Questions about Hyperinsulinemia/Diabetes

[Deetee]

Because we are completely frustrated by explaining things carefully to you, and having these explanations consistently ignored or misrepresented.

It's not true to say that you only want to learn. If you wanted to learn, you would now be quite knowledgeable about diabetes and its various complications, from all the good and correct information you have been given. And you would take the advice of so many posters and go and read a few books.

You don't want to learn. You want to find some way which will allow you to claim that reality is the way you want it to be. When told anything that seems to argue against the explanation you want, you ignore it, or contradict it, or imply that the poster doesn't know what they're talking about.

This becomes very wearing after a while.

For example, I have told you several times that glycosuria is simply an inevitable side-effect of the blood glucose concentration rising above the renal threshold. For any reason at all, not only in diabetes. And irrespective of what the insulin is doing. And that no matter how much glucose is lost in the urine, it doesn't make any practical difference to the blood glucose level. And that this is not a regulatory system, but merely a by-product of the way the kidney works.

And then you simply come along and say totally stupid things such asThis is absolute proof that you don't want to learn, you just want to imagine your own (wrong) explanations.

Kumar, as I said to you the first day you came on this forum, diabetes is one of the most extensively studied conditions in all medicine. An enormous amount is known about it. It is vanishingly improbable that you have discovered something that all these armies of specialist diabetologists around the world have missed. And the only way to see if you're right, is to learn what is already known about diabetes, and see if there is a rational explanation for your observations there.

But no. You want to stick to your ignorant explanation of what you think you've seen going on, so you have to reject all the knowledge that is being given to you and try to pretend that it means something else.

Well, I've had it. Again. There are only so many times I'm prepared to post the same explanation and have it twisted out of all recognition to suit your fantasies. Same as with the hours I spent trying to explain the Cori cycle to you, or the differences between ions and salts and elements, and intracellular and extracellular fluid. All a waste of time.

And you can call this TTT is you like, but I'm sick of seeing your pathetic little ego insist that you are the only pure-motived person here, and contribute so much, while we are only vested interests and closed minds. You're unteachable.

Rolfe.

Hear, hear!

 

[MRC_Hans]

Mr. Hans,

Thanks & well explained by translating in simple/my language with good example.

Well, you're really welcome, but read it carefully, because I'm going to expect that unless you have specific questions (like below) you have now understood it.

In case of type2 with IR: when sugar is not able to go in cells, will this not result into hypoglycemic type episodes & weakness/death of cells due to less available glucose to them due to IR inspite of hyperglycemia?

What did I say about the hole in the wall, and the "keyholes"? I said they became small, not non-existent. There is still glucose entering the cells, although with difficulty. However, untreated, type 2 diabetes may progress to a state where it leads to death. It does not work like hypos, because a hypo episode is the acute effect of the brain being starved of glucose.

You see, the brain is totally dependent on glucose, being unable to use lipids for fuel. The rest of the body cells can get energy from lipids, if glucose is not available.

However, the effects of a soaring BG (like ketosis, etc.) will get you long before your cells are starved of glucose to an extent that can kill you.

Whether this codition of IR remains persistant in type2 patients for whole of their balance life or can be reversed?

No, as has earlier been explained to you, a number of factors can reduce IR. Medicine, weight loss, exercise, giving up smoking. Also, s suitable diet can work, both by reducing the glucose input, but also by influencing the insulin resistance. In early stage type 2 patients, these factors will often enable them to regain and maintain normal BG regulation for many years.

Hans

 

[Badly Shaved Monkey]

Mr. Hans,

Thanks & well explained by translating in simple/my language with good example.

In case of type2 with IR: when sugar is not able to go in cells, will this not result into hypoglycemic type episodes & weakness/death of cells due to less available glucose to them due to IR inspite of hyperglycemia?

Whether this codition of IR remains persistant in type2 patients for whole of their balance life or can be reversed?

In order to prevent a drop in intracellular glucose a feedback mechanism is initiated to raise the blood concentration of a certain hormone beginning with the letter I. Now what can that be? Thus a raised blood concentration of that hormone will co-exist with a raised blood concentration of glucose, all so that intracellular glucose availablility is preserved.

H-O-M-E-O-S-T-A-S-I-S.

The only sensible question you can ask about this is why glucose has difficulty getting into cells so that this increase in that hormone's blood concentration is needed.

Any other questions, any other theories or considerations are just TTTT.

