Insulin: understanding its action in health and disease

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Insulin: understanding its action in health and disease


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Old 03-25-2015, 15:35   #1
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Default Insulin: understanding its action in health and disease

Here is an interesting article. It says that the role of insulin is more of "applying brake" to processes like glycogenolysis (producing glucose from glycogen) or gluconeogenesis (producing glucose out of other stuff like amino acids) than of transporting glucose into cells. According to the paper, hyperglycemia (high BG levels) is not because glucose cannot enter our cells but because of the liver dumping glucose at a high enough rate to raise glucose levels in the blood. It also says that with hyperglycemia, the cells don't take in too little glucose, buy they take in more than normal.

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Old 03-25-2015, 20:33   #2
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Way too focused on the fasting state. I really like to eat, so I spend as little time in that state as possible.

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Old 03-26-2015, 00:45   #3
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Way too focused on the fasting state. I really like to eat, so I spend as little time in that state as possible.
I too like eating (and eat tasty food of around 200 g of carbohydrates / day) but did not at all feel that the article was focussed on the fasting state. As I understand it, the article was focussed on the following points:

- There is no peripheral insulin resistance
- The cells do not "close their doors" to glucose, but do allow glucose in
- Hyperglycemia is due to liver adding glucose to the blood stream and not because of the ingested glucose hanging in the blood
- In diabetes actually more glucose enters the cells than in the normal case and not less as previously thought

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Old 03-26-2015, 01:16   #4
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Interesting, if a bit "turgid".

I need to read it again.

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Old 03-26-2015, 05:33   #5
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Quote:
Originally Posted by Rad Warrier View Post
Here is an interesting article. It says that the role of insulin is more of "applying brake" to processes like glycogenolysis (producing glucose from glycogen) or gluconeogenesis (producing glucose out of other stuff like amino acids) than of transporting glucose into cells.
Partially, but not very accurate.
1) Insulin causes excess glucose to be converted to fat and stored in fat tissue.
2) Insulin blocks the mobilization and utilization of stored fat.
3) Insulin puts the brakes on glucogenolysis (converting existing glycogen to glucose, BUT
4) Insulin ENCOURAGES gluconeogenesis which is manufacturing and storing glycogen from various things.
5) Insulin facilitates the entry of glucose into cells "at the margin". Glucose can get into cells via concentration gradient (high blood sugar), exercise and some other ways but insulin pushes an additional amount in. Otherwise, we would need very high blood sugar all the time to get ENOUGH glucose into our cells.
Quote:

According to the paper, hyperglycemia (high BG levels) is not because glucose cannot enter our cells but because of the liver dumping glucose at a high enough rate to raise glucose levels in the blood. It also says that with hyperglycemia, the cells don't take in too little glucose, buy they take in more than normal.

Regards,
Rad
That's very over-simplified. It depends on the nature of your insulin resistant. Some have more liver problems, others have mainly peripheral muscle IR while others have adipose IR (skinny diabetics). When the liver is insulin resistant, it doesn't respond directly to #3 above and continues to secret glucose when it shouldn't. This varies from person to person. And in that case, yes, there may actually be too much glucose getting into cells.

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Old 03-26-2015, 17:19   #6
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It sure is backassward approach to what I've been reading. Think of this in a logically manner and it tends to fall apart a bit. Two people, equal size and weight eat the same meals for a very long time. One gets hyperglycemia while the other has normal glucose levels, the argument breaks down at that point.

While burning glucose for energy insulin/glucagon/glycogen maintain homeostasis of your glucose levels. In a ketogenic state insulin/gluconegenesis maintain homeostasis of glucose levels, glucagon release regulates ketones and lactate buildup regulates glycogen release from the liver.

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Old 03-26-2015, 19:47   #7
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The word hyperglycaemia in the article was only modified by the word fasting. He would then proceed from the fasting state directly to the general case without justification. Post-prandial was not in the discussion at all.
The article claims that fasting hyperglycaemia is the hallmark of diabetes without providing any support for the statement.
"HbA1c of 7% is effectively normal It is only when HbA1c is > than 9% when things begin to go wrong." Can I go back to eating carbs now?
Overall the article seems to deny the very existence of insulin resistance without ever using those words.

The article does however, provide an explanation for the dawn phenomenon, again without using the words we generally see used.

The journal is about anesthesia, so expect the peers who may have reviewed this thing may have the wrong credentials to fairly review an article on diabetes.

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Old 03-26-2015, 21:29   #8
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The hallmark of bad research: published in a little known journal that is in another medical field.

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Old 03-26-2015, 21:45   #9
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Quote:
Originally Posted by stevenal1 View Post
The word hyperglycaemia in the article was only modified by the word fasting. He would then proceed from the fasting state directly to the general case without justification. Post-prandial was not in the discussion at all.
The article claims that fasting hyperglycaemia is the hallmark of diabetes without providing any support for the statement.
"HbA1c of 7% is effectively normal It is only when HbA1c is > than 9% when things begin to go wrong." Can I go back to eating carbs now?
Overall the article seems to deny the very existence of insulin resistance without ever using those words.

The article does however, provide an explanation for the dawn phenomenon, again without using the words we generally see used.

The journal is about anesthesia, so expect the peers who may have reviewed this thing may have the wrong credentials to fairly review an article on diabetes.
Some of these questions came to my mind when I read the paper. I don't have hyperglycemia in the fasting state (except in the morning which problem has now resolved.) Even if I eat a lot of carbs, by 4 hours I will have reached normal BG levels. My hyperglycemia occurs immediately after food, like after 1 hour, after 2 hours and sometimes up to 3 hours. If liver is the culprit, why does the liver dump glucose more when I take food? Why doesn't it add abnormally high amounts of glucose when I am in the fasting state (i.e., 3+ hours after food)? There are many diabetics like me whose hyperglycemia manifests only in the immediate post prandial state (1-3 hours after food.) If liver contributed to high glucose levels why does it not contribute in the fasting state, i.e., say after 3 hours? What prevents it from adding glucose in the fasting state? And what prompts it to add glucose in the immediate post prandial state?

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Old 03-27-2015, 11:58   #10
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I think by and large the article agrees with the understanding that we have of the diabetic condition and metabolic processes. Except that it puts IR at the back end of the equation, and as Steven points out doesn't talk much about the post prandial state.

The one thing that caught me attention was that glycogen provides 2 kcal/gm. Considering that glycogen is a highly complex chain of bound glucose molecules I would have thought that this number is much higher and not half that of a carb gram.

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