drosophila melanogaster acetyl-coa-carboxylase sustains a fatty acid–dependent remote signal to waterproof the respiratory system黑腹果蝇acetyl-coa-carboxylase维持脂肪acid-dependent远程信号防水呼吸系统.pdfVIP
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drosophila melanogaster acetyl-coa-carboxylase sustains a fatty acid–dependent remote signal to waterproof the respiratory system黑腹果蝇acetyl-coa-carboxylase维持脂肪acid-dependent远程信号防水呼吸系统
Drosophila melanogaster Acetyl-CoA-Carboxylase
Sustains a Fatty Acid–Dependent Remote Signal to
Waterproof the Respiratory System
1,2. 1,3.¤a 1,3¤b 1,3 4
Jean-Philippe Parvy , Laura Napal , Thomas Rubin , Mickael Poidevin , Laurent Perrin ,
Claude Wicker-Thomas5, Jacques Montagne1,3*
´ ´ ´ ´ ´
1 CNRS, Centre de Genetique Moleculaire, UPR 3404, Gif-sur-Yvette, France, 2 Universite Pierre et Marie Curie- Paris 6, Paris, France, 3 Universite Paris-Sud 11, Orsay, France,
´ ´ ´
4 IBDML, Universite de la Mediterranee, Marseille, France, 5 CNRS, LEGS, UPR 9034, Gif-sur-Yvette, France
Abstract
Fatty acid (FA) metabolism plays a central role in body homeostasis and related diseases. Thus, FA metabolic enzymes are
attractive targets for drug therapy. Mouse studies on Acetyl-coenzymeA-carboxylase (ACC), the rate-limiting enzyme for FA
synthesis, have highlighted its homeostatic role in liver and adipose tissue. We took advantage of the powerful genetics of
Drosophila melanogaster to investigate the role of the unique Drosophila ACC homologue in the fat body and the
oenocytes. The fat body accomplishes hepatic and storage functions, whereas the oenocytes are proposed to produce the
cuticular lipids and to contribute to the hepatic function. RNA–interfering disruption of ACC in the fat body does not affect
viability but does result in a dramatic reduction in triglyceride storage and a concurrent increase in glycogen accumulation.
These metabolic perturbations further highlight the role of triglyc
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