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. Author manuscript; available in PMC: 2012 Apr 6.
Published in final edited form as: Cell Metab. 2011 Apr 6;13(4):450–460. doi: 10.1016/j.cmet.2011.03.013

Fig.6. Pancreatic abnormalities render PARP-2−/− mice glucose intolerant after high-fat feeding.

Fig.6

(A) Plasma glucose levels during an intraperitoneal glucose tolerance test (IPGTT) in 9-month old PARP-2+/+ and −/− male mice (n=7 and 9, respectively) fed a high fat diet for 12 weeks. The area under the curve of the glucose curves is shown at the right. (B) Insulin levels during the first hour of the IPGTT in (A). (C) Comparison of total pancreas weight between PARP-2+/+ and PARP-2−/− mice on chow and high-fat diet. (D) Pancreas from PARP-2+/+ and PARP-2−/− mice after high-fat diet were stained for insulin (scale bar = 50 μm) and (E) Mean islet size was quantified. (F) Total insulin content in pancreas was measured as described. (G) Gene expression in the pancreas of PARP-2+/+ and PARP-2−/− mice was measured by RT-qPCR. (H) Pancreatic total protein extracts were used to test the abundance of SIRT1, and subunits from the respiratory complexes I and III. FOXO1 was also immunoprecipitated to determine relative FOXO1 acetylation levels. Through the figure, white bars and circles represent PARP-2+/+ mice, while black bars and circles represent PARP-2−/− mice. * indicates statistical difference vs. PARP-2+/+ mice at p<0.05