1. Figure 2 Mechanisms of crosstalk between adipocytes and the kidney
Figure 2 | Mechanisms of crosstalk between adipocytes and the kidney. Adipose tissue exerts effects on the kidney through the actions of an array of secretory factors, such as cytokines, adipokines and metabolites — factors that at normal levels are important in maintaining kidney function. In response to excess caloric stress, adipose tissue expands through adipocyte hypertrophy and/or hyperplasia concomitantly with the development of insulin resistance and dysregulation of lipid metabolism. A shift in macrophage polarization from an anti-inflammatory M2 phenotype to a pro-inflammatory M1 phenotype also occurs, leading to the development of chronic inflammation through the excessive production of inflammatory cytokines and a reduction in anti-inflammatory adipokines, such as adiponectin. Adipocytes and macrophages coordinately orchestrate these inflammatory events and adipokine secretion. Renal dysfunction in the context of chronic kidney disease (CKD) is associated with high levels of adipose-derived molecules, such as leptin, adiponectin, angiotensin II, IL-6 and tumour necrosis factor (TNF) as well as dysregulated metabolites. Combined, these factors increase oxidative stress, inflammation and fibrotic transition in the kidney and eventually cause renal injury. Conversely, CKD exaggerates adipose tissue insulin resistance and inflammation potentially through the production of urea. Moreover, CKD promotes ‘beiging' of adipose tissue, which favours energy loss and might therefore worsen kidney injury.
Zhu, Q. & Scherer, P. E. (2017) Immunologic and endocrine functions of adipose tissue: implications for kidney disease
Nat. Rev. Nephrol. doi: /nrneph