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Disruption of MAM integrity and insulin signaling in liver of diet-induced diabetic mice.
Disruption of MAM integrity and insulin signaling in liver of diet-induced diabetic mice. A: Quantification of protein amount in MAM fractions following cellular subfraction of liver of SD, HFHSD, and HFHSD + rosiglitazone mice. *P < 0.05 vs. SD mice; #P < 0.05 vs. untreated HFHSD mice. n = 5. B: Representative Western blots (at top) and quantitative analysis (below) of proteins in MAM fractions of liver of SD, HFHSD, and HFHSD + rosiglitazone mice. C: Representative Western blot (at top) and quantitative analysis (below) of insulin-stimulated PKB and GSK3β phosphorylation in primary hepatocytes of SD, HFHSD, and HFHSD + rosiglitazone mice. *P < 0.05; **P < vs. respective control; #P < 0.01 vs. SD mice with insulin. n = 3. D: In situ PLA images (at left, ×63 and scale bar = 20 μm) and quantitative analysis (at right) of CypD/IP3R1, VDAC1/IP3R1, and Grp75/IP3R1 interactions in primary hepatocytes of SD, HFHSD, and HFHSD + rosiglitazone mice. *P < 0.01 vs. SD mice; **P < vs. SD mice. n = 3. Rosi, rosiglitazone. Emily Tubbs et al. Diabetes 2014;63: ©2014 by American Diabetes Association
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