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A more recent version of this article appeared on September 1, 2005

Papers In Press, published online ahead of print June 16, 2005
J. Lipid Res., doi:10.1194/jlr.M500081-JLR200
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Submitted on February 28, 2005
Revised on May 23, 2005
Accepted on June 14, 2005

Transgenic expression of human hormone-sensitive lipase (HSL) in white adipose tissue corrects the white adipose phenotype of HSL-deficient mice

Mélanie Fortier, Krishnakant Soni, Nancy Laurin, Shu Pei Wang, Pascale Mauriège, Frank R. Jirik, and Grant A. Mitchell

Pediatrics Dept., Sainte-Justine Hospital, Montreal, Quebec H3T 1C5

Corresponding Author: grant.mitchell{at}recherche-ste-justine.qc.ca

In white adipose tissue (WAT), hormone sensitive lipase (HSL) can mediate lipolysis, a central pathway in obesity and diabetes. Gene-targeted HSL-deficient (HSL-/-) mice with no detectable HSL peptide or activity (measured as cholesteryl esterase) have WAT abnormalities including low mass, marked heterogeneity of cell diameter, increased diacylglycerol content and low beta-adrenergic stimulation of adipocyte lipolysis. Three transgenic mouse strains preferentially expressing human HSL in WAT were bred to a HSL-/- background. One, HSL-/-N, expresses normal human HSL (41.3 +/- 9.1% of normal activity); two express a serine-to-alanine mutant (S554A) initially hypothesized to be constitutively active: HSL-/-ML, 50.3 +/- 12.3% and HSL-/-MH, 69.8 +/- 15.8% of normal. In WAT, HSL-/-N mice resembled HSL+/+ controls in WAT masses, histology, diacylglyceride content and lipolytic response to beta-adrenergic agents. In contrast, HSL-/-ML and HSL-/-MH mice resembled non-transgenic HSL-/- mice, except that diacylglycerol content and perirenal and inguinal WAT masses approached normal in HSL-/-MH mice. Therefore (1) WAT expression of normal human HSL markedly improves HSL-/- WAT biochemically, physiologically and morphologically; (2) similar levels of S554A HSL have low physiological effect despite being active in vitro and (3) diacylglycerol accumulation is not essential for development of the characteristic WAT pathology of HSL-/- mice.


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