Immunologic and endocrine functions of adipose tissue: implications for kidney disease

Key Points Adipocytes are metabolically active cells; they produce signalling lipids and metabolites and secrete protein factors (adipokines) The relative levels of these lipids, proteins and metabolites change under different nutritional and pathological states, with adipocytes integrating information regarding the metabolic status quo at any given time and adjusting their cellular physiological state to maintain systemic homeostasis Adipocyte-derived factors establish complex paracrine and endocrine signalling axes between local cell types in adipose tissue and other organs, including the kidney A number of adipokines, including leptin and adiponectin, have well-established effects on kidney function; adiponectin might also be produced locally within the kidney and exert important metabolic functions in an autocrine fashion As a source of pro-inflammatory cytokines, adipose tissue might exert important effects on the inflammatory state of the kidney The renin–angiotensin system is present in adipose tissue and mediates inflammation in response to nutritional interventions; activation of this axis triggers profound signalling events in the kidney Adipose is an important endocrine and immunologic organ, releasing various adipokines and cytokines that regulate the adipocyte microenvironment and systemic metabolism. Here, the authors discuss the immunologic and endocrine functions of adipose tissue that contribute to kidney disease and the converse effects of kidney dysfunction on adipose tissue. Excess adiposity can induce adverse sequelae in multiple cell types and organ systems. The transition from the lean to the obese state is characterized by fundamental cellular changes at the level of the adipocyte. These changes affect the local microenvironment within the respective adipose tissue but can also affect nonadipose systems. Adipocytes within fat pads respond to chronic nutrient excess through hyperplasia or hypertrophy, which can differentially affect interorgan crosstalk between various adipose depots and other organs. This crosstalk is dependent on the unique ability of the adipocyte to coordinate metabolic adjustments throughout the body and to integrate responses to maintain metabolic homeostasis. These actions occur through the release of free fatty acids and metabolites during times of energy need — a process that is altered in the obese state. In addition, adipocytes release a wide array of signalling molecules, such as sphingolipids, as well as