scholarly journals A C. elegans Model for Mitochondrial Fatty Acid Synthase II: The Longevity-Associated Gene W09H1.5/mecr-1 Encodes a 2-trans-Enoyl-Thioester Reductase

PLoS ONE ◽  
2009 ◽  
Vol 4 (11) ◽  
pp. e7791 ◽  
Author(s):  
Aner Gurvitz
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthase ◽  
C Elegans ◽  
Mitochondrial Fatty Acid

scholarly journals Mitochondrial Fatty Acid Synthase Utilizes Multiple Acyl Carrier Protein Isoforms

2020 ◽  
Vol 183 (2) ◽  
pp. 547-557
Author(s):  
Xinyu Fu ◽  
Xin Guan ◽  
Rachel Garlock ◽  
Basil J. Nikolau
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthase ◽  
Acyl Carrier Protein ◽  
Protein Isoforms ◽  
Carrier Protein ◽  
Mitochondrial Fatty Acid

scholarly journals Emodin, a Naturally Occurring Anthraquinone Derivative, Ameliorates Dyslipidemia by Activating AMP-Activated Protein Kinase in High-Fat-Diet-Fed Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Thing-Fong Tzeng ◽  
Hung-Jen Lu ◽  
Shorong-Shii Liou ◽  
Chia Ju Chang ◽  
I-Min Liu
Keyword(s):  
Fatty Acid ◽  
Protein Kinase ◽  
High Fat Diet ◽  
Fatty Acid Synthase ◽  
Risk Index ◽  
Atherogenic Index ◽  
High Fat ◽  
Mitochondrial Fatty Acid ◽  
Regulated Gene Expression ◽  
Amp Activated Protein Kinase

The aim of this study was to investigate the antiobesity and antihyperlipidaemic effects of emodin on high-fat diet (HFD)-induced obese rats, and on the regulation of the expression of the genes involved in lipid metabolism to elucidate the mechanisms. After being fed HFD for two weeks, Wistar rats were dosed orally with emodin (40 and 80 mg kg−1) or pioglitazone (20 mg kg−1), once daily for eight weeks. Emodin (80 mg kg−1per day) displayed similar characteristics to pioglitazone (20 mg kg−1per day) in reducing body weight gain, plasma lipid levels as well as coronary artery risk index and atherogenic index of HFD-fed rats. Emodin also caused dose related reductions in the hepatic triglyceride and cholesterol contents and lowered hepatic lipid droplets accumulation in HFD-fed rats. Emodin and pioglitazone enhanced the phosphorylation of AMP-activated protein kinase (AMPK) and its primary downstream targeting enzyme, acetyl-CoA carboxylase, up-regulated gene expression of carnitine palmitoyl transferase 1, and down-regulated sterol regulatory element binding protein 1 and fatty acid synthase protein levels in hepatocytes of HFD-fed rats. Our findings suggest emodin could attenuate lipid accumulation by decreasing lipogenesis and increasing mitochondrial fatty acidβ-oxidation mediated by activation of the AMPK signaling pathway.

scholarly journals Crystal structures of the acyl transferases involved in the human cytosolic and mitochondrial fatty acid synthase

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Stephanie A. Misquitta ◽  
Gabor Bunkoczi ◽  
Xiaoqiu Wu ◽  
Kathryn L. Kavanagh ◽  
Viktoria Hozjan ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Crystal Structures ◽  
Fatty Acid Synthase ◽  
Mitochondrial Fatty Acid

Two genes of the putative mitochondrial fatty acid synthase in the genome of Saccharomyces cerevisiae

1997 ◽  
Vol 32 (6) ◽  
pp. 384-388 ◽  
Author(s):  
R. Schneider ◽  
Benedikt Brors ◽  
Frank Bürger ◽  
Stefan Camrath ◽  
Hanns Weiss
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Fatty Acid ◽  
Fatty Acid Synthase ◽  
Mitochondrial Fatty Acid

scholarly journals Caenorhabditis elegansF09E10.3 Encodes a Putative 3-Oxoacyl-Thioester Reductase of Mitochondrial Type 2 Fatty Acid Synthase FASII that Is Functional in Yeast

2009 ◽  
Vol 2009 ◽  
pp. 1-6 ◽  
Author(s):  
Aner Gurvitz
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthase ◽  
Reductase Activity ◽  
Carbon Sources ◽  
Yeast Cells ◽  
C Elegans ◽  
Animal Physiology ◽  
Mutant Cells

Caenorhabditis elegansF09E10.3 (dhs-25) was identified as encoding a 3-oxoacyl-thioester reductase, potentially of the mitochondrial type 2 fatty acid synthase (FASII) system. Mitochondrial FASII is a relatively recent discovery in metazoans, and the relevance of this process to animal physiology has not been elucidated. A good animal model to study the role of FASII is the nematodeC. elegans. However, the components of nematode mitochondrial FASII have hitherto evaded positive identification. The nematode F09E10.3 protein was ectopically expressed without an additional mitochondrial targeting sequence inSaccharomyces cerevisiaemutant cells lacking the homologous mitochondrial FASII enzyme 3-oxoacyl-ACP reductase Oar1p. These yeastoar1Δmutants are unable to respire, grow on nonfermentable carbon sources, or synthesize sufficient levels of lipoic acid. Mutant yeast cells producing a full-length mitochondrial F09E10.3 protein containedNAD+-dependent 3-oxoacyl-thioester reductase activity and resembled the corresponding mutant overexpressing native Oar1p for the above-mentioned phenotype characteristics. This is the first identification of a metazoan 3-oxoacyl-thioester reductase (see Note Added in Proof).

scholarly journals Discovery and Characterization of the 3-Hydroxyacyl-ACP Dehydratase Component of the Plant Mitochondrial Fatty Acid Synthase System

2017 ◽  
Vol 173 (4) ◽  
pp. 2010-2028 ◽  
Author(s):  
Xin Guan ◽  
Yozo Okazaki ◽  
Andrew Lithio ◽  
Ling Li ◽  
Xuefeng Zhao ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthase ◽  
Mitochondrial Fatty Acid

scholarly journals DIETARY ADENINE ALLEVIATES FATTY LIVER INDUCED BY OROTIC ACID

2010 ◽  
Vol 10 (3) ◽  
pp. 363-369 ◽  
Author(s):  
Yohanes Buang
Keyword(s):  
Fatty Acid ◽  
Fatty Liver ◽  
Serum Lipid ◽  
Orotic Acid ◽  
Fatty Acid Synthase ◽  
Enzyme Assay ◽  
Liver Lipid ◽  
Hepatic Tissue ◽  
Mitochondrial Fatty Acid ◽  
Basal Group

The effects of dietary adenine in fatty liver induced by orotic acid (OA) were studied. Rats were paired-fed 1% OA-supplemented diets with/or without 0.25% adenine or a diet without OA for 10 days. Serum lipid profiles were measured using enzyme assay kits. Lipids of liver tissues were extracted and liver lipid contents were determined. A peach of liver was prepared to determine the activities of fatty acid synthase (FAS) and fatty acid β-oxidation. The results showed that liver TG content of OA-fed rats increased markedly in comparison to basal group.  However, the addition of adenine to the diet reversed promotion of liver TG content to basal level. It was also found that FAS activities decreased. Furthermore, these diets reversed the inhibition of fatty acid β-oxidation to basal level and induced the serum lipid levels secretion. Therefore, the alleviation of fatty liver in OA-treated rats given dietary adenine is associated with the inhibition of FAS activities accompanied with the promotion of mitochondrial fatty acid β-oxidation and the promotion of serum lipid secretion from the hepatic tissue into the bloodstream.

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