胰岛素抵抗骨骼肌中由超负荷诱导的热休克蛋白（HSPs）、丝裂原活化蛋白激酶（MAPK）和微小RNA（miR-1和miR-133a）反应
Overload induced heat shock proteins (HSPs), MAPK and miRNA (miR-1 and miR133a) response in insulin-resistant skeletal muscle.
作者信息
Katta Anjaiah, Thulluri Srinivasarao, Manne Nandini D P K, Addagarla Hari S, Arvapalli Ravikumar, Nalabotu Siva K, Gadde Muralikrishna, Rice Kevin M, Blough Eric R
机构信息
Department of Pharmacology, Physiology and Toxicology, Marshall University, Joan C. Edwards School of Medicine, Huntington, WV 25755-1090, USA.
出版信息
Cell Physiol Biochem. 2013;31(2-3):219-29. doi: 10.1159/000343363. Epub 2013 Feb 8.
BACKGROUND
Insulin resistance (IR) may decrease muscle adaptability. Heat shock proteins (HSPs), mitogen-activated protein kinases (MAPKs), and miRNA are thought to play a role in muscle hypertrophy but it is unclear if IR may affect their regulation.
METHODS
Soleus muscles of lean Zucker (LZ) and insulin resistant obese Zucker (OZ) rats were overloaded for 7 or 21 days and subjected to immunoblotting and RT-PCR.
RESULTS
IR was associated with decreased muscle hypertrophy. Overload increased HSP27 phosphorylation in both the LZ and OZ rats at day 7 but only in the LZ at day 21. IR was associated with diminished overload induced MAPK phosphorylation and decreased expression of miR-1 and miR133. Overload decreased mir-1 levels in both the LZ and OZ but to a greater extent in the LZ animals.
CONCLUSION
These results suggest that alterations in the regulation of HSPs, MAPKs and miRNA may be associated with the diminished hypertrophy of IR muscle.
背景
胰岛素抵抗（IR）可能会降低肌肉适应性。热休克蛋白（HSPs）、丝裂原活化蛋白激酶（MAPKs）和微小RNA（miRNA）被认为在肌肉肥大中起作用，但尚不清楚IR是否会影响它们的调控。
方法
对瘦型 Zucker（LZ）大鼠和胰岛素抵抗肥胖型 Zucker（OZ）大鼠的比目鱼肌进行7天或21天的超负荷处理，并进行免疫印迹和逆转录聚合酶链反应（RT-PCR）。
结果
IR与肌肉肥大减少有关。在第7天，超负荷使LZ和OZ大鼠的HSP27磷酸化增加，但在第21天仅使LZ大鼠的HSP27磷酸化增加。IR与超负荷诱导的MAPK磷酸化减少以及miR-1和miR133表达降低有关。超负荷使LZ和OZ大鼠的mir-1水平均降低，但在LZ动物中降低幅度更大。
结论
这些结果表明，HSPs、MAPKs和miRNA调控的改变可能与IR肌肉肥大减少有关。
Zotero 插件