scholarly journals The effect of chronic ethanol administration on lipogenesis in liver and adipose tissue in the rat

1983 ◽  
Vol 50 (3) ◽  
pp. 549-553 ◽  
Author(s):  
Carmen Cascales ◽  
Manuel Benito ◽  
María Cascales ◽  
Trinidad Caldés ◽  
Angel Santos-Ruiz
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
De Novo ◽  
Tritiated Water ◽  
Acid Synthesis ◽  
Male Rats ◽  
Ethanol Administration ◽  
Chronic Ethanol Administration ◽  
Food And Drink

1. Rates of lipogenesis de novo have been studied in liver and epididymal fat pads of male rats chronically treated with ethanol. A solution of ethanol (150 ml/l) was administered as the only drinking fluid for 3 months with a standard solid diet; both food and drink were available ad lib.2. Lipogenesis in vivo was measured by the incorporation of tritiated water into lipid fractions: non-saponifiable lipid and fatty acids. Non-saponifiable lipid, both in liver and in adipose tissue, was unaffected by ethanol treatment. However, fatty acid synthesis de novo was significantly enhanced in both liver and adipose tissue, by 150 and 300% respectively.3. Plasma triacylglycerol and non-esterified fatty acid levels were unchanged and plasma glucose concentration slightly increased by ethanol administration.4. The rate of lipogenesis increased when insulin: glucagon increased twofold due to the effect of ethanol.

scholarly journals Chronic ethanol administration depresses fatty acid synthesis in rat adipose tissue

1988 ◽  
Vol 251 (2) ◽  
pp. 547-551 ◽  
Author(s):  
J S Wilson ◽  
M A Korsten ◽  
L P Donnelly ◽  
P W Colley ◽  
J B Somer ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Fatty Acid Synthetase ◽  
Acid Synthesis ◽  
Chronic Ethanol ◽  
Ethanol Administration ◽  
Acetyl Coa Carboxylase ◽  
Acetyl Coa ◽  
Chronic Ethanol Administration

Administration of ethanol as part of a nutritionally adequate liquid diet to female Wistar rats was found to depress markedly incorporation of labelled glucose into adipose-tissue acylglycerol fatty acids. Similar results with labelled pyruvate and acetate suggested inhibition of the fatty-acid-synthesis pathway at, or distal to, the acetyl-CoA carboxylase step. Activities of acetyl-CoA carboxylase and fatty acid synthetase were markedly lower in ethanol-fed animals. The activity of another lipogenic enzyme, phosphatidate phosphohydrolase, was not affected by chronic ethanol feeding. These findings suggest that chronic ethanol administration has marked effects on adipose-tissue lipogenesis.

scholarly journals Ethanol administration and the relationship of malonyl-coenzyme A concentrations to the rate of fatty acid synthesis in rat liver

1973 ◽  
Vol 136 (3) ◽  
pp. 639-647 ◽  
Author(s):  
Robert W. Guynn ◽  
Dulce Veloso ◽  
Raymond L. Harris ◽  
J. W. Randolph Lawson ◽  
Richard L. Veech
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
De Novo ◽  
Fatty Acid Synthetase ◽  
Acid Synthesis ◽  
Ethanol Administration ◽  
Liver Fatty Acid ◽  
Malonyl Coa ◽  
Significant Difference

1. The effect of ethanol on liver fatty acid synthesis was studied in vivo in 24h-starved and ‘meal-fed’ rats (i.e. fed for 3h per day and not ad libitum). 2. In the fed animal3H2O was incorporated into fat at a rate of 0.46μmol of C2 units/min per g wet wt. of liver. Administration of either ethanol (3.2g/kg) or equicaloric amounts of glucose had no effect on the rate of3H2O incorporation into lipid. 3. In the 24h-starved animal, administration of the same dose of ethanol produced an increase in the rate of3H2O incorporation from 0.06 to 0.12μmol of C2 units/min per g fresh wt. after 3h whereas [malonyl-CoA] increased from 0.006 to 0.009μmol/g. Glucose given in amounts equicaloric to ethanol was significantly more lipogenic, increasing both the3H2O incorporation from 0.06 to 0.20μmol of C2 units/min per g and the malonyl-CoA content from 0.006 to 0.013 μmol/g wet wt. at 3h. 4. The decrease in the redox state of free cytoplasm NAD or NADP couples or the changes in content of citrate, glucose 6-phosphate and pyruvate of liver after ethanol administration had no measurable effect on the rate of fatty acid synthesis in vivo. 5. Under the conditions of the experiments there was no significant difference, among any of the groups, in the activity of liver fatty acid synthetase measured in vitro. A double-reciprocal plot of the rate of3H2O incorporation and the total tissue malonyl-CoA concentrations showed a striking relationship. It has been concluded that the rate of fatty acid synthesis in vivo is determined principally by the Vmax. of fatty acid synthetase and the concentration of free malonyl-CoA. 6. It has also been concluded that under the conditions of the present study, the synthesis of fatty acids de novo is unlikely to be an important factor in the increased liver lipid content associated with ethanol administration.

