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PLIN5 deletion remodels intracellular lipid composition and causes insulin resistance in muscle

Mason,RR, Mokhtar,R, Matzaris,M, Selathurai,A, Kowalski,GM, Mokbel,N, Meikle,PJ, Bruce,CR and Watt,MJ 2014, PLIN5 deletion remodels intracellular lipid composition and causes insulin resistance in muscle, Molecular metabolism, vol. 3, no. 6, pp. 652-663, doi: 10.1016/j.molmet.2014.06.002.

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Title PLIN5 deletion remodels intracellular lipid composition and causes insulin resistance in muscle
Author(s) Mason,RR
Mokhtar,R
Matzaris,M
Selathurai,A
Kowalski,GMORCID iD for Kowalski,GM orcid.org/0000-0002-1599-017X
Mokbel,N
Meikle,PJ
Bruce,CRORCID iD for Bruce,CR orcid.org/0000-0002-0515-3343
Watt,MJ
Journal name Molecular metabolism
Volume number 3
Issue number 6
Start page 652
End page 663
Publisher Elsevier BV
Place of publication Amsterdam, Netherlands
Publication date 2014-09
ISSN 2212-8778
Keyword(s) lipid metabolism
perilipin
lipid droplet
insulin resistance
skeletal muscle
Summary Defective control of lipid metabolism leading to lipotoxicity causes insulin resistance in skeletal muscle, a major factor leading to diabetes. Here, we demonstrate that perilipin (PLIN) 5 is required to couple intramyocellular triacylglycerol lipolysis with the metabolic demand for fatty acids. PLIN5 ablation depleted triacylglycerol stores but increased sphingolipids including ceramide, hydroxylceramides and sphingomyelin. We generated perilipin 5 (Plin5)-/- mice to determine the functional significance of PLIN5 in metabolic control and insulin action. Loss of PLIN5 had no effect on body weight, feeding or adiposity but increased whole-body carbohydrate oxidation. Plin5-/- mice developed skeletal muscle insulin resistance, which was associated with ceramide accumulation. Liver insulin sensitivity was improved in Plin5-/- mice, indicating tissue-specific effects of PLIN5 on insulin action. We conclude that PLIN5 plays a critical role in coordinating skeletal muscle triacylglycerol metabolism, which impacts sphingolipid metabolism, and is requisite for the maintenance of skeletal muscle insulin action. © 2014 The Authors.
Language eng
DOI 10.1016/j.molmet.2014.06.002
Field of Research 110699 Human Movement and Sports Science not elsewhere classified
Socio Economic Objective 929999 Health not elsewhere classified
HERDC Research category C1.1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Copyright notice ©2014, Elsevier
Free to Read? Yes
Persistent URL http://hdl.handle.net/10536/DRO/DU:30071514

Document type: Journal Article
Collections: School of Exercise and Nutrition Sciences
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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.