Hyperglycemia and its treatment

[mktsgm]

I have a few fundamental questions about diabetes and its treatment.

1. Are diabetes and hyperglycemia the same?

If not,
a) What is the difference?
b) Our current treatment seems to be against hyperglycemia. What are we doing for diabetes?

If both are same,

a) What are the ill effects of higher glucose circulation? Do we have direct pathological evidence?
b) Years on medication has not produced results. In short, are we merely treating the symptoms?
c) Insulin seems to be our primary target in the treatment. Roles of glucagon, leptin, ghrelin, cortisol and many more are not targeted although they are also implicated in hyperglycemia.

Are there any out of the box thinking in current research, with regard to such a serious, elusive and persistent problem for the past fifty years.

 

[jim mcnamara]

Wow. Huge topic.
Hyerglycemia can result from trauma and disease processes. In the shorter term. Long term hyperglycemia is usually diagnosed as diabetes.
We have LOTS of evidence of tissue damage due to hypergylcemia. Most times if left unchecked would result in horrible debilitation and early death.
There is active research to cure Type I. Type II is strongly environmental - diet and exercise. It already has a known cure that works well depending on patient compliance.
This is a great site to get current on diabetes:
http://www.diabetes.org/research-and-practice/we-are-research-leaders/recent-advances/

Diabetes mellitus is really two separate diseases.

Type I is an autoimmune disorder - the panceatic cells (islets of Langerhans) that make insulin are damaged or killed. Insufficient or zero insulin is produced. The only treatment now is replace missing insulin, almost always done by insulin injection. Other curative measures like implanting islet cells (think transplanting cells), or using cell culture methods to create islet cells the body does not attack have been tried. It is currently believed that Type I is largely genetic. It mostly is diagnosed in younger patients - like children.

Type II is the result insulin resistance, with some genetic aspects, but largely the result of environment. Think diet. This used to appear only in middle aged adults, but really young children as young as 10 years of age are now diagnosed. It is evident in epidemic proportions in the US, for example.
One pathway to Type II is to consume too many calories and get a substantial amount of those excess calories from simple sugars like fructose and glucose.
The pancreas produces more and more insulin to control hypergylcemia. Because on cells throughout the body, receptor sites on the cell membranes are hit with lots of insulin to which they no longer respond or respond weakly. Treatment is consists of both dietary modification and medications, sometimes insulin.

The problems secondary to long periods of hyperglycemia from either Type I or Type II are legion and nasty. Retinopathy > blindness, Nephropathy > permanent damage to kidneys. Cardiovascular problems... The list goes on. There are populations in the US with more than 40% of adults with Type II and persons under the age of 18 newly diagnosed at levels that are increasing. Example: Navajo Reservation (US)

It does not require out of the box thinking. The out of control part of the Western diet causes most cases of diabetes, Type II. If a country becomes westernized, it too will see diabetes rates rise in the near future. Some countries in Europe are taking steps to curb simple sugars in the diet.

 

[mktsgm]

Thanks Jim. Wonderful explanation.

Strangely with high glucose in circulation, glucagon which should have stopped by now, continues to pump in more glucose. Weird. Why would body do two mistakes simultaneously, one to reduce insulin and pump in more glucagon (thus glucose)?

Have you ever come across such double whammy by the body, where one mistake by the body begets another only to sustain the earlier mistake?

 

[jim mcnamara]

This requires a diabetologist - a physician whose practice is largely limited to diabetic patents. I cannot answer. Even if I could you really need to consult someone who practices in this area.

 

[berkeman]

Thread closed temporarily for Moderation.

 

[berkeman]

Thanks Jim. Wonderful explanation.

Strangely with high glucose in circulation, glucagon which should have stopped by now, continues to pump in more glucose. Weird. Why would body do two mistakes simultaneously, one to reduce insulin and pump in more glucagon (thus glucose)?

Have you ever come across such double whammy by the body, where one mistake by the body begets another only to sustain the earlier mistake?

We cannot diagnose medical conditions here at the PF, and we cannot give medical advice. But we should be able to discuss the biology of what is going on, as long as we stay clear of anything that we should be talking with a doctor about.

Thread re-opened for now, as long as we can stay within the PF rules. Thank you.

 

[Ygggdrasil]

Strangely with high glucose in circulation, glucagon which should have stopped by now, continues to pump in more glucose. Weird. Why would body do two mistakes simultaneously, one to reduce insulin and pump in more glucagon (thus glucose)?

Seems like this occurs because of either loss of insulin secretion by pancreatic beta cells in type I diabetes or insulin resistance in the glucagon-producing pancreatic alpha cells in type II diabetes:

The opposite effects of insulin and glucagon in fuel homeostasis, the paracrine/endocrine inhibitory effects of insulin on glucagon secretion and the hyperglucagonemia in the pathogenesis of type 2 diabetes (T2D) have long been recognized. Inappropriately increased alpha-cell function importantly contributes to hyperglycemia and reflects the loss of tonic restraint normally exerted by high local concentrations of insulin on alpha-cells, possibly as a result of beta-cell failure and alpha-cell insulin resistance, but additional mechanisms, such as the participation of incretin hormones in this response, have also been suggested.

https://dmsjournal.biomedcentral.com/articles/10.1186/1758-5996-6-91