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. Author manuscript; available in PMC: 2014 Jul 10.
Published in final edited form as: Nat Immunol. 2011 Apr 10;12(5):408–415. doi: 10.1038/ni.2022

Figure 8.

Figure 8

The NLRP3-PYCARD inflammasome promotes insulin resistance in vivo. (a) Blood glucose and insulin levels were measured in WT (n=6), Nlrp3−/− (n=5) or Pycard−/− (n=6) mice under fasting or re-fed conditions after HFD feeding for 12 weeks. (b-e) Glucose tolerance test (GTT) (b, d) and insulin tolerance test (ITT) (c, e) were performed for WT, Nlrp3−/− (b, c) and Pycard−/− (d, e) mice on HFD for 12 weeks. (f) GTT was conducted on the indicated bone marrow chimeric mice on HFD for 12 weeks. (g, h) Insulin-stimulated phosphorylation of IRβ, IRS1 and Akt (Ser473) in liver tissues of individual WT and Pycard−/− mice (g), and phospho-Akt (Ser473) in liver, white adipose (WAT) and muscle tissues of individual WT and Nlrp3−/− mice (h) on HFD for 12 weeks after insulin (2 IU/kg body weight) infusion. Graphs at right of blots show the quantitation of each molecule. (i, j) Expression of Tnfa and Mcp1 mRNA relative to Actb in liver tissues of Nlrp3−/− mice (i) and Pycard−/− mice (j) on RD or HFD for 12 weeks. One of two independent experiments is shown (mean ± s.d.). * P < 0.05, versus controls.