Sorry folks, I broke my vow of silence. It'll not be broken again. unless Kumar shows he has understood this explanation.

Bye Bye Kumar.

 

[Kumar]

Kumar, as I told you on the last page, the low pH in the stomach is to enable the digestion of proteins there. It has nothing to do with carbohydrate digestion.

Digestion of Dietary Carbohydrates

Dietary carbohydrate from which humans gain energy enter the body in complex forms, such as disaccharides and the polymers starch (amylose and amylopectin) and glycogen. The polymer cellulose is also consumed but not digested. The first step in the metabolism of digestible carbohydrate is the conversion of the higher polymers to simpler, soluble forms that can be transported across the intestinal wall and delivered to the tissues. The breakdown of polymeric sugars begins in the mouth. Saliva has a slightly acidic pH of 6.8 and contains lingual amylase that begins the digestion of carbohydrates. The action of lingual amylase is limited to the area of the mouth and the esophagus; it is virtually inactivated by the much stronger acid pH of the stomach. Once the food has arrived in the stomach, acid hydrolysis contributes to its degradation; specific gastric proteases and lipases aid this process for proteins and fats, respectively. The mixture of gastric secretions, saliva, and food, known collectively as chyme, moves to the small intestine.
http://web.indstate.edu/thcme/mwking/glycolysis.html

 

[Deetee]

The action of lingual amylase is limited to the area of the mouth and the esophagus; it is virtually inactivated by the much stronger acid pH of the stomach. Once the food has arrived in the stomach, acid hydrolysis contributes to its degradation; specific gastric proteases and lipases aid this process for proteins and fats, respectively.

Yup.......
Proteases = Protein
Lipases = Fats

Nothing there about carbohydrates, as Mojo said.

Pay attention, will you

 

[Kumar]

In order to prevent a drop in intracellular glucose a feedback mechanism is initiated to raise the blood concentration of a certain hormone beginning with the letter I. Now what can that be? Thus a raised blood concentration of that hormone will co-exist with a raised blood concentration of glucose, all so that intracellular glucose availablility is preserved.

H-O-M-E-O-S-T-A-S-I-S.

The only sensible question you can ask about this is why glucose has difficulty getting into cells so that this increase in that hormone's blood concentration is needed.

Any other questions, any other theories or considerations are just TTTT.

Sorry folks, I broke my vow of silence. It'll not be broken again. unless Kumar shows he has understood this explanation.

Bye Bye Kumar.

OK.

Why glucose has difficulty getting into cells so that this increase in that hormone's blood concentration is needed?

There are possible multiple effects leading to insulin resistance. Inefficient transport of glucose, damaged insulin receptors, obesity, and many other aspects involving insulin and glucose, may all promote insulin resistance. It is often noted that glucose gets inside the cell, but is not utilized. This results in glucose not being converted into the energy currency of the body, called ATP. The glucose accumulates inside cells. This is a form of insulin insensitivity...
..The respiratory chain (citric acid cycle) works less efficiently, when fatty oxidation levels are increasing. From Harper's Biochemistry, "fatty acids inhibit glycolysis (the conversion of glucose into ATP) at several steps and stimulate gluconeogenesis (Page 617)." Glucose will accumulate in cells when fats inhibit the respiratory process. So reducing triglycerides and fats in the bloodstream will improve insulin sensitivity.
http://www.restoreunity.org/insulin_resistance.htm

I don't know how much above link tells the truth?

 

[Kumar]

Yup.......
Proteases = Protein
Lipases = Fats

Nothing there about carbohydrates, as Mojo said.

Pay attention, will you

I think you read upto here;

The first step in the metabolism of digestible carbohydrate is the conversion of the higher polymers to simpler, soluble forms that can be transported across the intestinal wall and delivered to the tissues. The breakdown of polymeric sugars begins in the mouth. Saliva has a slightly acidic pH of 6.8 and contains lingual amylase that begins the digestion of carbohydrates. The action of lingual amylase is limited to the area of the mouth and the esophagus; it is virtually inactivated by the much stronger acid pH of the stomach. Once the food has arrived in the stomach, acid hydrolysis contributes to its degradation

Is it all not regarding carbohydrates?

 

[Donks]

I think you read upto here;

Thanks for saying "I think," that's how I knew you were wrong before I even googled.
Let's see the sentence that's causing you so much trouble:
"Once the food has arrived in the stomach, acid hydrolysis contributes to its degradation"

Is it all not regarding carbohydrates?

What do you think? Hint: No.

