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Ablation of the very-long-chain fatty acid elongase ELOVL3 in mice leads to constrained lipid storage and resistance to diet-induced obesity.

Artikel i vetenskaplig tidskrift
Författare Damir Zadravec
Annelie Brolinson
Rachel M Fisher
Claes Carneheim
Robert I Csikasz
Justine Bertrand-Michel
Jan Borén
Hervé Guillou
Mats Rudling
Anders Jacobsson
Publicerad i The FASEB journal : official publication of the Federation of American Societies for Experimental Biology
Volym 24
Nummer/häfte 11
Sidor 4366-77
ISSN 1530-6860
Publiceringsår 2010
Publicerad vid Institutionen för medicin, avdelningen för molekylär och klinisk medicin
Sidor 4366-77
Språk en
Länkar dx.doi.org/10.1096/fj.09-152298
Ämnesord Acetyltransferases, genetics, metabolism, Adipokines, secretion, Adiponectin, blood, Adipose Tissue, metabolism, Animals, Basal Metabolism, genetics, Cells, Cultured, Diet, Eating, genetics, Female, Gene Expression Regulation, Enzymologic, Lipogenesis, genetics, Lipoproteins, VLDL, biosynthesis, blood, Liver, metabolism, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Obesity, enzymology, metabolism, Sex Factors, Triglycerides, biosynthesis, blood
Ämneskategorier Molekylär medicin (genetik och patologi), Kardiovaskulär medicin

Sammanfattning

Although saturated and monounsaturated very-long-chain fatty acids (VLCFAs) have long been associated with undesirable effects on health, including obesity, heart failure, and atherosclerosis, the physiological role of endogenous synthesis is largely unknown. The fatty acid elongase ELOVL3 is involved in the synthesis of C20-C24 saturated and monounsaturated VLCFAs mainly in liver, brown and white adipose tissue, and triglyceride-rich glands such as the sebaceous and meibomian glands. Here we show that ablation of ELOVL3 leads to reduced adiponectin levels, constrained expansion of adipose tissue, and resistance against diet-induced obesity, a situation that is more exaggerated in female mice. Both female and male knockout mice show reduced hepatic lipogenic gene expression and triglyceride content, a situation that is associated with reduced de novo fatty acid synthesis and uptake. As a consequence, the VLDL-triglyceride level in serum is significantly reduced. Remarkably, despite increased energy expenditure, markedly reduced serum levels of leptin, and increased expression of orexigenic peptides in the hypothalamus, the Elovl3(-/-) mice do not compensate by increased food intake. Thus, these results reveal that C20-C22 saturated and monounsaturated VLCFAs produced by ELOVL3 are indispensable for appropriate synthesis of liver triglycerides, fatty acid uptake, and storage in adipose tissue.

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