scholarly journals Fatty acid synthesis and the oxidative pentose phosphate pathway in developing embryos of oilseed rape (Brassica napus L.)

2005 ◽  
Vol 56 (412) ◽  
pp. 577-585 ◽  
Author(s):  
D. Hutchings
2000 ◽  
Vol 28 (6) ◽  
pp. 665-666 ◽  
Author(s):  
S. E. Kubis ◽  
S. Rawsthorne

The phosphoenolpyruvate transporter (PPT) is one of several important transporters for channelling carbon intermediates utilized for fatty acid synthesis and other plastidial pathways from the cytosol into the plastid. In this paper we show results on how the activity of the PPT changes between two important, physiologically different developmental stages of oilseed rape embryos.


2000 ◽  
Vol 352 (2) ◽  
pp. 525-532 ◽  
Author(s):  
Simon R. FOX ◽  
Lionel M. HILL ◽  
Stephen RAWSTHORNE ◽  
Matthew J. HILLS

Addition of oleoyl-CoA (1µM), or other acyl-CoA thioesters with a chain length of C16 or greater, to oilseed rape plastids (Brassica napus L.) inhibited the rate of D-glucose 6-phosphate (Glc6P) uptake by 70% after 2min. The IC50 value for oleoyl-CoA inhibition of the transporter was approx. 0.2–0.3µM. Inhibition was alleviated by the addition of acyl-CoA binding protein (ACBP) or BSA at slightly higher concentrations. Oleic acid (5–25µM), Tween 40 (10µM), Triton-X 100 (10µM) and palmitoylcarnitine (5µM) had no effect on Glc6P uptake. The uptake of [1-14C]Glc6P occurred in exchange for Pi, 3-phosphoglycerate or Glc6P at a typical rate of 30nmol Glc6P/min per unit of glyceraldehyde-3-phosphate dehydrogenase (NADP+). The Km(app) of the Glc6P transporter for Glc6P was 100µM. Neither CoA (0.3mM) nor ATP (3mM) inhibited Glc6P uptake, but the transporter was inhibited by 72% when ATP and CoA were added together. This inhibition was attributable to the synthesis of acyl-CoA thioesters, predominantly oleoyl-CoA and palmitoyl-CoA, by long-chain fatty acid-CoA ligase (EC 6.2.1.3) from endogenous fatty acids in the plastid preparations. Acyl-CoA thioesters did not inhibit the uptake of [2-14C]pyruvate or D-[1-14C]glucose into plastids. In vivo quantities of oleoyl-CoA and other long-chain acyl-CoA thioesters were lower than those for ACBP in early cotyledonary embryos, 0.7±0.2pmol/embryo and 2.2±0.2pmol/embryo respectively, but in late cotyledonary embryos quantities of long-chain acyl-CoA thioesters were greater than ACBP, 3±0.4pmol/embryo and 1.9±0.2pmol/embryo respectively.


2000 ◽  
Vol 348 (1) ◽  
pp. 145-150 ◽  
Author(s):  
Philip E. JOHNSON ◽  
Simon R. FOX ◽  
Matthew J. HILLS ◽  
Stephen RAWSTHORNE

The effects of long-chain acyl-CoA (lcACoA) esters (both added exogenously and synthesized de novo) and acyl-CoA binding protein (ACBP) on plastidial glucose 6-phosphate (Glc6P) and pyruvate metabolism were examined using isolated plastids. The binding of lcACoA esters by ACBP stimulated the utilization of Glc6P for fatty acid synthesis, starch synthesis and reductant supply via the oxidative pentose phosphate (OPP) pathway. Stimulation occurred at low (1-10 μM) concentrations of ACBP. Pyruvate-dependent fatty acid synthesis was not directly affected by ACBP. However, addition of ACBP did increase the Glc6P-dependent stimulation of pyruvate utilization mediated through the OPP pathway. On the basis of these experiments, we conclude that lcACoA esters may inhibit Glc6P uptake into plastids, and that this inhibition is relieved by ACBP. We also suggest that utilization of other substrates for fatty acid synthesis may be affected by lcACoA/ACBP via their effects on the OPP pathway.


2013 ◽  
Vol 12 (6) ◽  
pp. 962-970 ◽  
Author(s):  
Gang XIAO ◽  
Zhen-qian ZHANG ◽  
Rui-yang LIU ◽  
Chang-fa YIN ◽  
Xian-meng WU ◽  
...  

1983 ◽  
Vol 97 (2) ◽  
pp. 207-212 ◽  
Author(s):  
M.-Th Sutter-Dub ◽  
A. Sfaxi ◽  
P. Strozza

Pregnancy and progesterone treatment of ovariectomized rats decrease glucose metabolism through the pentose-phosphate pathway in isolated female rat adipocytes. As demonstrated in previous studies, progesterone directly decreases [1-14C]glucose oxidation through the pentose-phosphate pathway and lipogenesis from [6-14C]glucose; the present study therefore compared glucose-induced lipid synthesis during pregnancy (10, 16 and 20 days of pregnancy) with the effect of progesterone treatment (5 mg/rat per day for 14 days) to shed more light on the role of this steroid in glucose metabolism during pregnancy. The inhibition of [6-14C]glucose incorporation into triacylglycerols in the progesterone-treated rats was comparable to that which occurs during late (20 days) and mid-pregnancy (16 days) but not during early pregnancy (10 days). The inhibition of fatty acid synthesis was more important as pregnancy advanced and was different from the decrease in fatty acid synthesis induced by progesterone treatment. The sensitivity to insulin was comparable in virgin, ovariectomized and progesterone-treated ovariectomized rats but not in pregnant rats. This implies that progesterone and insulin affect glucose-induced lipid synthesis by distinct processes and that the impaired glucose metabolism is characterized by a reduction in basal glucose utilization rather than by an impaired insulin response.


1971 ◽  
Vol 49 (2) ◽  
pp. 267-272 ◽  
Author(s):  
P. K. Agrawal ◽  
D. T. Canvin

Glucose-1-14C, glucose-6-14C, and glucose-U-14C were used to calculate the contribution of the PPP in developing castor bean endosperm tissues. Depending on the age of the seed 5–12% of the glucose-14C used was metabolized via the PPP and 88–95% via the EMP pathway. When lipid synthesis was rapid (20- to 28-day period) the PPP contribution was also at a maximum. During the 30- to 51-day period when lipid synthesis decreased so did the PPP contribution.With the data obtained from the PPP contribution the amount of NADPH produced during the experimental period was calculated. Also, the amount of fatty acids synthesized during that period was determined from glucose-U-14C data and thus the amount of NADPH required was calculated. Assuming that all the NADPH produced in the PPP was utilizable in fatty acid synthesis it was found that it was only sufficient to supply 50–75% of the reducing hydrogen required for fat synthesis. Therefore, the rest of the reducing hydrogen must come from some other sources, possibly NADH.


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