We could look for another source on how carbohydrates are digested:

Polysaccharides and oligosaccharides must be hydrolyzed to their component monosaccharides before being absorbed. The digestion of starch begins with salivary amylase, but this activity is much less important than that of pancreatic amylase in the small intestine. Amylase hydrolyzes starch, with the primary end products being maltose, maltotriose, and a -dextrins, although some glucose is also produced. The products of a -amylase digestion are hydrolyzed into their component monosaccharides by enzymes expressed on the brash border of the small intestinal cells, the most important of which are maltase, sucrase, isomaltase and lactase (69). With typical refined Western diets, carbohydrate digestion is rapid and carbohydrate absorption occurs primarily in the upper small intestine. This is reflected by the presence of finger-like villi in the mucosa of the upper small intestine, with wider and shorter villi in the lower half of the small intestine. However, carbohydrate digestion and absorption can occur along the entire length of the small intestine, and is shifted toward the ileum when the diet contains less readily digested carbohydrates, or when intestinal glucosidase inhibitors which may be used to treat diabetes are present. In this situation, the upper small intestine exhibits wide villous structures with leaf-like arrays, while in the ileum the villi become longer and more finger-like.source

Or you could have read the complete page were you got your paragraph from, instead of quoting selectively and pretending the rest didn't exist.

 

[Mojo]

I think you read upto here;

Saliva has a slightly acidic pH of 6.8 and contains lingual amylase that begins the digestion of carbohydrates. The action of lingual amylase is limited to the area of the mouth and the esophagus; it is virtually inactivated by the much stronger acid pH of the stomach.

Is it all not regarding carbohydrates?

Well, you've posted this twice, so I assume you've read it. It's apparent, though, that you don't understand it at all.

Saliva contains an enzyme that digests carbohydrates. It is capable of digesting starch to sugars, which is why a piece of bread placed in the mouth will soon start to taste sweet. This enzyme works best at the pH found in the mouth, which is typically around 6.8. although your quotation describes this as "slightly acidic," it is really quite close to neutral pH.

Your quotation states that this enzyme is "virtually inactivated by the much stronger acid pH of the stomach." This means that the enzyme doesn't work significantly in the stomach, because of the gastric acid in the stomach. In fact, the more acid the stomach is, the more the enzyme will be deactivated.

So your contention that "higher gastric acid" will lead to "better digestion of carbs so more absorption" is clearly utter nonsense.

And, look at the second half of the last sentence from your quotation, which you mysteriously omitted the second time you posted it:

Once the food has arrived in the stomach, acid hydrolysis contributes to its degradation; specific gastric proteases and lipases aid this process for proteins and fats, respectively.

Note, this sentence explains that proteins and fats are digested in the stomach, which makes your question

Originally posted by Kumar
Is it all not regarding carbohydrates?

look at best remarkably stupid, and at worst totally dishonest.

 

[Kumar]

What did I say about the hole in the wall, and the "keyholes"? I said they became small, not non-existent. There is still glucose entering the cells, although with difficulty. However, untreated, type 2 diabetes may progress to a state where it leads to death. It does not work like hypos, because a hypo episode is the acute effect of the brain being starved of glucose.

You see, the brain is totally dependent on glucose, being unable to use lipids for fuel. The rest of the body cells can get energy from lipids, if glucose is not available.

However, the effects of a soaring BG (like ketosis, etc.) will get you long before your cells are starved of glucose to an extent that can kill you.

Hypo effect due to lowsugar is clear to me. How high sugar level in IR condition can effect the brain(without ketosis)?

Can you tell sopmething about BSM's indicated question;

Why glucose has difficulty getting into cells so that this increase in that hormone's blood concentration is needed?

 

[Donks]

which makes your questionlook at best remarkably stupid, and at worst totally dishonest.

Couldn't the same be said of every single post Kumar has made on this board? It's been a while since we debated if Kumar was truly that stupid or if he was just pretending.

 

[Kumar]

Once the food has arrived in the stomach, acid hydrolysis contributes to its degradation

Mojo I have posted part of that post to how carbohydrate part.
The above part of that post tell that it is for whole food including carbohydrates. Deactivated enzyme is due to low pH in stomach & that may not be only enzyme for carbs digestion. Will degredation/sepration of food will not make more carbs available for absorption? Can't some carbs be not dissovable? Do we lose some carbs in stool? Can some carbs be better digested/degraded in low gastric pH?

 

[Kumar]

Finally;

What causes IR condition, primarily?

