Signalling pathways involved in the stimulation of fatty acid synthesis by insulin

1997 ◽  
Vol 25 (4) ◽  
pp. 1238-1242 ◽  
Author(s):  
R. M. Denton ◽  
K. J. Heesom ◽  
S. K. Moule ◽  
N. J. Edgell ◽  
P. Burnett
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.


1998 ◽  
Vol 16 ◽  
pp. S87
Author(s):  
Christoph Huschka ◽  
Wolfgang Wohlrab ◽  
Reinhard Neubert

Author(s):  
Linda W. Gonzales ◽  
Robert Ertsey ◽  
Philip L. Ballard ◽  
Deborah Froh ◽  
Jon Goerke ◽  
...  

1960 ◽  
Vol 76 (2) ◽  
pp. 297-301 ◽  
Author(s):  
N. Hosoya ◽  
D. Hagerman ◽  
C. Villee

1994 ◽  
Vol 302 (1) ◽  
pp. 141-146 ◽  
Author(s):  
M J H Geelen

Short-term exposure of isolated rat hepatocytes to short- and medium-chain fatty acids led to an activation of acetyl-CoA carboxylase as measured in digitonin-permeabilized hepatocytes. Up to a certain concentration, typical for each of the fatty acids used, fatty acid-dependent activation of acetyl-CoA carboxylase coincided with an increase in the rate of fatty acid synthesis in intact hepatocytes, as determined by the incorporation of 3H from 3H2O water into fatty acids. At higher concentrations loss of stimulation of fatty acid synthesis occurred, but not the enhancement of carboxylase activity. With the fatty acids tested (C8:0-C14:0), the peak in fatty acid synthesis coincided with a peak in the level of malonyl-CoA. The onset of the stimulation of carboxylase activity coincided with the start of the peak in both fatty acid synthesis and malonyl-CoA. The longer the chain length of the fatty acid added, the lower the concentration at which the rate of fatty acid synthesis and the level of malonyl-CoA reached a peak and carboxylase activity started to become elevated. In cell suspensions incubated with increasing concentrations of fatty acids, accumulation of lactate decreased progressively. The latter observation, in combination with the fact that the activity of acetyl-CoA carboxylase is not always related to the rate of fatty acid biosynthesis, suggests that under these conditions not the activity of the carboxylase but the flux through the glycolytic sequence determines, at least in part, the rate of fatty acid synthesis de novo.


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