Fatty Acid Synthesis in the Perfused Liver of Adrenalectomized Rats

1975 ◽  
Vol 3 (4) ◽  
pp. 515-518 ◽  
Author(s):  
CHRISTOPHER J. KIRK ◽  
TERENCE R. VERRINDER ◽  
DOUGLAS A. HEMS
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Acid Synthesis ◽  
Perfused Liver ◽  
Adrenalectomized Rats

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.

scholarly journals Effects of glucagon and insulin on fatty acid synthesis and glycogen degradation in the perfused liver of normal and genetically obese (ob/ob) mice

1978 ◽  
Vol 174 (3) ◽  
pp. 761-768 ◽  
Author(s):  
G Y Ma ◽  
C D Gove ◽  
D A Hems
Keyword(s):  
Fatty Acid ◽  
Food Deprivation ◽  
Fatty Acid Synthesis ◽  
Fatty Acid Biosynthesis ◽  
Glycogen Metabolism ◽  
Acid Synthesis ◽  
Significant Inhibition ◽  
Perfused Liver ◽  
Glucagon And Insulin ◽  
Glycogen Breakdown

1. Rapid effects of hormones on glycogen metabolism and fatty acid synthesis in the perfused liver of the mouse were studied. 2. In perfusions lasting 2h, of livers from normal mice, glucagon in successive doses, each producing concentrations of 10(-10) or 10(-9)M, inhibited fatty acid and cholesterol synthesis. In perfusions lasting 40–50 min, in which medium was not recycled, inhibition of fatty acid synthesis was only observed with glucagon at concentrations greater than 10(-9)M. This concentration was about two orders of magnitude higher than that required for the stimulation of glycogen breakdown. Glucagon did not inhibit the activity of acetyl-CoA carboxylase, assayed 10 or 20 min after addition of glucagon (10(-9) or 10(-10)M). It is proposed that the action of glucagon on hepatic fatty acid biosynthesis could be secondary in time to depletion of glycogen. Insulin prevented the effect of glucagon (10(-10)M) on glycogenolysis, but not that of vasopressin. 3. Livers of genetically obese (ob/ob) mice did not show significant inhibition of lipid biosynthesis in response to glucagon, although there was normal acceleration of glycogen breakdown. This resistance to glucagon action was not reversed by food deprivation. Livers of obese mice exhibited resistance to the counteraction by insulin of glucagon-stimulated glycogenolysis, which was reversible by partial food deprivation.

scholarly journals Resistance to hepatic action of vasopressin in genetically obese (ob/ob) mice

1976 ◽  
Vol 160 (1) ◽  
pp. 23-28 ◽  
Author(s):  
D A Hems ◽  
G Y Ma
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Inborn Error ◽  
Cholesterol Synthesis ◽  
Acid Synthesis ◽  
Hepatic Glycogen ◽  
Perfused Liver ◽  
Obese Mice ◽  
Hepatic Action ◽  
Glycogen Breakdown

1. Fatty acid synthesis, measured in the perfused liver of genetically obese (ob/ob) mice with 3H2O or [14C]actate, did not show the inhibition by [8-arginine]vasopressin (antidiuretic hormone) that is observed in livers from normal mice. 2. Hepatic glycogen breakdown in obese mice was stimuulated by vasopressin, but not as extensively as in lean mice. 3. If obese mice received a restricted amount of food, then fatty acid synthesis still did not respond to vasopressin, but glycogen breakdown was fully stimulated. 4. Cholesterol synthesis was not inhibited by vasopressin in livers from obese mice. 5. Vasopressin inhibited fatty acid synthesis in intact lean mice, but not in obese animals. 6. These results suggest that genetic obesity could be due to an inborn error within the mechanisms (other than adenylate cyclase) which mediate responses to extracellular effectors.

In silico Mapping and Structure Analysis of Key Enzyme Genes in Fatty Acid Synthesis of Soybean

2009 ◽  
Vol 35 (10) ◽  
pp. 1942-1947
Author(s):  
Wan-Kun SONG ◽  
Ming-Xi ZHU ◽  
Yang-Lin ZHAO ◽  
Jing WANG ◽  
Wen-Fu LI ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Structure Analysis ◽  
Fatty Acid Synthesis ◽  
In Silico ◽  
Acid Synthesis ◽  
In Silico Mapping ◽  
Key Enzyme
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