liveonearth: (Default)
It's a free, online, educational event about how to interpret and act on your own genotypes.  There will be some fascinating lectures here, and some very basic ones.  I definitely want to hear the one about ketogenic diet.  You can sign up here.

EDIT: I did listen to one lecture per day, or at least part of each one.  Genetics and Epigenetics since it became a thing have been an interest of mine.  The programs were oriented at the general public, and I garnered no new information.  I was hoping that it would go a little deeper and nerdier for me.  Would be very useful for folks who are just getting introduced to the significance of modern science with regard to their genetic makeup and health.  Lots of correlates.  Very interesting.

The funny thing is that the clinicians all say the same thing, that your SNPs (single nucleotide polymorphisms) for the most part won't do you harm if you keep your general level of physical health strong.  There's a lot of redundancy build into human genetics and systems.  If someone forgets to cross a T somewhere in your genetics, you'll probably be fine, long as you don't wear yourself to a frazzle, skip sleep, and consider trips to the refrigerator to be adequate exercise.
liveonearth: (moon)
EPIGENETICS OF DM2: GLUCOCORTICOID AND VIT D RECEPTORS MEDIATE
ALSO TNF ALPHA OR DEXAMETHASONE INDUCES IR
http://www.nature.com/ncb/journal/v17/n1/full/ncb3080.html
Identification of nuclear hormone receptor pathways causing insulin resistance by transcriptional and epigenomic analysis
Sona Kang, Linus T. Tsai, Yiming Zhou, Adam Evertts, Su Xu, Michael J. Griffin, Robbyn Issner, Holly J. Whitton, Benjamin A. Garcia, Charles B. Epstein, Tarjei S. Mikkelsen & Evan D. Rosen
Nature Cell Biology 17, 44–56 (2015) doi:10.1038/ncb3080
Received 06 August 2014 Accepted Nov 2014 Published online 15 Dec 2014
Abstract
Insulin resistance is a cardinal feature of Type 2 diabetes (T2D) and a frequent complication of multiple clinical conditions, including obesity, ageing and steroid use, among others. How such a panoply of insults can result in a common phenotype is incompletely understood. Furthermore, very little is known about the transcriptional and epigenetic basis of this disorder, despite evidence that such pathways are likely to play a fundamental role. Here, we compare cell autonomous models of insulin resistance induced by the cytokine tumour necrosis factor-α or by the steroid dexamethasone to construct detailed transcriptional and epigenomic maps associated with cellular insulin resistance. These data predict that the glucocorticoid receptor and vitamin D receptor are common mediators of insulin resistance, which we validate using gain- and loss-of-function studies. These studies define a common transcriptional and epigenomic signature in cellular insulin resistance enabling the identification of pathogenic mechanisms.

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