#EBJS_Q_AND_A [DIABETIC MYOPATHY] FOLLOW-UP QUESTION ON POSTING 12/08/14 #AN_ARTICLE_A_DAY Q: 이상목 굳이 diabetes에 대한 인위적인 모델을 만들어 실험에 사용한 것이 근육atrophy에 대한 miRNA182의 기능을 알아보는 데에 도움이 될까요? 당뇨모델 사용을 통해 muscle atrophy를 확인했다는 결과가 있는건지 궁금합니다 A: Am J Physiol Endocrinol Metab. 2012 Feb 1;302(3):E307-15. (Page E307) MUSCLE ATROPHY in poorly controlled diabetes, also called diabetic myopathy, is a clinical condition in which skeletal muscle size and strength/endurance are reduced (21, 39). 21. Jakobsen J, Reske-Nielsen E. Diffuse muscle fiber atrophy in newly diagnosed diabetes. Clin Neuropathol 5: 73–77, 1986. 39. Riddell MC, Iscoe KE. Physical activity, sport, and pediatric diabetes. Pediatr Diabetes 7: 60 –70, 2006. (ABSTRACT) Altered REDD1, myostatin, and Akt/mTOR/FoxO/MAPK signaling in streptozotocin-induceddiabetic muscle atrophy. Hulmi JJ, Silvennoinen M, Lehti M, Kivelä R, Kainulainen H Type 1 diabetes, if poorly controlled, leads to skeletal muscle atrophy, decreasing the quality of life. We aimed to search highly responsive genes in diabetic muscle atrophy in a common diabetes model and to further characterize associatedsignaling pathways. Mice were killed 1, 3, or 5 wk after streptozotocin or control. Gene expression of calf muscles was analyzed using microarray and protein signaling with Western blotting. We identified translational repressor protein REDD1(regulated in development and DNA damage responses) that increased seven- to eightfold and was associated with muscleatrophy in diabetes. The diabetes-induced increase in REDD1 was confirmed at the protein level. This result was accompanied by the increased gene expression of DNA damage/repair pathways and decreased expression in ATP production pathways. Concomitantly, increased phosphorylation of AMPK and dephosphorylation of theAkt/mTOR/S6K1/FoxO pathway of proteins were observed together with increased protein ubiquitination. These changes were especially evident during the first 3 wk, along with the strong decrease in muscle mass. Diabetes also induced an increase inmyostatin protein and decreased MAPK signaling. These, together with decreased serum insulin and increased serum glucose, remained altered throughout the 5-wk period. In conclusion, diabetic myopathy induced by streptozotocin led to alteration of multiple signaling pathways. Of those, increased REDD1 and myostatin together with decreased Akt/mTOR/FoxOsignaling are associated with diabetic muscle atrophy. The increased REDD1 and decreased Akt/mTOR/FoxO signalingfollowed a similar time course and thus may be explained, in part, by increased expression of genes in DNA damage/repair and possibly also decrease in ATP-production pathways.
Posted on: Sat, 13 Dec 2014 03:20:49 +0000
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