Team of Japanese scientists discovers insulin-resistant protein

[kristopher]

Team of Japanese scientists discovers insulin-resistant protein

A team of Japanese scientists has identified an insulin-resistant protein that could be a major cause of obesity and diabetes, a discovery that could help medical practitioners diagnose and treat lifestyle diseases.

The finding was released through the online version of the U.S. science magazine Cell Metabolism on Jan. 4. The state of insulin resistance is widely seen in people who are suffering from type 2 diabetes caused mainly by lifestyle related factors such as overeating, inadequate exercise and obesity.

Using a method called "comparative proteomic analysis," the team of scientists from Kobe University, Shimadzu Corp. and other groups found the insulin-resistant protein in mice after conducting detailed analysis of various kinds of protein. The analysis showed that the levels of the insulin-resistant protein in the blood of obese mice were twice to three times higher than normal. When the protein was injected into other mice, those mice that were not obese became resistant to insulin.

Moreover, those mice that were made incapable of producing the protein did not become obese even when they were fed fatty foods and showed no resistance to insulin. The same protein exists in humans and it is known to be effective in treating inflammation and injuries...

http://mdn.mainichi.jp/mdnnews/news/20120105p2a00m0na006000c.html

[eridani]

1. So, why in bloody hell, having just reported that type II diabetes is a genetic disease--

---do the writers persist in calling it a "lifestyle" disease?

[Saving Hawaii]

2. I don't think they did that.

And it is a lifestyle disease. Identifying a major component of what is happening though would be a great way to identify ways to treat it.

[eridani]

3. It is most assuredly not a lifestyle disease, any more than PKU is

If your parents feed you a low phenylalanine diet until you are 6 years old or so, thereby preventing mental retardation, that doesn't do jackshit to fix the gene that is the cause of PKU.

Analogously, being active and eating a healthy diet certainly postpones the age of onset of diabetes, but it does jackshit to fix the genes involved.

[TheMadMonk]

5. It IS a lifestyle disease, because a NORMAL diet doesn't trigger it. /nt

[eridani]

6. Nonsense

People who are genetically diabetic are guaranteed to become diabetic eventually. In the old days, people usually died of something else before that happened. The effect of a bad diet is to lower the age of onset, period. That is of course a very serious problem.

If you are not genetically diabetic, there is no diet that will trigger diabetes.

[TheMadMonk]

7. By your same argument, gout and heart disease aren't lifestyle diseases...

...either.

Genetics may predispose a person to certain medical conditons, but it's lifestyle (or other environmental factors) which is the final trigger, that sets those triggers off.

Obesity (the single biggest risk factor for Type 2 diabetes) is NOT an inevitable condition. It's the result of a lifestyle choice made too easy by an overabundance of highly processed food. 25 plus percent of the people in the developed world DID NOT mutate into lard magnets over the course of a single generation.

The predispostion to obesity has always been there. As a highly preseved survival trait. People who stack on the weight quickly and efficiently are far more likely to survive a lean season. It would not surprise me at all to learn that this protein was a part of that survival mechanism.

[eridani]

8. Your reasoning is exactly backwards

Being genetically diabetic is a risk factor for diabetes and weight gain, not the other way around. 25% of the population has always been diabetic and prone to weight gain. Ironically, the less likely you are to be able to lose weight easily, the more excercise and a good diet benefit you and postpone onset of diabetes. Emphasis on weight loss is a major public health risk by itself.

[TheMadMonk]

9. And for all but the last two generations of our existence as a species...

...this predisposition was mostly beneficial. Just as being a sickle cell carrier is beneficial in areas where malaria is prevalent, despite the lethality to the 25% of offspring where two carriers come together.

Being able to stack on +50% bodyweight in a few weeks in Autumn has been, for most of our existence, a good thing. However, when it's "Harvest" every day, and no true winter ever eventuates to properly burn that stored energy away, we get fat and STAY fat.

Something my mother brought to my attention a little while back. AC and winter heating to shirtsleeve comfort levels means we burn a lot, lot fewer calories simply modulating our body temperatures today, than when I was a child.

More processed food means we spend less calories digesting it.

Portion sizes are ludicrous; 5lb pizza's; 10lb challenge burgers; multigallon buckets of popcorn. 1/2 gallon [s]bucket[/s]cups of softdrink.

Less physically mobile.

Kids with this fucking END OF LIFE disease. AND cardiac disease. AND hypertension and more. Call them syndromes, conditions any self excusing bloody thing you please in their proper place, in the final 25 years of a long life. However, in a seven year old it's a 100 fucking percent preventable DISEASE.

It's not fair to genetics to blame it on genes that have been there for dozens if not hundreds of generations. Environmental/lifestyle changes in our caloric landscape are what has changed.

[eridani]

10. The disease is preventable by death from some other cause

The number of potential diabetics is determined by genetics. Bad lifestyle factors do not change that, but they do lower the age of onset by quite a bit. THAT is the problem.

If you can't produce the recently discovered protein, there is no way in hell you become diabetic, crappy diet or no.

[TheMadMonk]

13. Some other cause oftimes being OLD FUCKING AGE.

Some people are proteonomicallly predisposed to high blood pressure, high cholesterol, ecxema, Huntington's, Haemophilia,... you flippin' name it. ALL diseases, conditions or syndromes (same bloody difference) by the diagnostician's book.

