Dr Raymond Ng, PhD,
Singapore Institute for Clinical Sciences,
A*STAR
Date: Thursday, 5 March, 2015
Time: 4:30 pm – 5:30 pm
Venue: MD6-01-01B
Chairperson: Dr. Deron R. Herr
microRNA-32 promotes Beige Cell Emergence During Cold Thermogenesis by Inhibiting Tob1 and Activating p38/MAPK Signaling
Proper control of metabolism is critical to maintain human physiology and health. However, throughout the globe, obesity and associated metabolic diseases such as type 2 diabetes have become increasingly prevalent leading to increased interest in adipose biology and metabolism. Mammals, including humans, possess both white (WAT) and brown adipose tissue (BAT). WAT serves as a depot for excess calories whereas BAT dissipates chemical energy stored in white fat as heat to maintain optimal body temperature. We wish to harness this unique ability of BAT to combat obesity and metabolic syndrome. Recent studies have shown that adult humans contain significant deposits of BAT which renewed interest in BAT differentiation and its physiological role in adults.
microRNAs (miRNAs), a class of small non-coding RNAs, have been recently discovered to regulate metabolic homeostasis. miRNAs exert modest effects on multiple target genes and modulate gene expression through target mRNA degradation and translation inhibition. miRNAs have recently emerged as crucial regulators in adipogenesis and lipid metabolism. Specific miRNAs like miR-33a/b have been shown to regulate cholesterol and lipid metabolism and are currently in various phases of therapeutic development. Preliminary data shows that miR-32 inhibition in vivo inhibits the emergence of beige cells which function like BAT cells, within WAT. This inhibition of beige cell emergence is most likely due to a drop in serum fgf21 levels due to reduced p38/MAPK signaling in brown adipose tissue leading to decreased secretion of fgf21 during cold exposure. In conclusion, our study shows that miR-32 plays a crucial role in stimulating beige cell emergence by activating p38/MAPK signaling during cold thermogenesis.
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