Fatty acid synthesis in adipose tissues of physically trained rats in vivo

1983 ◽  
Vol 245 (1) ◽  
pp. E8-E13
Author(s):  
K. Tokuyama ◽  
H. Okuda
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Physical Training ◽  
Dark Period ◽  
Acid Synthesis ◽  
Free Access ◽  
Adipose Tissues ◽  
Brown Adipose

The effect of physical training on fatty acid synthesis in vivo was studied. After the rats had free access to a running wheel for 50 days, the rate of fatty acid synthesis estimated using 3H2O in adipose tissues of trained rats was about three times higher than that of sedentary rats in both the light and dark period. The rate of fatty acid synthesis in the liver but not in the brown adipose tissue was also slightly enhanced by physical training. The number of adipocytes was not affected, but the size of adipocytes was reduced by physical training. In trained rats, the rate of fatty acid synthesis in adipocytes whose diameter was similar to that of sedentary rats was about 10 times higher than that of sedentary rats. Within adipose tissue, the rate of fatty acid synthesis correlated positively to the diameter of adipocytes both in the sedentary and trained rats. These findings mean that the adaptive increase in fatty acid synthesis seen in adipocytes of trained rats is not secondary to the reduction in size of adipocytes.

Fatty acid synthesis and generation of glycerol-3-phosphate in brown adipose tissue from rats fed a cafeteria diet

2008 ◽  
Vol 86 (7) ◽  
pp. 416-423 ◽  
Author(s):  
Valéria E. Chaves ◽  
Danúbia Frasson ◽  
Maria E.S. Martins-Santos ◽  
Luiz C.C. Navegantes ◽  
Victor D. Galban ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Brown Adipose Tissue ◽  
Glucose Uptake ◽  
Fatty Acid Synthesis ◽  
Fatty Acid Content ◽  
Acid Synthesis ◽  
Cafeteria Diet ◽  
Brown Adipose

In vivo fatty acid synthesis and the pathways of glycerol-3-phosphate (G3P) production were investigated in brown adipose tissue (BAT) from rats fed a cafeteria diet for 3 weeks. In spite of BAT activation, the diet promoted an increase in the carcass fatty acid content. Plasma insulin levels were markedly increased in cafeteria diet-fed rats. Two insulin-sensitive processes, in vivo fatty acid synthesis and in vivo glucose uptake (which was used to evaluate G3P generation via glycolysis) were increased in BAT from rats fed the cafeteria diet. Direct glycerol phosphorylation, evaluated by glycerokinase (GyK) activity and incorporation of [U-14C]glycerol into triacylglycerol (TAG)–glycerol, was also markedly increased in BAT from these rats. In contrast, the cafeteria diet induced a marked reduction of BAT glyceroneogenesis, evaluated by phosphoenolpyruvate carboxykinase-C activity and incorporation of [1-14C]pyruvate into TAG–glycerol. BAT denervation resulted in an approximately 50% reduction of GyK activity, but did not significantly affect BAT in vivo fatty acid synthesis, in vivo glucose uptake, or glyceroneogenesis. The data suggest that the supply of G3P for BAT TAG synthesis can be adjusted independently from the sympathetic nervous system and solely by reciprocal changes in the generation of G3P via glycolysis and via glyceroneogenesis, with no participation of direct phosphorylation of glycerol by GyK.

scholarly journals Downregulation of de Novo Fatty Acid Synthesis in Subcutaneous Adipose Tissue of Moderately Obese Women

2015 ◽  
Vol 16 (12) ◽  
pp. 29911-29922 ◽  
Author(s):  
Esther Guiu-Jurado ◽  
Teresa Auguet ◽  
Alba Berlanga ◽  
Gemma Aragonès ◽  
Carmen Aguilar ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Subcutaneous Adipose Tissue ◽  
De Novo ◽  
Acid Synthesis ◽  
Obese Women ◽  
Subcutaneous Adipose

scholarly journals USP22-dependent accumulation of lipidomes drives hepatocellular carcinoma progression by stabilizing PPARγ

2020 ◽  
Author(s):  
Zhen Ning ◽  
Xin Guo ◽  
Xiaolong Liu ◽  
Chang Lu ◽  
Aman Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Fatty Acid ◽  
Molecular Mechanism ◽  
Fatty Acid Synthesis ◽  
De Novo ◽  
Acid Synthesis ◽  
Specific Protease ◽  
Pparγ Expression

