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Sonksen and Sonksen, Insulin and ketogenic diet

Insulin is still misunderstood almost invariably. The doctrine that insulin is required for glucose transport is false. The role insulin has in storage of fat on cellular level often goes unnoticed. To me it seems to be why insulin is a major component in development of common mortalities, like atherosclerosis, obesity and Type 2 diabetes.

Here is my pedestrian piece of mind on the common insulin myths.

The Olden Med School Text Books

I spent some of this Sunday browsing an old finnish-language anatomy textbook from 1974.

I found this textbook at the Recycling Center. Nienstedt, Hänninen, Arstila: "Ihmisen fysiologia ja anatomia". It notes that insulin is a peptide, and that small intestine hormones increase insulin secretion.

Insulin paragraphs from old anatomy textbookThis textbook - once a great benefit to finnish students - also incorrectly assumes that muscle or adipose cells only gain glucose via insulin activated transport, and that it is this transport that causes reduction in blood glucose. This textbook also fails to note that insulin can command cells to store tons of fat.

Old Myths

As far as I can tell, these myths have been perpetuated from at least the early 1970's to the first years of 2000's. Very, very sad show.

The section on endocrinology is just a couple of pages, and makes note of popular notions of insulin as an important component of glucose transport. Wrong, just like most pre-2000 books are. The books that don't know what insulin receptor is. Or know of glucose transporters on the cell surface. And that most glucose transporters seem to be passive.

Insulin trumps Glucagon

As a lead further into the topic, of importance is the fact that insulin-production works as an antagonist of glucagon.

Graph of actions of amylin. In effect, amylin is produced in pancreatic beta-cells along with insulin. Amylin down-signals glucagon from pancreas, and glucagon is down-signaled also via activation of GABA. Sadly this detail is lost.

From this misunderstanding follows a lot of confusion around ketogenic diets. Such as the misconception that DKA and ketogenic diet are linked, when in fact DKA only occurs if glucagon levels go unchecked. In other words: only in radical absence of insulin, pancreatic deficiency.

Enter Sonksen and Sonksen 2000

Soenksen on nature of fasting hyperglycemiaGiants of insulin metabolism, for me. What a joyous day it was for me to find their papers!

They elaborate insulin function and related details well. They ended the confusing misconceptions that some still carry on. If you are a diabetic, a student, a nurse or a MD, it may be worthwhile to understand the details of Insulin: understanding its action in health and disease, in British Journal of Anesthesia 2000, issue 85. It is not new, but it is still new information to most.

So what is insulin if not for glucose transport?

Insulin is for countering the glucagon, for digestion of dietary nutrients, for fat storing and for cellular growth, as far as I can read. For anabolic state.

Understand that insulin does not lower blood glucose

Soenksen on linear relation of plasma glucagon to glucoseInsulin-signal instead limits the release of glucose from liver: hepatic glucose production, through glucagon, according to Sonksen and Sonksen.

For a slightly easier intro, with more entertaining history on the topic of insulin action, also read Peter H. Sonksen's lucid article Insulin, growth hormone and sport in Journal Of Endocrinology Volume 170, 2001. A true champion!

Most GLUT work passively without insulin

Besides, most glucose transporter proteins in human cells are passive and do not require any insulin to function. graphic of cell surface glucose and insulin receptor signaling Currently it is thought that GLUT4-transporters in muscle cells are insulin regulated, and can provide extra glucose transport. I'm probably at fault in many ways, but I think its effect may be trivial.

So, in this view, hyperglycemic DKA is caused by breakaway glucagon signaling, in the (almost complete) absence of amylin and insulin. As far as I can see it would only happen in advanced diabetes, or injury to pancreas or its blood flow.

Insulin myths die slowly

Also make note of the typical phrase that insulin the cause of primary glucose uptake. I keep thinking it's simply not correct. This type of generalization is common. I'm probably just missing better part of it.

Insulin is too difficult to comprehend for many

The Olden Idea of History that insulin regulates blood sugar levels through muscle glucose uptake dies so very slowly. The research of insulin receptor seems to find its way into gray matter very slowly. The knowledge of GLUT, sadly the privilege of the cell-biology crowd, and knowledge of glucagon the endocrino-cult?

Copyright Casimir Pohjanraito 2022

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