Supplementary Figure 4: Insulin stimulates the secretion of IL-1β by macrophages via metabolism and the NLRP3 inflammasome. | Nature Immunology

Supplementary Figure 4: Insulin stimulates the secretion of IL-1β by macrophages via metabolism and the NLRP3 inflammasome.

From: Postprandial macrophage-derived IL-1β stimulates insulin, and both synergistically promote glucose disposal and inflammation

Supplementary Figure 4

(a) InsR protein levels in naive (M0), pro-inflammatory M1 and alternative M2 polarized macrophages (n=3 experiments). (b) Insulin-induced (s473) phospho-AKT in M0, M1 and M2 polarized macrophages, data presented as ratio of insulin to non-insulin treated cells after normalization to total AKT (n=3 experiments). (c) Extracellular acidification rate (ECAR; mpH/min) from M0 or M2 polarized macrophages incubated for 2 hours in the presence or absence of 1 μg/ml insulin (n=12 and 15, respecively; 3 experiments). (d) Two-hour TNFα, IL-6, and CXCL1 secretion from 2 hour M1 polarized WT or Nlrp3-/- macrophages treated with or without 1 μg/ml insulin (n=5 mice each). (e) Gene expression profiles in M1 polarized macrophages with or without 2-hour treatment with 1 μg/ml insulin; data are expressed as fold change from untreated M0 controls (n=9, 3 experiments). (f) Cell survival as detected by annexin V and dapi staining of 2-hour M1 polarized macrophages treated for 2 hours with or without 1 μg/ml insulin. (g) Circulating CXCL1 protein concentration in mice treated with or without 1 unit/kg insulin (60 minutes post injection; n=10). *P < 0.05, **P<0.01. Statistical significance (P) was determined by ANOVA and in (g) by student’s t test. All error bars denote s.e.m.

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