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. Author manuscript; available in PMC: 2014 Sep 1.
Published in final edited form as: J Endocrinol. 2013 Oct 4;219(2):109–117. doi: 10.1530/JOE-13-0124

Fig. 5.

Fig. 5

(A) Hepatic total mTOR protein level (using primary antibody from Cell Signaling Technology, Inc., Danvers, MA) in normal (N) and transgenic mice over-expressing bovine growth hormone (Tg) without pioglitazone (PIO) treatment, and after PIO treatment in normal (N-Pio) and transgenic mice over-expressing bovine growth hormone (Tg-Pio); (B) hepatic mTOR phosphorylated at a tyrosine residue (mTOR-pY) protein level (using primary antibody from Cell Signaling Technology, Inc., Danvers, MA) in N and Tg mice without pioglitazone (PIO) treatment, and after PIO treatment in N (N-Pio) and Tg mice (Tg-Pio); (C) hepatic AKT2 protein level (using primary antibody from Cell Signaling Technology, Inc., Danvers, MA) in N and Tg mice without pioglitazone (PIO) treatment, and after PIO treatment in N (N-Pio) and Tg mice (Tg-Pio). Values are means ± SEM. a, b, c – values that do not share the same letter in the superscript are significantly different (p<0.05).