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. 2012 Jul 17;61(8):1949–1958. doi: 10.2337/db11-1502

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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. 1. — Increased Shp1 protein and gene expression in diet-induced obesity and generation of hepatocyte-specific Shp1 knockout mice (Ptpn6^H-KO). A: Shp1 protein detection by Western blotting in gastrocnemius muscle (Gastroc), epididymal white adipose tissue (EWAT), perirenal white adipose tissue (PWAT), and liver of Ptpn6^f/f mice fed an SD or HFD for 8 weeks (n = 12–13 per diet group), with eEF2 and β-actin as loading controls. B: Quantitative PCR analysis of hepatic Shp1 gene expression with Actb as the sample control (n = 11–12 per diet group). Dotted lines on blots separate noncontiguous sections of the same gel (^P < 0.05 and ^^^P < 0.005 diet effect). Western blot detection of Shp1 in liver (C), purified hepatocytes and Kupffer cells (D) isolated from Ptpn6^H-KO mice with either hemizygous (+/−) or homozygous (^+/+) expression of Alb-Cre (Alb-Cre), and from their Alb-Cre (^−/−) Ptpn6^f/f littermates. Shp1 level in J774 macrophages (M) acted as a blotting control. α-Tubulin (C) and β-actin (D) were loading controls.