It appears that you are currently using Ad Blocking software. What are the consequences? Click here to learn more.

Obesity, Diabetes and Hormones

Does Too Much Glucagon, not Insulin Resistance, Cause Type 2 Diabetes?

By David Mendosa


The press release from the Eleanor Roosevelt Institute in Denver announces that “Scientists Discover Connection between Obesity and Diabetes.” That’s exciting news, but just half of the story.

You may only appear to be insulin resistant.

The research report in the December 2003 issue of journal Endocrinology is so dense that even the institute’s PR people missed the point. The title indicates how tough going the report is: “Altered Glucose Homeostatic in Proopiomelanocortin-Null Mouse Mutants Lacking Central and Peripheral Melanocortin.”

Even after reading the press release, the article itself, and talking with one of its principal authors I really don’t know what the title is saying. However, what the authors found is exciting news.

The press release focuses on the connection between the melanocyte-stimulating hormone (MSH) and diabetes. The study authors found that diabetes in obese mice requires MSH, which is made by the proopiomelanocortin (POMC) gene that is found in both mice and humans. Mice without the MSH hormone were obese, but did not develop diabetes.

Administration of the MSH hormone to these mice increased resistance to insulin and directly affected blood sugar levels. Therefore, MSH may be a factor in the development of Type 2 Diabetes.

“Our findings show that obese people with high levels of the hormone MSH may be more likely to be diabetic than obese people with low levels of the MSH hormone,” explains the study’s lead author Miles B. Brennan, Ph.D., and ERI scientist. “This is the first time that the link between the hormone MSH and blood sugar levels has been established.”

A hormonal basis of the connection between diabetes and obesity had been previously suspected. Last year I reported in my Diabetes Update number 5 that the journal Nature published “The hormone resistin links obesity to diabetes” in its January 18, 2001, issue.

Other scientists believe beta cells in the pancreas that are not functioning properly cause both diabetes and obesity. This was the crux of my article in the January 2001 issue of Diabetes Wellness Letter.

Beta cells produce the hormone insulin. The new research, however, focuses on a different hormone, one produced by the alpha cells of the pancreas. This in the hormone glucagon.

“What we are saying is that it is a pancreatic change,” Dr. Brennan tells me. “But it is not related to the beta cells so much as to the alpha cells, which secrete glucagon, which has an opposite effect to insulin, and so we’re looking at what in general people think of insulin resistance. You are not really solely responsive to insulin but rather your metabolic state relates to the ratio of insulin to glucagon, and what you are seeing in type 2 diabetes is certainly a rise in insulin, but an even greater rise in glucagon, which is countervailing to the rise in insulin.”

What really surprised me was what Dr. Brennan says next.

“A lot of work has gone into the idea that your peripheral tissues somehow become resistant to the effect of insulin, and what we think is a more significant aspect of this is that your hormonal state has changed and not your peripheral tissues and that your ratio of insulin to glucagon is different and that is why you appear to be resistant to insulin, merely because we are not really paying attention to your glucagon levels.”

Then what is the connection between MSH and glucagon?

“When we took MSH away,” Dr. Brennan replies, “what we did was completely severe the relationship of diabetes and obesity. The mice which lacked that, despite being morbidly obese, they weren’t insulin resistant. In fact, they were hypersensitive to the effects of insulin. And when we tracked this down it wasn’t really that they were hypersensitive to the effect of insulin, but that in the absence of MSH they didn't induce any glucagon. So it was the absence of glucagon that was responsible for what looked like hypersensitivity to insulin.”

Then, I ask Dr. Brennan if they say this in the article, or is it something they discovered since then.

“It’s in the article,” he replies. “It is sort of buried. You need to know the jargon to be able to get it out.”

“But the press release doesn’t even mention glucagon,” I pointed out.

“We tried to put glucagon in," Dr. Brennan replies. "But our publicity people told us that we were just muddying the waters.”

What a shame. I’ve seen this research reported in about a dozen websites, journals, and news feeds, but not one mentions glucagon, because they didn’t do any more than recycle the press release. In this case their slothfulness is obvious, because every case reprinted a serious error.

The press release says the research is in the Journal of Endocrinology. It’s published by the Society for Endocrinology in England. As soon as I received the press release I searched PubMed for the article in that journal. It isn't there.

Instead, the article appears in Endocrinology, published by the Endocrine Society in Chevy Chase, Maryland.

Often people blame those of us with type 2 diabetes calling it a “lifestyle disease.” They imply that we could be thinner if we wanted to and not have diabetes. Blaming the victim is a popular sport, and people aren’t going to stop just because research with rats establishes a hormonal imbalance as the root cause of type 2 diabetes. But it’s a start. 


This article originally appeared on Mendosa.com, December 24, 2003.


Last modified: December 24, 2003

[Go Back] Go back to Home Page

[Go Back] Go back to Diabetes Directory

Advertisment
Never Miss An Update!
I comply with the HONcode standard for trustworthy health information. You can verify my HONcode certificate here.