TY - JOUR
T1 - Regulation of glucose and lipid homeostasis by adiponectin
T2 - Effects on hepatocytes, pancreatic β cells and adipocytes
AU - Tao, Caroline
AU - Sifuentes, Angelica
AU - Holland, William L.
N1 - Funding Information:
The authors would like to acknowledge the National Institutes of Health ( K99-DK094973 ) and American Heart Association ( 12BGI-A8910006 ) for funding to W.L.H.
PY - 2014/1
Y1 - 2014/1
N2 - 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.
AB - 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.
KW - ceramide
KW - insulin resistance
KW - obesity
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U2 - 10.1016/j.beem.2013.11.003
DO - 10.1016/j.beem.2013.11.003
M3 - Article
C2 - 24417945
AN - SCOPUS:85047687709
SN - 1521-690X
VL - 28
SP - 43
EP - 58
JO - Best Practice and Research: Clinical Endocrinology and Metabolism
JF - Best Practice and Research: Clinical Endocrinology and Metabolism
IS - 1
ER -