[9] Fatty acid synthase from human liver

Roncari, Daniel A. K.

doi:10.1016/0076-6879(81)71011-5

Cited by 52 publications

(34 citation statements)

References 3 publications

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“…Particularly high yields were observed from liver Kim et al 1981 ;Muesing & Porter, 1975 ;Roncari, 1981), often from animals fed on a carbohydrate-based diet, and from fat producing glands, including the lactating mammary gland (Kumar & Dodds, 1981 ;Smith & Abraham, 1975) and the uropygial gland of birds (Kolattukudy et al 1981). High yields of purified human FAS were also obtained from a mammary epithelial cell line (Thompson et al 1981).…”

Section: Purification and Crystallization Of Animal Fasmentioning

confidence: 99%

Structure and function of eukaryotic fatty acid synthases

Maier

Leibundgut

Boehringer

et al. 2010

Quart. Rev. Biophys.

123

127

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Abstract. In all organisms, fatty acid synthesis is achieved in variations of a common cyclic reaction pathway by stepwise, iterative elongation of precursors with two-carbon extender units. In bacteria, all individual reaction steps are carried out by monofunctional dissociated enzymes, whereas in eukaryotes the fatty acid synthases (FASs) have evolved into large multifunctional enzymes that integrate the whole process of fatty acid synthesis. During the last few years, important advances in understanding the structural and functional organization of eukaryotic FASs have been made through a combination of biochemical, electron microscopic and X-ray crystallographic approaches. They have revealed the strikingly different architectures of the two distinct types of eukaryotic FASs, the fungal and the animal enzyme system. Fungal FAS is a 2Á6 MDa a 6 b 6 heterododecamer with a barrel shape enclosing two large chambers, each containing three sets of active sites separated by a central wheel-like structure. It represents a highly specialized micro-compartment strictly optimized for the production of saturated fatty acids. In contrast, the animal FAS is a 540 kDa X-shaped homodimer with two lateral reaction clefts characterized by a modular domain architecture and large extent of conformational flexibility that appears to contribute to catalytic efficiency.

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Section: Purification and Crystallization Of Animal Fasmentioning

confidence: 99%

Structure and function of eukaryotic fatty acid synthases

Maier

Leibundgut

Boehringer

et al. 2010

Quart. Rev. Biophys.

123

127

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“…The day after collection, the SF samples were analyzed in duplicate for glucose-6-phosphate dehydrogenase (G6PDH, EC 1.1.1.49), malic enzyme (ME, EC 1.1.1.40) and fatty acid synthase (FAS, EC 2.3.1.85) using the methods of Lö hr and Bee, Jacot, Guex and Biolley Waller (1974), Hsu and Lardy (1969) and Roncari (1981), respectively. The NADPH formation (G6PDH and ME) or oxidation (FAS) was measured at 378C by absorbance at 340 nm.…”

Section: Experimental Dietsmentioning

confidence: 99%

Effects of two supplementation levels of linseed combined with CLA or tallow on meat quality traits and fatty acid profile of adipose and different muscle tissues in slaughter pigs

Bee

Jacot

Guex

et al. 2008

Animal

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Dietary linseed supply efficiently elevates the linolenic acid concentration of pork. The main problem of increasing the n-3 fatty acid tissue levels arises from a higher susceptibility to lipid oxidation. Increasing the saturation level of tissue lipids by the dietary inclusion of conjugated linoleic acids (CLA) or tallow might prevent oxidation. Thus, the aim of the study was to evaluate the impact of dietary CLA or tallow supplementation combined with extruded linseed on the growth performance, carcass characteristics and fatty acid profile of muscles (longissimus, semimembranosus, biceps femoris) and subcutaneous fat (SF). The enzyme activity of the de novo lipogenesis and stearoyl-CoA desaturase in the SF was also assessed. From 18 to 104 kg BW, 32 Swiss Large White barrows were fed a diet supplemented with either: (1) 2% linseed (L2); (2) 3% linseed (L3); (3) 2% linseed 1 1% CLA (L2-C) or (4) 2% linseed 1 1% tallow (L2-T). The linolenic and eicosatrienoic acid concentrations were higher (P , 0.01) and the P n-6/ P n-3 ratio was lower (P , 0.01) in all tissues of L3 than L2 and L2-T barrows. Only in the SF the docosapentaenoic acid concentration was increased (P , 0.01) in L3 barrows. Compared with the other three diets, feeding the L2-C diets increased (P , 0.01) the amount of myristic, palmitic, stearic and palmitoleic acid at the expense of the oleic and eicosenoic acid content in the intramuscular and SF lipids. Except for the lower (P , 0.05) eicosadienoic acid concentration in the muscles, feeding the L2-C treatment resulted in similar polyunsaturated fatty acid concentrations and P n-6/ P n-3 ratio than feeding L2 or L2-T diets. Both the c9,t11-and t10,c12-CLA isomers found in the CLA-supplemented diet were also detected in the tissues, but the c9,t11-isomer was more abundant than the t10,c12-isomer. De novo lipogenesis was not (P . 0.05) affected by the dietary fats, whereas D9-desaturase activity was depressed (P , 0.05) by CLA inclusion (L2-C). Only when oxidation was challenged by cooking and subsequent storage for 4 days at 48C values of thiobarbituric acid-reactive substances were lower (P , 0.05) in longissimus muscle chops of L2-C compared with L2, L3 and L2-T barrows. The present findings revealed that CLA, but not tallow, combined with extruded linseed enhanced the oxidative stability of pork probably by lowering the degree of unsaturation of the lipids without affecting the improved P n-6/ P n-3 ratio.

