfe.

I realize my wording did more or less imply deliberation, which is of course wrong. The body does not do anything at all deliberately, but evolutionary traits will make it react to certain conditions. Since it is probably of limited evolutionary advantage to be able to deal with hyperglycaemia (in a natural environment nearly all diabetics will be type 1, and a temporal ability to curb BG at moderately high levels is not likely to improve an individual's reproductive success), I think you are probably right: It is just the way things happen to work.

Hans

 

[MRC_Hans]

Do you have any documentation on this revolutionary claim? Or is it just in your fantasy?

How then "weight stay constant or gain weight" can happen in many IR/T2 patients? Can it happen without fat stores?

They are not totally unable to metabolize glucose. But you imply that the excess glucose is converted directly by the excess insulin. This cannot happen.

Central obesity is more related to IR condition.

Yeah, but the reason is speculative. Either, the position of the fat somehow poses a greater load on the body, or it simply happens that the genentic disposition to be centrally fat goes together wit hincreases risk of diabetes.

You may take it as "Excess insulin secretion due to gluco-toxicity or induced, may trigger IR condition & its persistence may result into pesistent of IR condition".

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.


Is it not in physiology that secretion of any harmone, enzyme or body's fluid will stop when it is in sufficient/excess quantity at the target sites? In IR patients, is insulin not remain in excess/sufficient quantity?

Duh, that is the regulation that breaks down in type 2 diabetes. But strictly speaking, it is not excess insulin. The abnormally high level of insulin is the regulation system's response to IR: In order to keep the glucose metabolism going, the pressure is raised, that is, both BG and insulin levels are raised.

I think you are just talking about diabetes. IR can be one condition related to diabetic patients, not whole diabetes.

Psst, Kumar, this is a thread about diabetes. You started it yourself. Of course I talk about diabetes . IR is a condition related to type 2 diabetes. Do you STILL not understand the distinction between type 1 and type 2?

Thanks, but then why a diabetic patient don't get controlled BG levels when excess sugar can be excreted in urine?

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.

What is then glucose conversion into fats & its store?

It requires the glucose to be metabolized in cells, and well, that is what it doesn't get.

Anyway this point is related to WHY all excesses of glucose couldn't be excreted in urine? When excretion is possible, why diabetic patients experiances high BG levels? Can it be resulted due to any disorder in system of this excretion OR hyperinsulinemia?

Normally I would just refer a poster to the answer above, but things cannot seem to be itereted enough for you: None of the excretion systems are able to cope with a diabetes condition. Urine excretion may take the top off, but no more.

Can any disorder in excretion of excess glucose in urine be also a reason to getting gluco/Insulin-toxicity, IR or diabetes?

No.

This is a new point & deep understandings may be needed. can you bit satisfy me on this point otherwise I will check it properly.

By all means, Kumar, do check it properly. Time YOU did some of the work around here . I'm waiting for the result of your researches .

Hans

 

[MRC_Hans]

On animal insulin: Especially in Asean countries, there is still some local production of animal insulin (it is a relatively cheap and low-tech process). The international market, OTOH is entirely dominated by the modern synthetic and analogues.

Hans