Figure 3 The fat–intestine–kidney axis

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Presentation transcript:

Figure 3 The fat–intestine–kidney axis Figure 3 | The fat–intestine–kidney axis. Tissue homeostasis in healthy individuals requires fine-tuned interactions between a regulatory network of cells and bacteria that is maintained through the correct function of organs, such as the kidney, liver, adipose and intestine, and by the secretion of regulatory molecules from immune and parenchymal cells. In individuals with chronic kidney disease (CKD) or who are obese, this homeostasis is disrupted by kidney or adipose dysfunction, which culminates in systemic inflammation. Inflammation leads to intestinal disbiosis and increased gut permeability. Dysbiosis can also alter intestinal function and induces local and systemic inflammation that could induce the migration of immune cells into adipose tissue and the kidney, causing renal dysfunction and favouring further increases in adipose deposition. NK cells, natural killer cells; RAS, renin–angiotensin system; SCFA, short-chain fatty acid; SNS, sympathetic nervous system. Câmara, N. O. S. et al. (2017) Kidney disease and obesity: epidemiology, mechanisms and treatment Nat. Rev. Nephrol. doi:10.1038/nrneph.2016.191