Vetten die niet gevoelig zijn insuline [Jan 2003]

[3XL]

[Boston, MA, January, 2003]: Imagine being able to throw away those diet books and eat whatever you want without becoming fat, and - as a bonus - not develop diabetes and live longer as well. A new study led by Joslin Diabetes Center researchers and published in the Jan. 24 issue of the journal Science brings scientists one step closer to turning this scenario - no doubt the dream of the estimated 60 million overweight American adults - into a reality.

The study, conducted in laboratory animals, raises the possibility that new drugs can be developed to make fat cells in the body less sensitive to insulin. Perhaps one day humans, like the genetically altered mice studied, may be able to eat whatever they want and still stay slim - and live longer.

The researchers, headed by C. Ronald Kahn, M.D., at the Joslin Diabetes Center, reported on their experiments with mice that have been genetically altered to have no insulin receptor in fat. These FIRKO mice were able to eat all they wanted and remain lean. In fact, even when they were stimulated to overeat, they failed to gain any extra weight. What’s even more important is that these mice live longer than brother/sister controls that ate the same amount of food but did not have this genetic knockout. Matthias Bluher, M.D., of Joslin, and Barbara B. Kahn, M.D., of Boston’s Beth Israel Deaconess Medical Center's Department of Medicine, also participated in the study. Both institutions are affiliated with Harvard Medical School, where Dr. C. Ronald Kahn is the Mary K. Iacocca Professor of Medicine and Dr. Barbara Kahn is Professor of Medicine.

Why did the mice stay slim? The mice in the study had fat that could not respond to insulin. "Since insulin is needed to help fat cells store fat, these animals had less fat and were protected against the obesity that occurs with aging or overeating. They also were protected against the metabolic abnormalities associated with obesity, including type 2 diabetes," Dr. C. Ronald Kahn said.

"In this interesting mouse model, a reduction in fat mass, achieved without caloric restriction, significantly extends lifespan. These exciting results demonstrate how the NIH investment in fundamental research continues to generate new insights with major implications for preventing and treating diabetes and obesity," said Dr. Judith Fradkin. Dr. Fradkin heads the Endocrinology, and Metabolic Diseases Division of the National Institute of Diabetes and Digestive and Kidney Diseases Diabetes, part of the National Institutes of Health, which funded the study.

Scientists know that how long an organism lives depends on many factors, including genetics, hormone signaling, body weight, body fat content and environmental factors such as food or caloric intake. It also has been known for some time that caloric restriction increases longevity in various organisms, ranging from yeast to mammals. What was not clear was if diet restriction increased longevity directly or whether the longevity was due to the associated leanness.

In the current study, the researchers found FIRKO mice at all ages had a 50 to 70 percent reduction in fat mass, despite the fact that they ate normally or even more than the controls. Moreover, they were protected against obesity and its related metabolic disorders, including type 2
diabetes, which affects at least 17 million Americans and is associated with obesity in at least 80 percent of cases.

The researchers found both male and female FIRKO mice on average had a lifespan increase of 18 percent or 134 days - from 753 to 887 days. Furthermore, the researchers found at 30 months of age when 45 to 54 percent of control mice had died that more than 80 percent of FIRKO mice were still alive.

While the researchers do not know if the same outcome would occur in other mammals or humans, the findings in the FIRKO mice study provide hope. "Perhaps one day if we are able to find a drug to reduce or block insulin action in fat cells in humans, we might be able to prevent obesity, as well as type 2 diabetes and other metabolic diseases," Dr. C. Ronald Kahn said. "And who knows, they might also live longer too."

[kingnbajam]

heeft een insuline resistentie van vetcellen geen gevolg voor hormonale processen in het menselijk lichaam? En wat voor gevolgen zou het kunnen hebben voor spiercellen? Daar wordt volgens mij niets over gezegd. Wat als je geen vet meer kunt opslaan, maar ook vertraagde opname spiercellen?

[Big T]

Laten we realistisch zijn: er bestaan nog geen medicijnen om dit te bereiken, de muis is genetisch behandeld (net als bij het myostatine-gen) om dit aan te tonen.

En nee het zal geen effect hebben gehad op de spier receptor, enkel de vetcel receptor.
Zelfs wanneer het lukt bij muizen, dan nog duurt het 10tallen jaren om dit te kunnen omzetten voor de mens. Net als bij klonen ed.

De vraag is wel wat er gebeurd met al de extra vetzuren in de bloedbaan, als het niet word opgeslagen in vetweefsel, wat moet er dan mee gebeuren? Word het afgescheiden? Daar heb ik niets over gelezen.

[Deejay_Spike]

vet schijten

(nee maar serieus, ik denk dat als het niet wordt opgeslagen, het gewoon wordt afgescheiden.)

[Martinus]

Spetterpoep!
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[dandyman]

Origineel gepost door TylW

De vraag is wel wat er gebeurd met al de extra vetzuren in de bloedbaan, als het niet word opgeslagen in vetweefsel, wat moet er dan mee gebeuren? Word het afgescheiden? Daar heb ik niets over gelezen.

lijkt me idd een vraag die ook bij hun moet opkomen zou je zeggen ja