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10.1152/ajplung.00091.2015

http://scihub22266oqcxt.onion/10.1152/ajplung.00091.2015
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C4867352!4867352!26919895
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suck abstract from ncbi


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pmid26919895      Am+J+Physiol+Lung+Cell+Mol+Physiol 2016 ; 310 (9): L837-45
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  • Hyperinsulinemia adversely affects lung structure and function #MMPMID26919895
  • Singh S; Bodas M; Bhatraju NK; Pattnaik B; Gheware A; Parameswaran PK; Thompson M; Freeman M; Mabalirajan U; Gosens R; Ghosh B; Pabelick C; Linneberg A; Prakash YS; Agrawal A
  • Am J Physiol Lung Cell Mol Physiol 2016[May]; 310 (9): L837-45 PMID26919895show ga
  • There is limited knowledge regarding the consequences of hyperinsulinemia on the lung. Given the increasing prevalence of obesity, insulin resistance, and epidemiological associations with asthma, this is a critical lacuna, more so with inhaled insulin on the horizon. Here, we demonstrate that insulin can adversely affect respiratory health. Insulin treatment (1 ?g/ml) significantly (P < 0.05) increased the proliferation of primary human airway smooth muscle (ASM) cells and induced collagen release. Additionally, ASM cells showed a significant increase in calcium response and mitochondrial respiration upon insulin exposure. Mice administered intranasal insulin showed increased collagen deposition in the lungs as well as a significant increase in airway hyperresponsiveness. PI3K/Akt mediated activation of ?-catenin, a positive regulator of epithelial-mesenchymal transition and fibrosis, was observed in the lungs of insulin-treated mice and lung cells. Our data suggests that hyperinsulinemia may have adverse effects on airway structure and function. Insulin-induced activation of ?-catenin in lung tissue and the contractile effects on ASM cells may be causally related to the development of asthma-like phenotype.
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