Supplementary Figure 3: Acute exposure to IL-1β induces insulin secretion without changing insulin sensitivity. | Nature Immunology

Supplementary Figure 3: Acute exposure to IL-1β induces insulin secretion without changing insulin sensitivity.

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

Supplementary Figure 3

(a) Circulating active GLP-1 protein levels in WT mice injected with saline or 1 μg/kg IL-1β. (b) Glucose and (c) insulin levels during i.p. GTT with Gipr-/-/Glp1r-/- double knockout (KO; n=7) or WT (n=8) mice. (d) Insulin tolerance test 18 minutes after an injection of saline (n=5) or 1 μg/kg IL-1β (n=6) in WT mice. (e) Circulating glucose and (f) insulin levels during an i.p. GTT with IRAK4 knockout mice, pretreated with saline or 1 μg/kg IL-1β (n=6). (g-i) Insulin concentrations in culture media of islets isolated from mice (g; left to right: n=9, 13, 9, 12; 3 experiments) and humans (h; left to right: n=44, 9, 34, 15; 8 experiments) and of human ENDOC cells (i; n=9; 3 experiments) pre-incubated with the indicated doses of IL-1β (priming) during glucose stimulated insulin secretion assays. *P < 0.05, **P < 0.001, ***P < 0.0001. Statistical significance (P) was determined by Student's t test and in (g-i) by ANOVA. All error bars denote s.e.m.

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