Group items tagged

Obesity-induced insulin resistance and hepatic steatosis are alleviated by {omega}-3 fatty acids: a role for resolvins and protectins. González-Périz A, Horrillo R, Ferré N, Gronert K, Dong B, Morán-Salvador E, Titos E, Martínez-Clemente M, López-Parra M, Arroyo V, Clària J. FASEB J. 2009 Feb 23. [Epub ahead of print] PMID: 19211925 doi: 10.1096/fj.08-125674

RvE1 protects from local inflammation and osteoclast- mediated bone destruction in periodontitis. Hasturk H, Kantarci A, Ohira T, Arita M, Ebrahimi N, Chiang N, Petasis NA, Levy BD, Serhan CN, Van Dyke TE. FASEB J. 2006 Feb;20(2):401-3. Epub 2005 Dec 22. PMID: 16373400 doi:10.1096/fj.05-4724fje

Glucose restriction can extend normal cell lifespan and impair precancerous cell growth through epigenetic control of hTERT and p16 expression. Li Y, Liu L, Tollefsbol TO. FASEB J. 2009 Dec 17. [Epub ahead of print] PMID: 20019239 doi: 10.1096/fj.09-149328 Cancer cells metabolize glucose at elevated rates and have a higher sensitivity to glucose reduction. However, the precise molecular mechanisms leading to different responses to glucose restriction between normal and cancer cells are not fully understood. We analyzed normal WI-38 and immortalized WI-38/S fetal lung fibroblasts and found that glucose restriction resulted in growth inhibition and apoptosis in WI-38/S cells, whereas it induced lifespan extension in WI-38 cells. Moreover, in WI-38/S cells glucose restriction decreased expression of hTERT (human telomerase reverse transcriptase) and increased expression of p16(INK4a). Opposite effects were found in the gene expression of hTERT and p16 in WI-38 cells in response to glucose restriction. The altered gene expression was partly due to glucose restriction-induced DNA methylation changes and chromatin remodeling of the hTERT and p16 promoters in normal and immortalized WI-38 cells. Furthermore, glucose restriction resulted in altered hTERT and p16 expression in response to epigenetic regulators in WI-38 rather than WI-38/S cells, suggesting that energy stress-induced differential epigenetic regulation may lead to different cellular fates in normal and precancerous cells. Collectively, these results provide new insights into the epigenetic mechanisms of a nutrient control strategy that may contribute to cancer therapy as well as antiaging approaches.

25-hydroxyvitamin D3 is an active hormone in human primary prostatic stromal cells. Lou YR, Laaksi I, Syvälä H, Bläuer M, Tammela TL, Ylikomi T, Tuohimaa P. FASEB J. 2004 Feb;18(2):332-4. Epub 2003 Dec 4. PMID: 14657005

Human cathelicidin antimicrobial peptide (CAMP) gene is a direct target of the vitamin D receptor and is strongly up-regulated in myeloid cells by 1,25-dihydroxyvitamin D3.\nGombart AF, Borregaard N, Koeffler HP.\nFASEB J. 2005 Jul;19(9):1067-77.\nPMID: 15985530

In the July 2005 FASEB Journal, Adrian F. Gombart of the University of California, Los Angeles (UCLA) and his colleagues reported that vitamin D boosts production in white blood cells of one of the antimicrobial compounds that defends the body against germs.\n\nImmediately, Cannell says, the proverbial lightbulb went on in his head: Maybe the high doses of vitamin D that he had been prescribing to virtually all the men on his ward had boosted their natural arsenal of the antimicrobial, called cathelicidin, and protected them from flu. Cannell had been administering the vitamin D because his patients, like many other people in the industrial world, had shown a deficiency:

Medical, Biology and Nutrition Journal

"(NaturalNews) New research published in The Journal of the Federation of American Societies for Experimental Biology (FASEB) has found that the "Western" diet, typically high in sugar and fat, may be responsible for activating genes that signal the body to become fatter. According to scientists, the body's response to high amounts of energy-dense food is to activate the kappa opioid receptor which triggers increased fat storage. Researchers arrived at this conclusion by conducting an experiment on two groups of mice. One group had its kappa opioid receptors genetically deactivated while the other remained intact. Both groups were fed diets high in fat and sugar for 16 weeks. At the end of 16 weeks, the group with the deactivated receptor remained lean while the control group gained significant weight. Besides limiting their bodies' ability to store energy-dense food in their fat stores, the mice whose receptors had been deactivated were noted to also have a limited ability to assimilate and store nutrients from the foods they ingested. Traci Ann Czyzyk-Morgan, one of the study's researchers, indicated that the findings prove the hypothesis long held by many in the scientific community that the kappa opioid receptor may be responsible for causing widespread obesity in Western countries. She and others continue to encourage people to avoid diets high in fat and sugar. "

"ScienceDaily (Dec. 26, 2009) - Going back for a second dessert after your holiday meal might not be the best strategy for living a long, cancer-free life say researchers from the University of Alabama at Birmingham. That's because they've shown exactly how restricted calorie diets -- specifically in the form of restricted glucose -- help human cells live longer. They found that the normal cells lived longer, and many of the precancerous cells died, when given less glucose. Gene activity was also measured under these same conditions. The reduced glucose caused normal cells to have a higher activity of the gene that dictates the level of telomerase, an enzyme that extends their lifespan and lower activity of a gene (p16) that slows their growth. Epigenetic effects (effects not due to gene mutations) were found to be a major cause in changing the activity of these genes as they reacted to decreased glucose levels. "Western science is on the cusp of developing a pharmaceutical fountain of youth" said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "This study confirms that we are on the path to persuading human cells to let us to live longer, and perhaps cancer-free, lives.""

Heart scan scores starting dropping not just 2%, or 8% . . . but 24%, 30%, 50% and more. We also began to see a larger proportion of people achieving these larger successes. Why? I attribute the surge in success to the addition of vitamin D. With vitamin D added to the mix of strategies in Track Your Plaque, HDL cholesterols went up much higher, LDL dropped further, blood sugars dropped, blood pressures dropped. People felt better, had more energy, gained more clarity in thought. And heart scan scores dropped more readily.