Posted on 02/16/2011 8:37:12 AM PST by decimon
Researchers from Mount Sinai School of Medicine have discovered a novel function of brain insulin, indicating that impaired brain insulin action may be the cause of the unrestrained lipolysis that initiates and worsens type 2 diabetes in humans. The research is published this month in the journal Cell Metabolism.
Led by Christoph Buettner, MD, Assistant Professor of Medicine in the Division of Endocrinology, Diabetes and Bone Disease at Mount Sinai School of Medicine, the research team first infused a tiny amount of insulin into the brains of rats and then assessed glucose and lipid metabolism in the whole body. In doing so, they found that brain insulin suppressed lipolysis, a process during which triglycerides in fat are broken down and fatty acids are released.
Furthermore, in mice that lacked the brain insulin receptor, lipolysis was unrestrained. While fatty acids are important energy sources during fasting, they can worsen diabetes, especially when they are released after the person has eaten, as happens in people with diabetes. Researchers previously believed that insulin's ability to suppress lipolysis was entirely mediated through insulin receptors expressed on adipocytes, or fat tissue cells.
"We knew that insulin has this fundamentally important ability of suppressing lipolysis, but the finding that this is mediated in a large part by the brain is surprising," said Dr. Buettner. "The major lipolysis-inducing pathway in our bodies is the sympathetic nervous system and here the studies showed that brain insulin reduces sympathetic nervous system activity in fat tissue. In patients who are obese or have diabetes, insulin fails to inhibit lipolysis and fatty acid levels are increased. The low-grade inflammation throughout the body's tissue that is commonly present in these conditions is believed to be mainly a consequence of these increased fatty acid levels."
Dr. Buettner added, "When brain insulin function is impaired, the release of fatty acids is increased. This induces inflammation, which can further worsen insulin resistance, the core defect in type 2 diabetes. Therefore, impaired brain insulin signaling can start a vicious cycle since inflammation can impair brain insulin signaling." This cycle is perpetuated and can lead to type 2 diabetes. Our research raises the possibility that enhancing brain insulin signaling could have therapeutic benefits with less danger of the major complication of insulin therapy, which is hypoglycemia."
Dr. Buettner's team plans to further study conditions that lead to diabetes such as overfeeding to test if excessive caloric intake impairs brain insulin function. A major second goal will be to find ways of improving brain insulin function that could break the vicious cycle by restraining lipolysis and improving insulin resistance. This study is supported by a grant from the National Institutes of Health and the American Diabetes Association. First author of the study is Thomas Scherer, PhD, postdoctoral fellow in the Department of Medicine in the Division of Endocrinology, Diabetes and Bone Disease.
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About The Mount Sinai Medical Center
The Mount Sinai Medical Center encompasses both The Mount Sinai Hospital and Mount Sinai School of Medicine. Established in 1968, Mount Sinai School of Medicine is one of few medical schools embedded in a hospital in the United States. It has more than 3,400 faculty in 32 departments and 15 institutes, and ranks among the top 20 medical schools both in National Institute of Health funding and by U.S. News & World Report. The school received the 2009 Spencer Foreman Award for Outstanding Community Service from the Association of American Medical Colleges.
The Mount Sinai Hospital, founded in 1852, is a 1,171-bed tertiary- and quaternary-care teaching facility and one of the nation's oldest, largest and most-respected voluntary hospitals. U.S. News & World Report consistently ranks The Mount Sinai Hospital among the nation's best hospitals based on reputation, patient safety, and other patient-care factors. Nearly 60,000 people were treated at Mount Sinai as inpatients last year, and approximately 530,000 outpatient visits took place.
For more information, visit www.mountsinai.org. Follow us on Twitter @mountsinainyc.
Ping
Interesting research, but to cure or prevent type two diabetes, stop eating sugar, fake sugar, and grains. And start walking or otherwise exercising. That is all you have to do.
Would you care to cite medical evidence for your opinion?
“That’s all you have to do” to get me to consider your opinion.
Most doubtful.
Thanks for posting this! It was an interesting read, even if they are only using mouse models at this time.
It works for some but many have something far more serious.
Although I would say this is oversimplified, in defense of the poster, I tried this, with astonishing success. My fasting blood numbers in late 2009 were tested at 110 glucose, low 160s triglycerides. In March 2010, started moderate exercise program and eliminated sugar, corn syrup products and grain products of any kind. Three months later, another fasting blood test, glucose at low 90s, triglycerides dropped all the way down to high 60s.
fasting glucose of 110 isn’t considered diabetic, to my knowledge. Did the ADA screw with the numbers again? The upper limit that I am familiar with is 123.
The triglycerides number is interesting.
I had a fasting glucose in the 110+ range despite the fact that I'm in great shape, exercise for long periods every day, and never let sugar or grain products touch my lips. I also had a low body weight. Taking off another ten pounds has made me really too thin but it did get the blood sugar down. I live on chicken, fish, and vegetables. It's not a fun diet but losing a foot isn't fun either.
I knew a guy who got off the needle through carefully regulating his diet through the day. He had the discipline to do that. His doctor then said he knew this could be done but that people most often don’t have the discipline for it.
You’re right, 110 is not diabetic, but it did make me little nervous, as 123 didn’t seem so far off.
I think those numbers are too tight. The range of “acceptable” blood sugar is apparently 80-100, now. “Pre-diabetic” is akin to “a little bit pregnant”.
I understand susceptability, but the loosening of the definition of diabetic suffers from suspectability, IMO.
“It’s not a fun diet but losing a foot isn’t fun either. “ You have a great attitude! Have you experimented w/herbs and spices to add more flavor dimensions?
Bookmarked for wife.
7 - “It works for some but many have something far more serious.”
Most of these folks here don’t have any idea of what you are talking about, however those of us who suffer from it certainly do.
There are numerous variation of type ‘2’ diabetes.
7 - “It works for some but many have something far more serious.”
Most of these folks here don’t have any idea of what you are talking about, however those of us who suffer from it certainly do.
There are numerous variation of type ‘2’ diabetes.
Does obesity cause diabetes or does diabetes cause obesity?
You call that diabetes?
“You call that diabetes?”
I’m not sure which statement of mine would lead you to believe that I consider 110 mg/dl blood glucose to be diabetes. But just in case there was any ambiguity in my comments, I will clarify things now by stating forcefully that no, I don’t call that diabetes at all. Many doctors will define that as prediabetes, and the American Diabetes Association defines prediabetes as being between 100 and 125 fasting glucose. So I think it is high enough to cause some concern so as to keep it from going any higher, if possible.
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