There are any number of "good protein"/"bad protein" diseases, and more being discovered all the time. Some are manageable by diet, and some are not.

The way you're arguing is a total cop out. "I can't help it. I have a gene." "It's not my fault my kid is getting their first bypass at age 12. It's genetics."

BULLSHIT! You CAN help it. You can choose to die SOONER or LATER. You can choose to feed your kid a decent (or at the very least calorically restricted) diet, or you can help them into an early grave by letting them gorge on concentrated grease products and corn derived sugars.

[eridani]

14. But you can't change their genes

People who are the least likely to lose weight benefit the most by exercising and following a good diet, so why are you making weight loss the criterion here? This amounts to public abuse of people for a genetic trait, and it has no health benefits.

BTW, diagnosed type II diabetics see sugar control and blood pressure improve IMMEDIATELY on such a regimen, well before any weight loss. Therefore weight loss isn't causing this effect. Furthermore, success in controlling symptoms has no correlation whatsoever with the amount of weight lost.

[TheMadMonk]

15. Nowhere have I said it's about weight loss.

It's about not excusing uncontrolled weight gain with a genetic copout.

It's about not using that copout to excuse setting kids up for a (short) lifetime of health woes.

[eridani]

16. You say copout, I say reality

Can't find the study, as it's old to be online, but someone compared black men who believed that all black people start out behind the eightball with those Herman Cain types who believed that racism was now irrelevant. Turned out that the former were much less likely to leave their spouses or quit their educations when faced with adversity. Looks like it helps to have a worldview that is more closely connected with reality in order to effectively deal with reality.

When will the born insulin resistant living in a society where most jobs are sedentary be average weight? Never. Realizing that can help them develop realistic plans to cope with that, including finding ways to stay active and learning to minimize intake of foods with a high glycemic index.

[TheMadMonk]

17. I say copout, because that's what it is.

"I can't help it. I have a glandular condition." seems to be the whine of choice with which to wash down the third Big Mac.

WTF has average weight got to do with it? There's a fucking huge difference between "solid" and morbidly obese.

Knowing the exact mechanism of insulin resistance should be entirely irrelevant to the general population. Exact methods of propper management have been known for decades. I strongly suspect that these findings will see greater use as an excuse for even larger helpings and more couch time, than reason to "stay active, and learning to minimize intake of foods with a high glycemic index."

[eridani]

18. Herman Cain, is that you?

I guess people who complain about racial discrimination should just suck it up and quit blaming society too. Proper management is rendered useless if health care workers focus on weight rather than sugar control, and most of them do that. That results in a 90% fail rate.

Programs like this have much higher success rates http://cinderernst.com/why-no-weight-loss
http://www.haescommunity.org/resources.php?rType=r

Astrup et al [International Journal of Obesity Vol 11, p 51-66 (1987)] have demonstrated that it is fat people who eat the least who have abnormal insulin response. He compared two groups of fat people, one of which ate less than 1500 calories a day, and the other of which ate more than 3000. Every one of the former group had abnormal insulin response, and none of the latter group. The people who are most at risk genetically for developing type II diabetes are therefore those who are least likely to lose weight, and the most likely to benefit from more exercise and improvements in diet composition.

If fat (rather than the underlying genetic trait of insulin resistance) is such a problem, why are fat type II diabetics less insulin-dependent, less likely to develop the complications of diabetes, and less likely to die from it than type II diabetics of average weight? [Turkington, R.W. and Weidling, H.K., JAMA Vol 240, p. 833-836 (1987)] Why do diabetic Pima Indian women (the human population with the largest known genetic concentration of insulin resistance) experience the lowest levels of mortality when they weigh twice the actuarial ideal? [Pettitt, D.J., et al Am. J. Epidemiol. Vol 115, p. 359-366 (1982)] (Pima men with the longest life spans weigh 45% more.)

[Lionel Mandrake]

11. The link in the OP points to a newspaper article which refers to "lifestyle diseases", but

the word "lifestyle" does not appear in the scientific article which is the source of the newspaper story.

(See my previous post for a link to this original source.)

Your quarrel is with the author(s) of the newspaper article, not with the scientists whose work they are reporting.

[eridani]

12. I thought I made the contrast between the newspaper and the publication clear

The news almost always reflects official predjudices.

[Lionel Mandrake]

4. For more information, browse

Last edited Mon Jan 9, 2012, 08:58 PM - Edit history (2)

http://www.cell.com/cell-metabolism/

Look for the cartoon of a sumo wrestler biting into a hamburger. That cartoon will lead to the source of the Mainichi Daily News story that the OP points to:

"PGRN is a Key Adipokine Mediating High Fat Diet-Induced Insulin Resistance and Obesity through IL-6 in Adipose Tissue"

by Toshiya Matsubara, Ayako Mita, Kohtaro Minami, Tetsuya Hosooka, Sohei Kitazawa, Kenichi Takahashi, Yoshikazu Tamori, Norihide Yokoi, Makoto Watanabe, Ei-ichi Matsuo, Osamu Nishimura, and Susumu Seino,

Cell Metabolism 15, 38–50, January 4, 2012.

You should be able to download this article for free if you are a student or teacher at a university. Otherwise, you will have to pay for it. (Don't bother if you haven't studied molecular biology.)