http://medgadget.com/2012/04/in-study-altering-heart-molecules-protects-against-obesity.html
In short, researchers at UT Southwestern found that a regulatory molecule in the heart, in this case mi-RNA-208a, that actually has an effect on the body's metabolism by effecting MED13 (mediator complex subunit 13), which is known to control transcription of thyroid hormone. micoRNA-208 has been shown to negatively regulate MED13 and in this particular study researchers show that cardiac-specific over-expression of MED13 OR pharmacologic inhibition of miRNA-208a provides mice with a resistance to high-fat diet induced obesity.
- I'll back track for a sec to explain what miRNAs (micro RNAs) are: mi-RNA are short, single stranded RNA molecules usually around 20-25 nucleotides in length and are known to regulate gene expression. Unlike mRNA, miRNAs don't actually encode for proteins but function by preventing translation of mRNA. So, in the case of miRNA-208a, we see prevention of MED13 translation.
So, we've all learned that obesity, type 2 diabetes, and stroke are all inflammatory disorders; my big question now is how does regulation of MED13 affect inflammation in the body??
Will we see prevention of chronic inflammation along with prevention of metabolic issues?
What would happen if an obese person with chronic inflammation was treated with miRNA-208a inhibition? -Would we see a reduction in that person's inflammation also??
If we do see a reduction in inflammation, would this treatment help in other inflammatory diseases??
There's lots more interesting research to be done!!
If you'd like to take a look at the journal article, search "A cardiac MicroRNA Governs Systemic Energy Homeostatis by Regulation of MED13" CE Grueter
This does sound promising, but then again everything is so interconnected that there is a great chance that the miRNA will lead to other undesirable effects. Also, i wonder how easy it is to isolate miRNA, since I've seen conflicting reports on this. It will be essential to isolate the miRNA-208a only, since unwanted segments may lead to complications.
ReplyDeleteOver and over this semester we have seen examples where studies proved promising in animal models only to be met with spectacular failures in human trials. Previous research into curving obesity by controlling leptin (decreases hunger) and ghrelin (increases hunger) proved initially successful. As the trials progressed however the subjects all regressed. Despite these two powerful hormone cascades being tightly regulated, alternative pathways were engaged. These pathways stimulated the hunger response preventing weight loss. This research gave credence to the theory that adipose tissue acts as an organ, sending and receiving chemical messengers in the body. It seems the body is biologically engineered to have an overriding hunger stimulus. I would like to know more about the length of time this trial ran to see if the end result would be similar to the leptin/ghrelin trials. Also I would be curious to see the side effects this treatment would have in humans. This protein could have numerous interactions elsewhere causing adverse effects. All in all this is an exciting topic and I looking forward to the upcoming research. Hopefully it yields a new treatment curbing obesity and maybe even inflammation!
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