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

Qingzhang Zhu, Philipp E. Scherer

Research output: Contribution to journalReview articlepeer-review

45 Scopus citations

Abstract

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 inflammatory and hormonal factors (adipokines) that are critical for interorgan crosstalk. The interactions of adipose tissue with the kidney-referred to as the adipo-renal axis-are important for normal kidney function as well as the response of the kidney to injury. Here, we discuss the mechanistic basis of this interorgan crosstalk, which clearly has great therapeutic potential given the increasing rates of chronic kidney disease secondary to obesity and type 2 diabetes mellitus.

Original languageEnglish (US)
Pages (from-to)105-120
Number of pages16
JournalNature Reviews Nephrology
Volume14
Issue number2
DOIs
StatePublished - Feb 1 2018

ASJC Scopus subject areas

  • Nephrology

Fingerprint

Dive into the research topics of 'Immunologic and endocrine functions of adipose tissue: implications for kidney disease'. Together they form a unique fingerprint.

Cite this