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“…The livers were homogenized and fractionated (14), and the palmitoyl-CoA oxidation (measured as acid-soluble products) (15) and the activities of ACAT (16), acetyl-coenzyme A carboxylase (ACC) (17), fatty acyl-coenzyme A oxidase (ACO) (18), carnitine palmitoyltransferase (CPT)-I and CPT-II (19), diacylglycerol acyltransferase (DGAT) (20), FAS (21,22), and glycerol-3-phosphate acyltransferase (GPAT) (23) were measured in the postnuclear fraction. HMG-CoA synthase activity (24) was measured in the mitochondrial fraction.…”

Section: Enzyme Activitiesmentioning

confidence: 99%

Causes and prevention of tamoxifen-induced accumulation of triacylglycerol in rat liver

Gudbrandsen¹,

Røst²,

Berge

2006

Journal of Lipid Research

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Tamoxifen can induce hepatic steatosis in women. In this study, we wanted to elucidate the mechanism behind the tamoxifen-induced accumulation of triacylglycerol in liver in female rats, and we hoped to prevent this development by combination treatment with the modified fatty acid tetradecylthioacetic acid (TTA). The increased hepatic triacylglycerol level after tamoxifen treatment was accompanied by decreased acetyl-coenzyme A carboxylase (ACC) and FAS activities, increased glycerol-3-phosphate acyltransferase (GPAT) activity, and a tendency to increased diacylglycerol acyltransferase (DGAT) activity. The activities and mRNA levels of enzymes involved in b-oxidation, ketogenesis, and uptake of lipids from liver were unaffected by tamoxifen, whereas the uptake of lipoproteins was unchanged and the uptake of fatty acids was decreased. Combination treatment with tamoxifen and TTA (Tam1TTA) normalized the hepatic triacylglycerol level and increased the activities of ACC, FAS, GPAT, and DGAT compared with tamoxifentreated rats. The activities and mRNA levels of enzymes involved in b-oxidation, ketogenesis, and uptake of lipids were increased after Tam1TTA treatment. In conclusion, tamoxifen increased the hepatic triacylglycerol level, probably as a result of increased triacylglycerol biosynthesis combined with unchanged b-oxidation. The tamoxifen-induced accumulation of triacylglycerol was prevented by cotreatment with TTA, through mechanisms of increased mitochondrial and peroxisomal b-oxidation. The anti-estrogen agent tamoxifen has been used as an effective treatment for estrogen receptor-positive breast cancers for several years (1). However, tamoxifen treatment is associated with an increased risk of developing fatty liver (steatosis) (2-4), and it is reported that as many as 43% of women with breast cancer treated with tamoxifen may develop steatosis within the first 2 years of treatment (4). It has been hypothesized that impaired fatty acid b-oxidation could be the cause of fatty liver after tamoxifen treatment (5, 6).The modified fatty acid tetradecylthioacetic acid (TTA) is a ligand for all peroxisome proliferator-activated receptors (PPARs) (7) and has shown promise in the prevention and treatment of common lipid disorders and insulin resistance (8). TTA increases both mitochondrial and peroxisomal b-oxidation in liver (9) and therefore may be a valuable tool for the treatment of fatty liver.In this study, female rats with 7,12-dimethylbenz[a]anthracene-induced mammary tumors were treated with tamoxifen, TTA, or a combination of tamoxifen and TTA (Tam1TTA) for 14 days after palpable tumors developed. We had two aims in this study: first, we wanted to elucidate the mechanism behind the accumulation of triacylglycerol in liver after tamoxifen treatment in this rat model; second, we wanted to investigate whether cotreatment with TTA could abolish this undesirable side effect of tamoxifen. To clarify the mechanisms involved, we measured the activities and gene expression of enzymes controlling the hep...

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[9] Fatty acid synthase from human liver

Cited by 52 publications

References 3 publications

Structure and function of eukaryotic fatty acid synthases

Structure and function of eukaryotic fatty acid synthases

Effects of two supplementation levels of linseed combined with CLA or tallow on meat quality traits and fatty acid profile of adipose and different muscle tissues in slaughter pigs

Causes and prevention of tamoxifen-induced accumulation of triacylglycerol in rat liver

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