Publication: Metabolomic profiling in liver of adiponectin-knockout mice uncovers lysophospholipid metabolism as an important target of adiponectin action
Issued Date
2015-07-01
Resource Type
ISSN
14708728
02646021
02646021
Other identifier(s)
2-s2.0-84935082866
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Biochemical Journal. Vol.469, No.1 (2015), 71-82
Suggested Citation
Ying Liu, Sanjana Sen, Sivaporn Wannaiampikul, Rengasamy Palanivel, Ruby L.C. Hoo, Ruth Isserlin, Gary D. Bader, Rungsunn Tungtrongchitr, Yves Deshaies, Aimin Xu, Gary Sweeney Metabolomic profiling in liver of adiponectin-knockout mice uncovers lysophospholipid metabolism as an important target of adiponectin action. Biochemical Journal. Vol.469, No.1 (2015), 71-82. doi:10.1042/BJ20141455 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/35428
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Metabolomic profiling in liver of adiponectin-knockout mice uncovers lysophospholipid metabolism as an important target of adiponectin action
Other Contributor(s)
Abstract
© 2015 Authors; published by Portland Press Limited. Adiponectin mediates anti-diabetic effects via increasing hepatic insulin sensitivity and direct metabolic effects. In the present study, we conducted a comprehensive and unbiased metabolomic profiling of liver tissue from AdKO (adiponectin-knockout) mice, with and without adiponectin supplementation, fed on an HFD (high-fat diet) to derive insight into the mechanisms and consequences of insulin resistance. Hepatic lipid accumulation and insulin resistance induced by the HFD were reduced by adiponectin. The HFD significantly altered levels of 147 metabolites, and bioinformatic analysis indicated that one of the most striking changes was the profile of increased lysophospholipids. These changes were largely corrected by adiponectin, at least in part via direct regulation of PLA2 (phospholipase A2) as palmitate-induced PLA2 activation was attenuated by adiponectin in primary hepatocytes. Notable decreases in several glycerolipids after the HFD were reversed by adiponectin, which also corrected elevations in several diacyglycerol and ceramide species. Our data also indicate that stimulation of ω-oxidation of fatty acids by the HFD is enhanced by adiponectin. In conclusion, this metabolomic profiling approach in AdKO mice identified important targets of adiponectin action, including PLA2, to regulate lysophospholipid metabolism and ω-oxidation of fatty acids.
