Nat. Rev. Endocrinol. doi:10.1038/nrendo.2015.189 Figure 2 Obesity induces inflammation in adipose tissue, the liver, skeletal muscle and the pancreas to cause dysbiosis in the intestine Figure 2 | Obesity induces inflammation in adipose tissue, the liver, skeletal muscle and the pancreas to cause dysbiosis in the intestine. In adipose tissue, proinflammatory signalling induces lipolysis and release of free fatty acids. This proinflammatory environment eventually results in insulin resistance. In the liver, obesity induces proinflammatory cytokine production and macrophage recruitment, which results in insulin resistance and steatosis. In skeletal muscle, lipid and proinflammatory macrophage accumulation inhibit insulin signalling in obesity. In the pancreas, obesity is associated with macrophage infiltration, IL-1β secretion and decreased insulin secretion. In the intestine, dysbiosis occurs as the composition of the microbial population changes. Obesity decreases the numbers of eosinophils and innate lymphoid cells in the gut, correlating with increased barrier permeability and increased systemic levels of lipopolysaccharide. Obesity induces macrophage accumulation and chronic inflammation in the adipose tissue, liver, skeletal muscle and pancreatic islets. TNF, tumour necrosis factor. Lackey, D. E. & OlefskyI, J. M. (2015) Regulation of metabolism by the innate immune system Nat. Rev. Endocrinol. doi:10.1038/nrendo.2015.189