scholarly journals Effects of anti-oxidant treatment on sciatic nerve dysfunction in streptozotocin-diabetic rats; comparison with essential fatty acids

Diabetologia ◽  
1995 ◽  
Vol 38 (2) ◽  
pp. 129-134 ◽  
Author(s):  
�. Karasu ◽  
M. Dewhurst ◽  
E. J. Stevens ◽  
D. R. Tomlinson
Keyword(s):  
Fatty Acids ