Glyceride Synthesis from Free Fattyacids and Glycerol

1996 ◽  
pp. 421-434 ◽  
Author(s):  
F. Ergan
Keyword(s):  
1972 ◽  
Vol 128 (5) ◽  
pp. 1057-1067 ◽  
Author(s):  
E. D Saggerson

1. 0.5mm-Palmitate stimulated incorporation of [U-14C]glucose into glyceride glycerol and fatty acids in normal fat cells in a manner dependent upon the glucose concentration. 2. In the presence of insulin the incorporation of 5mm-glucose into glyceride fatty acids was increased by concentrations of palmitate, adrenaline and 6-N-2′-O-dibutyryladenosine 3′:5′-cyclic monophosphate up to 0.5mm, 0.5μm and 0.5mm respectively. Higher concentrations of these agents produced progressive decreases in the rate of glucose incorporation into fatty acids. 3. The effects of palmitate and lipolytic agents upon the measured parameters of glucose utilization were similar, suggesting that the effects of lipolytic agents are mediated through increased concentrations of free fatty acids. 4. In fat cells from 24h-starved rats, maximal stimulation of glucose incorporation into fatty acids was achieved with 0.25mm-palmitate. Higher concentrations of palmitate were inhibitory. In fat cells from 72h-starved rats, palmitate only stimulated glucose incorporation into fatty acids at high concentrations of palmitate (1mm and above). 5. The ability of fat cells to incorporate glucose into glyceride glycerol in the presence of palmitate decreased with increasing periods of starvation. 6. It is suggested that low concentrations of free fatty acids stimulate fatty acid synthesis from glucose by increasing the utilization of ATP and cytoplasmic NADH for esterification of these free fatty acids. When esterification of free fatty acids does not keep pace with their provision, inhibition of fatty acid synthesis occurs. Provision of free fatty acids far in excess of the esterification capacity of the cells leads to uncoupling of oxidative phosphorylation and a secondary stimulation of fatty acid synthesis from glucose.


1964 ◽  
Vol 206 (6) ◽  
pp. 1217-1222 ◽  
Author(s):  
Irving B. Fritz

Carnitine increased oxidation of palmitate-1-C14 by rat heart and liver preparations, but decreased palmitate incorporation into glycerides. To determine which of the effects was derivative and which was primary, experiments were repeated using tissues whose rates of fatty acid oxidation had been depressed by Amytal poisoning. Under these conditions, carnitine inhibition of fatty acid conversion to glycerides was abolished. Similarly, low concentrations of carnitine were found to enhance palmitate oxidation without influencing palmitate esterification. Isolated liver microsomes which synthesized glycerides without oxidizing fatty acids showed no response to carnitine under all conditions tried. The inability of carnitine to alter glyceride formation in experiments described may signify that acyl-CoA generation from CoA and acylcarnitine is specifically directed toward the fatty acid oxidase system rather than to glyceride synthesis. It was also shown that, under conditions optimal for demonstration of carnitine augmentation of fatty acid oxidation by rat heart preparations, carnitine increased palmitate oxidation by a variety of other tissue homogenate preparations.


1998 ◽  
Vol 4 (6) ◽  
pp. 401-405 ◽  
Author(s):  
V.J. Robles ◽  
H.S. García ◽  
J.A. Monroy ◽  
O. Angulo

Menhaden oil was hydrolyzed using a lipase from Pseudomonas sp. The hydrolysate was cold frac tionated at-72°C. Glyceride synthesis was performed using the same lipase under different reaction environments. The best conditions for the esterification reaction were 39 °C for 18 h in a reaction mixture containing anhydrous glycerol, n-3 polyunsaturated fatty acids (PUFA) enriched solution (2% lipids in hexane), hexane, and phosphate buffer-lipase solution (1% w/v). Product composition was 81.33% triacylglycerides and 18.67% of free fatty acids (w/w). Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) accounted for 36.18% of the esterified fatty acids, of which 58% was EPA and 42% was DHA. This method offers an alternative to produce glycerides rich in n-3 PUFA.


2007 ◽  
Vol 293 (5) ◽  
pp. E1352-E1357 ◽  
Author(s):  
Maria Emilia Soares Martins-Santos ◽  
Valéria Ernestânia Chaves ◽  
Danúbia Frasson ◽  
Renata Polessi Boschini ◽  
Maria Antonieta Rissato Garófalo ◽  
...  

The pathways of glycerol-3-phosphate (G3P) generation for glyceride synthesis were examined in precision-cut liver slices of fasted and diabetic rats. The incorporation of 5 mM [U-14C]glucose into glyceride-glycerol, used to evaluate G3P generation via glycolysis, was reduced by ∼26–36% in liver slices of fasted and diabetic rats. The glycolytic flux was reduced by ∼60% in both groups. The incorporation of 1.0 mM [2-14C]pyruvate into glyceride-glycerol (glyceroneogenesis) increased ∼50% and ∼36% in slices of fasted and diabetic rats, respectively, which also showed a two-fold increase in the activity phospho enolpyruvate carboxykinase. The increased incorporation of 1.0 mM [2-14C]pyruvate into glyceride-glycerol by slices of fasted rats was not affected by the addition of 5 mM glucose to the incubation medium. The activity of glycerokinase and the incorporation of 1 mM [U-14C]glycerol into glyceride-glycerol, evaluators of G3P formation by direct glycerol phosphorylation, did not differ significantly from controls in slices of the two experimental groups. Rates of incorporation of 1 mM [2-14C]pyruvate and [U-14C]glycerol into glucose of incubation medium (gluconeogenesis) were ∼140 and ∼20% higher in fasted and diabetic slices than in control slices. It could be estimated that glyceroneogenesis by liver slices of fasted rats contributed with ∼20% of G3P generated for glyceride-glycerol synthesis, the glycolytic pathway with ∼5%, and direct phosphorylation of glycerol by glycerokinase with ∼75%. Pyruvate contributed with 54% and glycerol with 46% of gluconeogenesis. The present data indicate that glyceroneogenesis has a significant participation in the generation of G3P needed for the increased glyceride-glycerol synthesis in liver during fasting and diabetes.


1998 ◽  
Vol 75 (5) ◽  
pp. 643-650 ◽  
Author(s):  
Yu-Chih Yeh ◽  
Erdogan Gulari
Keyword(s):  

1975 ◽  
Vol 34 (3) ◽  
pp. 225-231 ◽  
Author(s):  
D. A. Hems
Keyword(s):  

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