Editing MicroRNA (section)

===Obesity===
miRNAs play crucial roles in the regulation of [[stem cell]] progenitors differentiating into [[adipocyte]]s.<ref name="pmid21844119">{{cite journal | vauthors = Romao JM, Jin W, Dodson MV, Hausman GJ, Moore SS, Guan LL | title = MicroRNA regulation in mammalian adipogenesis | journal = Experimental Biology and Medicine | volume = 236 | issue = 9 | pages = 997–1004 | date = September 2011 | pmid = 21844119 | doi = 10.1258/ebm.2011.011101 | s2cid = 30646787 }}</ref> Studies to determine what role [[pluripotent stem cells]] play in [[adipogenesis]], were examined in the immortalized human [[bone marrow]]-derived [[stromal cell]] line hMSC-Tert20.<ref name="pmid21756067">{{cite journal | vauthors = Skårn M, Namløs HM, Noordhuis P, Wang MY, Meza-Zepeda LA, Myklebost O | title = Adipocyte differentiation of human bone marrow-derived stromal cells is modulated by microRNA-155, microRNA-221, and microRNA-222 | journal = Stem Cells and Development | volume = 21 | issue = 6 | pages = 873–83 | date = April 2012 | pmid = 21756067 | doi = 10.1089/scd.2010.0503 | hdl = 10852/40423 | hdl-access = free }}</ref> Decreased expression of [[miR-155]], [[Mir-221 microRNA|miR-221]], and [[Mir-221 microRNA|miR-222]], have been found during the adipogenic programming of both immortalized and primary hMSCs, suggesting that they act as negative regulators of differentiation. Conversely, [[ectopic expression]] of the miRNAs [[MiR-155|155]], [[Mir-221 microRNA|221]], and [[Mir-221 microRNA|222]] significantly inhibited adipogenesis and repressed induction of the master regulators [[PPARγ]] and CCAAT/enhancer-binding protein alpha ([[CEBPA]]).<ref name="pmid16431920">{{cite journal | vauthors = Zuo Y, Qiang L, Farmer SR | title = Activation of CCAAT/enhancer-binding protein (C/EBP) alpha expression by C/EBP beta during adipogenesis requires a peroxisome proliferator-activated receptor-gamma-associated repression of HDAC1 at the C/ebp alpha gene promoter | journal = The Journal of Biological Chemistry | volume = 281 | issue = 12 | pages = 7960–67 | date = March 2006 | pmid = 16431920 | doi = 10.1074/jbc.M510682200 | doi-access = free }}</ref> This paves the way for possible genetic obesity treatments.

Another class of miRNAs that regulate [[insulin resistance]], [[obesity]], and [[diabetes]], is the [[Let-7 microRNA precursor|let-7]] family. Let-7 accumulates in human tissues during the course of [[aging]].<ref name="Jun-HaoGupta2016">{{cite journal | vauthors = Jun-Hao ET, Gupta RR, Shyh-Chang N | title = Lin28 and let-7 in the Metabolic Physiology of Aging | journal = Trends in Endocrinology and Metabolism | volume = 27 | issue = 3 | pages = 132–141 | date = March 2016 | pmid = 26811207 | doi = 10.1016/j.tem.2015.12.006 | s2cid = 3614126 }}</ref> When let-7 was ectopically overexpressed to mimic accelerated aging, mice became insulin-resistant, and thus more prone to high fat diet-induced obesity and [[diabetes]].<ref name="pmid21962509">{{cite journal | vauthors = Zhu H, Shyh-Chang N, Segrè AV, Shinoda G, Shah SP, Einhorn WS, Takeuchi A, Engreitz JM, Hagan JP, Kharas MG, Urbach A, Thornton JE, Triboulet R, Gregory RI, Altshuler D, Daley GQ | title = The Lin28/let-7 axis regulates glucose metabolism | journal = Cell | volume = 147 | issue = 1 | pages = 81–94 | date = September 2011 | pmid = 21962509 | pmc = 3353524 | doi = 10.1016/j.cell.2011.08.033  }}</ref> In contrast when let-7 was inhibited by injections of let-7-specific [[antagomir]]s, mice become more insulin-sensitive and remarkably resistant to high fat diet-induced obesity and diabetes. Not only could let-7 inhibition prevent obesity and diabetes, it could also reverse and cure the condition.<ref name="pmid22160727">{{cite journal | vauthors = Frost RJ, Olson EN | title = Control of glucose homeostasis and insulin sensitivity by the Let-7 family of microRNAs | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 108 | issue = 52 | pages = 21075–80 | date = December 2011 | pmid = 22160727 | pmc = 3248488 | doi = 10.1073/pnas.1118922109 | bibcode = 2011PNAS..10821075F | doi-access = free }}</ref> These experimental findings suggest that let-7 inhibition could represent a new therapy for [[obesity]] and type 2 diabetes.