scholarly journals Stimulation of fatty acid synthesis by oestradiol in vitro

1960 ◽  
Vol 76 (2) ◽  
pp. 297-301 ◽  
Author(s):  
N. Hosoya ◽  
D. Hagerman ◽  
C. Villee
1970 ◽  
Vol 118 (2) ◽  
pp. 259-263 ◽  
Author(s):  
Alan G. Goodridge

1. A single glucose meal stimulated the incorporation of acetate into fatty acids in liver slices. If the glucose was added in vitro, it had no effect. Fructose and glycerol in vitro markedly stimulated fatty acid synthesis from acetate. Fructose and glycerol probably by-passed a rate-controlling reaction between glucose and triose phosphate. This reaction may have been stimulated by glucose administered in vivo. 2. The stimulation of fatty acid synthesis caused by fructose did not require the synthesis of enzyme, thus indicating that fatty acid-synthesizing enzymes were present in a latent form in the livers from unfed chicks.


1968 ◽  
Vol 108 (1) ◽  
pp. 147-152 ◽  
Author(s):  
Ajit Goswami ◽  
James K. Skipper ◽  
William L. Williams

RNA from testes of hypophysectomized rats treated with follicle-stimulating hormone and luteinizing hormone markedly stimulates in vitro the incorporation of acetate and malonate (as CoA derivatives) into polyunsaturated fatty acids. The system in vitro contains the components necessary for both protein and fatty acid synthesis. That the RNA is a hormone-induced messenger type that causes enzyme synthesis that then causes fatty acid synthesis is supported by the following observations: (1) the stimulation of RNA synthesis by follicle-stimulating hormone and luteinizing hormone is decreased by injection of the animals with actinomycin D; (2) puromycin in the system in vitro decreases the synthesis of polyunsaturated fatty acids; (3) the activity of the RNA preparation is destroyed by digestion with ribonuclease; in fact, the digest is inhibitory, which is a characteristic of messenger-RNA-mediated protein synthesis; (4) protein that might be denatured enzyme is virtually absent from the effective RNA preparations.


1952 ◽  
Vol 197 (1) ◽  
pp. 181-191 ◽  
Author(s):  
Grace. Medes ◽  
Alice. Thomas ◽  
Sidney. Weinhouse

1959 ◽  
Vol 234 (12) ◽  
pp. 3111-3114 ◽  
Author(s):  
Albert I. Winegrad ◽  
Walter N. Shaw ◽  
Francis D.W. Lukens ◽  
William C. Stadie

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.


1982 ◽  
Vol 28 (2) ◽  
pp. 223-230 ◽  
Author(s):  
Adrian J. Cutler ◽  
Robley J. Light

The yeast Candida bogoriensis produced large quantities of an extracellular glycolipid, the diacetyl sophoroside of 13-hydroxydocosanoic acid, when grown on a standard glucose rich medium (3% glucose, 0.15% yeast extract), but not when grown on a low glucose medium (0.5% glucose, 0.4% yeast extract) (A. J. Cutler and R. J. Light. 1979. J. Biol. Chem. 254: 1944–1950). Glucose levels also affected the quantity and distribution of the free fatty acid and triglyceride fractions synthesized by this organism. Cells grown on the low glucose medium contained palmitate and stearate as the major fatty acids in these two fractions, and a 3-h incubation with [1-14C]acetate led primarily to the labeling of these two acids. Cells grown on the standard enriched glucose medium contained relatively less stearate and more behenate than the low glucose grown cells, and the incorporation of [1-14C]acetate into stearate was decreased, while that into behenate was increased.Supplementation of low glucose grown cells with glucose led to a rapid stimulation of fatty acid synthesis, primarily palmitate and stearate in the free fatty acid fraction and stearate in the triglyceride fraction. Total triglyceride began to increase a few hours after supplementation, but synthesis of the extracellular glycolipid, and hence 13-hydroxydocosanoic acid, did not occur until 12–24 h after supplementation. The stimulation by glucose of long chain fatty acid synthesis in C. bogoriensis was therefore a process distinct from the glucose stimulation of palmitate and stearate synthesis, though the two events may be causally related.


2000 ◽  
Vol 80 (1) ◽  
pp. 59-67 ◽  
Author(s):  
J. A. Moibi ◽  
R. J. Christopherson ◽  
E. K. Okine

Twenty-four wether lambs were randomly allocated to six treatments to investigate the effect of temperature and dietary lipid supplements on fatty acid synthesis and metabolic activity in sheep. The treatments consisted of four groups exposed to either cold (0 °C) or warm temperature (+23 °C) and given ad libitum access to either a control barley-based diet or with lipid supplementation. Two other groups were placed on the dietary regimen at 0 °C, but pair-fed to intake of animals in the +23 °C environment. At 5 wk, fatty acid synthesis was measured by [1-14C]acetate incorporation into tissue lipids. Cold exposure and dietary lipid supplementation had no effect (P > 0.05) on in vivo fatty acid synthesis rates in either longissimus dorsi or the liver. In both subcutaneous and mesenteric adipose tissue depots, the rate of acetate incorporation into tissue lipid was not significantly affected by cold exposure. In the perirenal fat depot, cold exposure increased (P < 0.05) the rate of fatty acid synthesis, while lipid supplementation decreased (P < 0.05) the rate in all tissue adipose depots. In vitro, mesenteric and perirenal adipose tissues from cold pair-fed animals had higher (P < 0.05) rates of fatty acid synthesis compared to tissues from animals in the warm environment. However, there was no effect of dietary lipid supplementation in these two fat depots. Metabolic heat production, and energy and nitrogen excretion by animals were increased (P < 0.05) by cold exposure while lipid supplementation had the opposite effect (P < 0.05). The relationship between average daily gain and feed intake was linear at both warm and cold environments, but with higher (P < 0.05) average daily gain at all levels of intake in the cold compared to the warm environment. Results indicate that both environment and diet regulate metabolic activity in sheep. However, there were differences in lipogenic response by tissues to the treatments. Key words: Environmental temperature, dietary lipid, fatty acid synthesis, metabolic rate, sheep


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