Why glucose has difficulty getting into cells so that this increase in insulin blood concentration is needed?

How fats/obesity can be a contributing factor to getting IR?

These may not yet be known in science, so we can think dynamically & discuss. Probably then, we may add/know something.

 

[Badly Shaved Monkey]

Finally;

What causes IR condition, primarily?

For a very long time you have been resolutely asserting that the cause is too much insulin in spite of being told countless times this assertion is wrong. Are you now dropping that assertion?

 

[Kumar]

For a very long time you have been resolutely asserting that the cause is too much insulin in spite of being told countless times this assertion is wrong. Are you now dropping that assertion?

I think so in view of your so much representations. But you know anything can change anytime due to any new finding. I don't understand, why it is named as Insulin resistance when insulin don't resist it, why cells resist only glucose when both glucose & insulin are higher? Anyway, let us progress otherwise, leaving this issue? Pls teach me:-

What causes IR condition, primarily?

Why glucose has difficulty getting into cells so that this increase in insulin blood concentration is needed?

How fats/obesity can be a contributing factor to getting IR?

 

[Kumar]

Mojo,

Furthur, excess HCL can add to NaCl in intestines(Na being Cotransported with sugar) :-

Neutralization
In duodenum, gastric acid gets neutralized by sodium bicarbonate. This also blocks gastric enzymes that have their optima in the acid range of pH. The secretion of sodium bicarbonate from pancreas is stimulated by gastrin. This polypeptide hormone gets activated and secreted from so-called S cells in the mucosa of the duodenum and jejunum when the pH in duodenum falls below 4,5 to 5,0. The neutralization is described by the equation:

HCl + NaHCO3 → NaCl + H2CO3
The carbonic acid instantly dissociates into carbon dioxide and water.
http://www.answers.com/topic/gastric-acid

The ingredients in the stomach cell that make hydrochloric acid (HCl) are carbon dioxide (CO2), water (H2O), and sodium chloride (NaCl) or potassium chloride (KCl).

NaCl + H2O + CO2 = HCl + NaHCO3, or

KCl + H2O + CO2 = HCl + KHCO3

As we can see, the byproduct of making hydrochloric acid is sodium bicarbonate (NaHCO3) or potassium bicarbonate (KHCO3), which goes into blood stream. These bicarbonates are the alkaline buffers that neutralize excess acids in the blood;
http://www.heartspring.net/alkaline_water_health.html

 

[Mojo]

Mojo I have posted part of that post to how carbohydrate part.

In other words, you have deliberately omitted the phrase

specific gastric proteases and lipases aid this process for proteins and fats, respectively.

and then asked

Is it all not regarding carbohydrates?

Do you not realise that this makes you look dishonest ?

 

[Kumar]

In other words, you have deliberately omitted the phrase and then asked Do you not realise that this makes you look dishonest ?

No, since we were talking about carbs & that para was about carbs, I indicated the point of discussions. Fats & protien digestion was an additional mentioning, but it was not our point of discussions, so I ignored.

Never think/use dishonest or other doubting words for me AS I am not & can't--mostly.

 

[Mojo]

No, since we were talking about carbs & that para was about carbs, I indicated the point of discussions. Fats & protien digestion was an additional mentioning, but it was not our point of discussions, so I ignored.

Exactly. It didn't fit your theory, so you ignored it.

Although the paragraph was mostly about carbohydrates, it was also about the early stages of digestion in general. This includes carbohydrate digestion in the mouth, and protein and fat digestion in the stomach. The stomach's enzymes do not digest carbohydrates.

The sentence

Once the food has arrived in the stomach, acid hydrolysis contributes to its degradation; specific gastric proteases and lipases aid this process for proteins and fats, respectively.

does not say anything about carbohydrate digestion in the stomach. It states that food continues to be digested in the stomach, as a result of of acid hydrolysis and the action of enzymes to catalyse this for proteins and fats.

 

[Donks]

No, since we were talking about carbs & that para was about carbs, I indicated the point of discussions. Fats & protien digestion was an additional mentioning, but it was not our point of discussions, so I ignored.

That's part of the problem with you, you ignore the parts you don't understand or agree with. Stop reading half a sentence just because you don't like the other half.

Never think/use dishonest or other doubting words for me AS I am not & can't--mostly.

You demonstrate time and time again an utter dishonesty. Actions speak louder than words. If you don't want to keep being labeled as dishonest, stop misrepresenting what others say.