Miami, FL (PRWEB) May 02, 2012
A newly published study offers promising results in obesity research. In particular, research in NYGGF4, a recently discovered gene found in fat cells, which its over-activity induces insulin resistance and reduces the cellular energy, mitochondria (cellular energy plant) mass and its DNA, as well as being associated with excessive free radicals. This study suggests that pre-treatment with Alpha Lipoic Acid "strikingly enhanced" absorption of glucose by fat cells with over-active NYGGF4. In another word, there was an improvement in insulin resistance in such cells.
Alpha Lipoic acid, in its reduced from, is a vital co-enzyme associated with the production of energy. However, Alpha Lipoic acid is also classified as a dietary nutrient.
In Germany, Alpha Lipoic Acid has been used as a co-therapy in the treatment of Diabetic poly-neuropathy for decades and first human clinical studies of Alpha Lipoic Acid in the United States was carried out in 70's by Dr. Fredrick C. Bartter and Dr. Burton M. Berkson, two associates of the National Institutes of Health for the treatment of chronic liver damage.
In 1996, Professor Lester Packer a senior anti-oxidant researcher and scientist at the University of California (Berkley) declared R-Alpha Lipoic a universal antioxidant.
In Japan, Alpha Lipoic Acid had been previously sold only as a medicine. In June 2004, the Ministry of Health, Labor, and Welfare of Japan reclassified Alpha Lipoic Acid as a food.
While Alpha Lipoic Acid is dietary supplements, overwhelming number of studies have suggested its beneficial role in diabetes related complications and, now, this study points to its beneficial role for improving insulin resistance in fat cells (3T3L-1) through increasing a biological signalling pathway (Akt).
The cell line 3T3L-1 is pre-adipogenic (fat), to which under hormonal or cellular redox imbalance transforms to fat cells, storing triglycerides.
In general, obesity is associated with a number of factors including non-insulin-dependent diabetes, and cardiovascular diseases.
Studies have shown that Alpha Lipoic Acid activates the insulin signaling pathway, not only in adipose (fat) cells but also in muscle cells and that its application opposes unnecessary formation of 3T3-L1 (pre-fat cells). Treatment of 3T3-L1 with Alpha Lipoic Acid has opposed both insulin or the hormonal mixture-induced formation of 3T3-L1 pre-adipocytes by modulating the MAPK pathway. (1)
MAPK/Akt pathways, where Alpha Lipoic Acid has shown promising results, are biological pathways that promote acceptance of glucose by the cells, in another word oppose insulin resistance.
In conclusion, Nutri-Med Logic Corp agrees with this and other studies, to which Alpha Lipoic Acid improves insulin resistance in both pre-fat and muscle cells. Nutri-Med Logic Corp adds that Alpha Lipoic Acid is also classified as a nutrient and its dietary supplementation is beneficial not only in obesity but also diabetes.
Nutri-Med Logic Corp is also a producer of dietary supplements such as a Pharmaceutical Grade R-Alpha Lipoic Acid (the natural type of Lipoic Acid), a universal anti-oxidant and the dietary supplement of choice for the Diabetics, in Germany for decades;
Producer of PolyEnylPhosphatidylCholine (PPC 425mg), an extract of soy, a pure and effective dietary source of choline and the recommended dietary supplement for those with Fatty Liver and Alcoholic Liver Disease, in Europe for decades.
Nutri-Med Logic Corp invites you to visit its News Archives and Review its News Releases on other potential benefits of Omega-3 Fatty Acids.
Nutri-Med Logic's products are Formulated Based on Nutritional Logic, made from the highest quality raw materials that are manufactured in pharmaceutical facilities, encapsulated in pharmaceutical facilities and packaged in pharmaceutical facilities.
It must be noted that the studies, statements or sources above and below have not been evaluated by The FDA and, thus, one should not relate the cause of any diseases, stated herein, to lack of the dietary supplements, stated herein, nor equate their supplementation to prevention, treatment or cure.
1. Sept 12, 2003. J. of Biol Chem, 278, 34823-34833