A biotin analog inhibits acetyl-CoA carboxylase activity and adipogenesis.

Abstract	Acetyl-CoA carboxylase catalyzes the first committed step in the synthesis of long chain fatty acids. In this study, we observed that treatment of 3T3-L1 cells with biotin chloroacetylated at the 1' nitrogen reduced the enzymatic activity of cytosolic acetyl-CoA carboxylase and concomitantly inhibited the differentiation of 3T3-L1 cells in a dose-dependent manner. Treatment with chloroacetylated biotin blocked the induction of PPARgamma, STAT1, and STAT5A expression that normally occurs with adipogenesis. Moreover, addition of chloroacetylated biotin inhibited lipid accumulation, as judged by Oil Red O staining. Our results support recent studies that indicate that acetyl-CoA carboxylase may be a suitable target for an anti-obesity therapeutic.
Authors	Keith L Levert, Grover L Waldrop, Jacqueline M Stephens
Journal	The Journal of biological chemistry (J Biol Chem) Vol. 277 Issue 19 Pg. 16347-50 (May 10 2002) ISSN: 0021-9258 [Print] United States
PMID	11907024 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
Chemical References	Azo Compounds DNA-Binding Proteins Enzyme Inhibitors Milk Proteins Receptors, Cytoplasmic and Nuclear STAT1 Transcription Factor STAT5 Transcription Factor Stat1 protein, mouse Stat5a protein, mouse Trans-Activators Transcription Factors Biotin Acetyl-CoA Carboxylase oil red O
Topics	3T3 Cells Acetyl-CoA Carboxylase (antagonists & inhibitors) Adipocytes (metabolism) Adipose Tissue (drug effects) Animals Azo Compounds (pharmacology) Biotin (analogs & derivatives, pharmacology) Cell Differentiation Cells, Cultured DNA-Binding Proteins (metabolism) Dose-Response Relationship, Drug Electrophoresis, Polyacrylamide Gel Enzyme Inhibitors (pharmacology) Kinetics Lipid Metabolism Mice Milk Proteins Models, Chemical Receptors, Cytoplasmic and Nuclear (metabolism) STAT1 Transcription Factor STAT5 Transcription Factor Time Factors Trans-Activators (metabolism) Transcription Factors (metabolism) Transcription, Genetic

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