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. 2012 Nov 15;61(12):3156–3166. doi: 10.2337/db12-0418

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© 2012 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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FIG. 6. — Effects of nicotine on cell signaling and insulin sensitivity in L6 skeletal muscle myotubes. A: Serine phosphorylation of IRS-1 in response to nicotine exposure at 200 μmol. B: Stimulation of p44/p42 MAPK over time with continuous nicotine exposure at 200 μmol with and without MEK inhibitor UO126, the upstream kinase of p44/p42 activation. C: Stimulation of p70s6k over time with continuous nicotine exposure at 200 μmol with and without the mTOR inhibitor rapamycin. D: Effects of nicotine at 200 μmol on IRS-1^ser636 phosphorylation in L6 muscle cell culture with and without inhibitors against p44/p42 MAPK and mTOR. Values are mean ± SEM. §Significantly different than control, P < 0.05; ¥significantly different than time 0, P < 0.05; #significantly different than nicotine, P < 0.05.

FIG. 6. — Effects of nicotine on cell signaling and insulin sensitivity in L6 skeletal muscle myotubes. A: Serine phosphorylation of IRS-1 in response to nicotine exposure at 200 μmol. B: Stimulation of p44/p42 MAPK over time with continuous nicotine exposure at 200 μmol with and without MEK inhibitor UO126, the upstream kinase of p44/p42 activation. C: Stimulation of p70s6k over time with continuous nicotine exposure at 200 μmol with and without the mTOR inhibitor rapamycin. D: Effects of nicotine at 200 μmol on IRS-1^ser636 phosphorylation in L6 muscle cell culture with and without inhibitors against p44/p42 MAPK and mTOR. Values are mean ± SEM. §Significantly different than control, P < 0.05; ¥significantly different than time 0, P < 0.05; #significantly different than nicotine, P < 0.05.

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