Supplementary Figure 6: Proposed model for the physiological role of IL-1β and insulin in the regulation of glucose metabolism in response to food intake. | Nature Immunology

Supplementary Figure 6: Proposed model for the physiological role of IL-1β and insulin in the regulation of glucose metabolism in response to food intake.

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

Supplementary Figure 6

Food ingestion during feeding increases the number of peritoneal macrophages. These macrophages are stimulated by bacterial products and glucose to increase the production and release of IL-1β. Increased IL-1β concentrations will then enhance the continuous postprandial insulin secretion from pancreatic β cells via the highly expressed IL-1 receptor 1 (IL-1R1) and the IL-1 receptor-associated kinase-4 (IRAK4). The secreted insulin binds to its receptor (InsR) on macrophages, leading to enhanced glucose uptake through the glucose transporter GLUT1, AKT phosphorylation (pAKT) as well as hexokinase 2 (HK2) and glycolytic activity leading to ROS production. This further stimulates macrophage- derived pro-IL-1β-maturation by the NLRP3 inflammasome. Finally, increased levels of IL-1β and insulin stimulate glucose uptake into muscle, adipose tissue and immune cells that consequently decrease glycemia, thereby limiting the postprandial inflammatory response.

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