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Fat mass is increased in the acyl‐CoA synthetase‐isoform 1 (ACSL1) adipose‐specific knockout mouse
Author(s) -
Ellis Jessica Mary,
Li Lei,
Wu PeiChi,
Coleman Rosalind
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.147.1
Subject(s) - adipose tissue , white adipose tissue , medicine , endocrinology , lipolysis , chemistry , gene isoform , biology , biochemistry , gene
Long chain acyl‐CoA synthetase (ACSL) catalyses the conversion of fatty acids into their acyl‐CoA derivatives. Acyl‐CoAs have multiple fates including oxidation, and incorporation into phospholipids, cholesteryl esters, and triacylglycerol. ACSL1, one of five ACSL isoforms, is highly expressed in white adipose tissue and thought to be important for triacylglycerol formation. To investigate the role of ACSL1 in adipose tissue we have created an adipose‐specific knock out of ACSL1, the ACSL1 A−/− mouse. Although we expected mice with reduced fat mass, we report the contrary: the ACSL1 A−/− mice have increased fat mass on a low‐fat diet. Animal weights are similar to their littermate controls yet fat mass is increased ~30%. ACSL1 A−/− mice gain weight and fat mass similar to controls when fed a high‐fat diet. ACSL1 A−/− mice have a ~40% reduction in total ACS activity in white adipose depots on both low‐fat and high‐fat diet with no evidence of compensation. Interestingly, we observe a reduction in total ACSL activity in adipose of mice fed a high‐fat diet that inversely correlates with fat mass. Despite increased adiposity, the ACSL1 A−/− mice respond normally to glucose tolerance tests. The data suggest that the role of ACSL1 in adipocytes is not limited to the formation of triacylglycerol.