NDLI: Cathepsin K Null Mice Show Reduced Adiposity during the Rapid Accumulation of Fat Stores

Content Provider	PubMed Central
Author	Funicello, Marcella Novelli, Michela Ragni, Maurizio Vottari, Teresa Cocuzza, Cesare Soriano-lopez, Joaquin Chiellini, Chiara Boschi, Federico Marzola, Pasquina Masiello, Pellegrino Saftig, Paul Santini, Ferruccio Rene, St-jacques Desmarais, Sylvie Morin, Nicolas Mancini, Joseph Percival, M. David Aldo, Pinchera Maffei, Margherita
Editor	Bartolomucci, Alessandro
Copyright Year	2007
Abstract	Growing evidences indicate that proteases are implicated in adipogenesis and in the onset of obesity. We previously reported that the cysteine protease cathepsin K (ctsk) is overexpressed in the white adipose tissue (WAT) of obese individuals. We herein characterized the WAT and the metabolic phenotype of ctsk deficient animals (ctsk−/−). When the growth rate of ctsk−/− was compared to that of the wild type animals (WT), we could establish a time window (5–8 weeks of age) within which ctsk−/−display significantly lower body weight and WAT size as compared to WT. Such a difference was not observable in older mice. Upon treatment with high fat diet (HFD) for 12 weeks ctsk−/− gained significantly less weight than WT and showed reduced brown adipose tissue, liver mass and a lower percentage of body fat. Plasma triglycerides, cholesterol and leptin were significantly lower in HFD-fed-ctsk−/− as compared to HFD-fed WT animals. Adipocyte lipolysis rates were increased in both young and HFD-fed-ctsk−/−, as compared to WT. Carnitine palmitoyl transferase-1 activity, was higher in mitochondria isolated from the WAT of HFD treated ctsk−/− as compared to WT. Together, these data indicate that ctsk ablation in mice results in reduced body fat content under conditions requiring a rapid accumulation of fat stores. This observation could be partly explained by an increased release and/or utilization of FFA and by an augmented ratio of lipolysis/lipogenesis. These results also demonstrate that under a HFD, ctsk deficiency confers a partial resistance to the development of dyslipidemia.
Related Links	http://dx.doi.org/10.1371/journal.pone.0000683
Starting Page	683
File Format	PDF
ISSN	19326203
e-ISSN	19326203
Journal	PLoS ONE
Issue Number	8
Volume Number	2
Language	English
Publisher	Public Library of Science
Publisher Date	2007-08-01
Access Restriction	Open
Rights Holder	Public Library of Science
Subject Keyword	Biochemistry, Genetics and Molecular Biology(all) Agricultural and Biological Sciences(all) Medicine(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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