Regulation of glucose and lipid homeostasis by adiponectin

Effects on hepatocytes, pancreatic β cells and adipocytes

Caroline Tao, Angelica Sifuentes, William L. Holland

Research output: Contribution to journalArticle

56 Citations (Scopus)

Abstract

Adiponectin has received considerable attention for its potential anti-diabetic actions. The adipokine exerts control of glucose and lipid homeostasis via critical effects within the liver, adipose, and pancreas. By stimulating adipogenesis, opposing inflammation, and influencing rates of lipid oxidation and lipolysis, adiponectin critically governs lipid spillover into non-adipose tissues. Ceramide, a cytotoxic and insulin desensitizing lipid metabolite formed when peripheral tissues are exposed to excessive lipid deposition, is potently opposed by adiponectin. Via adiponectin receptors, AdipoR1 and AdipoR2, adiponectin stimulates the deacylation of ceramide- yielding sphingosine for conversion to sphingosine 1-phosphate (S1P) by sphingosine kinase. The resulting conversion from ceramide to S1P promotes survival of functional beta cell mass, allowing for insulin production to meet insulin demands. Alleviation of ceramide burden on the liver allows for improvements in hepatic insulin action. Here, we summarize how adiponectin-induced changes in these tissues lead to improvements in glucose metabolism, highlighting the sphingolipid signaling mechanisms linking adiponectin to each action. One sentence summary: We review the anti-diabetic actions of adiponectin.

Original languageEnglish (US)
Pages (from-to)43-58
Number of pages16
JournalBest Practice and Research: Clinical Endocrinology and Metabolism
Volume28
Issue number1
DOIs
StatePublished - Jan 1 2014

Fingerprint

Adiponectin
Adipocytes
Hepatocytes
Homeostasis
Lipids
Ceramides
Glucose
Insulin
Liver
Adiponectin Receptors
Adipogenesis
Sphingolipids
Sphingosine
Adipokines
Lipolysis
Pancreas
Inflammation

Keywords

  • ceramide
  • insulin resistance
  • obesity

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

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