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. 2009 Oct 6;59(1):6–16. doi: 10.2337/db09-0755

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© 2010 by the American Diabetes Association.

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FIG. 6. — Grp78 heterozygosity promotes adaptive UPR and improves ER homeostasis in WAT. Whole cell lysates were prepared from WAT of 25-week-old mice on regular diet (RD) or after 15-week HFD (n = 4–6 mice per condition) and subjected to Western blotting. The protein loading was normalized against β-actin. Quantitation of relative protein levels of indicated UPR signaling molecules (A) and ER chaperones (B) are presented as the means ± SE. *P < 0.05; **P < 0.01 for ^+/− vs. ^+/+; #P < 0.05; ##P < 0.01 for HFD vs. regular diet. □, ^+/+ regular diet; , ^+/− regular diet; ▧, ^+/+ HFD; ■, ^+/− HFD.

Inline graphic — Grp78 heterozygosity promotes adaptive UPR and improves ER homeostasis in WAT. Whole cell lysates were prepared from WAT of 25-week-old mice on regular diet (RD) or after 15-week HFD (n = 4–6 mice per condition) and subjected to Western blotting. The protein loading was normalized against β-actin. Quantitation of relative protein levels of indicated UPR signaling molecules (A) and ER chaperones (B) are presented as the means ± SE. *P < 0.05; **P < 0.01 for ^+/− vs. ^+/+; #P < 0.05; ##P < 0.01 for HFD vs. regular diet. □, ^+/+ regular diet; , ^+/− regular diet; ▧, ^+/+ HFD; ■, ^+/− HFD.