Autoimmune Thyroid Disease

An Unfortunate and Lengthy Adventure in Misdiagnosis

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ACE and weight gain

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Thanks to a yahoo group called TaubesTalk for the following news article and abstract:

SYDNEY (AFP) – Australian scientists may have discovered how to help people lose weight without cutting back on food, a breakthrough that could pave the way for fat-burning drugs.

Researchers in Melbourne found that by manipulating fat cells in mice they were able to speed up the animals’ metabolisms.

They found that when a particular enzyme, known as angiotensin converting enzyme (ACE), was removed, mice were able to eat the same amount as other mice but burn more calories and therefore gain less weight.

Animals without the enzyme were on average 20 percent lighter than normal mice and had 50 to 60 percent less body fat, senior researcher at the Howard Florey Institute Michael Mathai said.

“It is very clear that they do have less body fat,” he told AFP.

Mathai, who is also a lecturer in nutrition at Victoria University, said the slimmer mice also appeared to have less chance of developing diabetes because they processed sugar faster than normal mice.

He said the research, to be published Tuesday in the US-based Proceedings of the National Academy of Sciences, could be used to develop drugs to assist weight loss.

Drugs which impair the action of ACE already exist and are mostly used to combat high blood pressure.

“The drugs are out there because they are used for hypertension,” he said.

“So we know their safety and their tolerability. What we don’t know is whether or not they will work in humans. And we don’t know whether it will work in all obese humans.”

Mathai said it could be a question of finding the right dosage of hypertension medication, or developing a new type of drug of the same class, to be used as weight-loss pills.

“This might be one way in which you can increase metabolic rate in combination with managing nutrition to limit the intake of calories,” he said.

Mathai said the research, conducted at the Howard Florey Institute, Victoria University, La Trobe University, Deakin University, the Baker Institute and the University of Melbourne, was yet to pinpoint why the genetic manipulation led to weight loss.

“Because we deleted the gene, the gene is gone from the whole body, that means that it is gone from all tissues including the brain,” he said.

“And so we don’t know whether it’s a direct effect of the deficiency in the tissue or whether it’s something coming from the brain.” Australian scientists report weight loss breakthrough

And the abstract:

Angiotensin II (AII), acting via its G-protein linked receptor, is an important regulator of cardiac, vascular, and renal function. Following injection of AII into rats, we find that there is also a rapid tyrosine phosphorylation of the major insulin receptor substrates 1 and 2 (IRS-1 and IRS-2) in the heart. This phenomenon appears to involve JAK2 tyrosine kinase, which associates with the AT1 receptor and IRS-1/IRS-2 after AII stimulation. AII-induced phosphorylation leads to binding of phosphatidylinositol 3-kinase (PI 3-kinase) to IRS-1 and IRS-2; however, in contrast to other ligands, AII injection results in an acute inhibition of both basal and insulin-stimulated PI 3-kinase activity. The latter occurs without any reduction in insulin receptor or IRS phosphorylation or in the interaction of the p85 and p110 subunits of PI 3-kinase with each other or with IRS-1/IRS-2. These effects of AII are inhibited by AT1 receptor antagonists. Thus, there is direct cross-talk between insulin and AII signaling pathways at the level of both tyrosine phosphorylation and PI 3-kinase activation. These interactions may play an important role in the association of insulin resistance, hypertension, and cardiovascular disease. Cross-talk between the insulin and angiotensin signaling systems

I think this may be why low carbohydrate diets help so many people with food chemical intolerance. Lower your insulin levels, and I bet you lower your ACE output.

Written by alienrobotgirl

1 May, 2008 at 6:24 pm

Posted in The Genetics of FCI?

Tagged with , , ,

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