Abstract Elevated de novo lipogenesis (DNL) is considered to be a crucial factor in hepatocellular carcinoma (HCC) development. However, the molecular mechanism for its occurrence in HCC is still unclear. Herein, we identified ubiquitin-specific protease 22 (USP22) as a key regulator for de novo fatty acid synthesis, which directly interacts with, deubiquitinates and stabilizes PPARγ through K48-linked deubiquitination, and in turn, this stabilization increases ACC and ACLY transcription. In addition, we found that USP22 promoted the de novo synthesis of fatty acid labeling from glucose tracers. USP22-dysregulated de novo fatty acid synthesis contributes to HCC progression, but USP22 was functionality suppressed by inhibiting the expression of PPARγ, ACLY, or ACC in in vitro cell proliferation and in vivo tumorigenesis experiments. In HCC, USP22 expression positively correlates with PPARγ expression, and simultaneously, high expression of USP22 and PPARγ or USP22, ACC and ACLY is associated with a poor prognosis. Taken together, we identified a previously undescribed USP22-regulated lipogenesis molecular mechanism that involves the PPARγ-ACLY/ACC axis in HCC tumorigenesis and provide a rationale for therapeutic targeting of lipogenesis via USP22 inhibition.

Effects of pregnancy and ovarian steroids on fatty acid synthesis and uptake in Syrian hamsters

1991 ◽  
Vol 260 (1) ◽  
pp. R153-R158 ◽  
Author(s):  
A. J. Bhatia ◽  
G. N. Wade
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
White Adipose Tissue ◽  
Fatty Acid Synthesis ◽  
De Novo ◽  
Acid Synthesis ◽  
De Novo Lipogenesis ◽  
Ovarian Steroids ◽  
Syrian Hamsters

The effects of pregnancy and ovarian steroids on the in vivo distribution of newly synthesized fatty acids (incorporation of tritium from 3H2O into fatty acid) in Syrian hamsters (Mesocricetus auratus) were examined. During late, but not early, gestation hamsters had reduced levels of newly synthesized fatty acids in heart, liver, uterus, and white adipose tissues (parametrial and inguinal fat pads). Treatment of ovariectomized hamsters with estradiol + progesterone significantly decreased fatty acid synthesis-uptake in heart, liver, and inguinal white adipose tissue. Treatment with either estradiol or progesterone alone was without significant effect in any tissue. Pretreatment of hamsters with Triton WR-1339 (tyloxapol), an inhibitor of lipoprotein lipase activity and tissue triglyceride uptake, abolished the effects of estradiol + progesterone in white adipose tissue and heart but not in liver. Thus hamsters lose body fat during pregnancy in part because of decreased de novo lipogenesis. The effect of pregnancy on lipogenesis is mimicked by treatment with estradiol + progesterone but not by either hormone alone. Furthermore, it appears that the liver is the principal site of estradiol + progesterone action on lipogenesis in Syrian hamsters.

scholarly journals Fatty acid synthesis in the perfused liver of adrenalectomized rats

1976 ◽  
Vol 156 (3) ◽  
pp. 593-602 ◽  
Author(s):  
C J Kirk ◽  
T R Verrinder ◽  
D A Hems
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
De Novo ◽  
Direct Action ◽  
Acid Synthesis ◽  
Diabetic Rats ◽  
Perfused Liver ◽  
Control Sham ◽  
Adrenalectomized Rats

1. Fatty acid synthesis, measured in the perfused liver of fed adrenalectomized rats with 3H2O and 14C-labelled precursors, was less than in control sham-operated rats. 2. This defect was more extensive for synthesis of fatty acids incorporated into triacylglycerols than into phospholipids. 3. There was impairment in desaturation and export of newly synthesized fatty acid. 4. Fatty acid synthesis and desaturation were restored to normal rates 5h after treatment with cortisol in vivo. 5. Fatty acid synthesis was seasonally variable, being highest in the winter; the impairment after adrenalectomy was observed in all seasons. 6. In perfusions with oleate (0.7 mM), no further impairment in fatty acid synthesis was discerned in livers from adrenalectomized rats, in which the rate resembled that in control livers. 7. No defect in the incorporation of oleate into glycerides was discerned in livers from adrenalectomized rats. 8. Cortisol exerted no stimulatory effect on fatty acid synthesis when added to perfusion media. 9. The impairment in hepatic lipogenesis, demonstrable after adrenalectomy, shows that adrenal glucocorticoids promote hepatic capacity for fatty acid synthesis de novo, at least in intact non-diabetic rats. It is suggested that this effect is mediated by insulin, perhaps through direct action on the liver.

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