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Posted on 26th Mar 2015 @ 6:46 AM
Recently, the renowned international academic journal of nature medicine published online a latest research progress of Chinese scientists , Ming-Hui Zou research group, which disclosed that they found nicotine in tobacco would activate protein kinase AMPKα2 within adipocytes , leading to the activation of downstream signaling pathways, increased lipolysis process in adipose cells , despite weight reduced, however it would result in severe insulin resistance. Prior studies have found that smoking would promote weight loss, while it would also lead to insulin resistance and hyperinsulinemia, the molecular mechanism hidden behind has not been studied. The researchers found that nicotine in tobacco could selectively activate AMPKα2 in adipose cells , AMPKα2 as a protein kinase was capable of phosphorylating 334 serine of MAP kinase phosphatase 1 (MKP1) , promoting MKP1 proteasome pathway degradation.
The deduction of nicotine dependent MKP1 would induce the abnormal activation of p38 mitogen-activated protein kinase (p38MAPK) as well as c-jun N-terminal kinase (JNK) , leading to insulin receptor substrate 1 (IRS1) 307 serine phosphorylation. Phosphorylated IRS1 would accelerate the degradation and inhibition of protein kinase B (PKB), resulting in cell deficient insulin -mediated inhibition on lipolysis process. Eventually, nicotine increased lipolysis process of adipocytes, leading to weight loss, however , while increasing lipolysis process , it also elevated the level of free fatty acids in circulating system, causing insulin resistance in insulin-sensitive tissues. These results demonstrated AMPKα2 acting as as a crucial regulatory factor played an important role in promoting nicotine-induced systemic insulin resistance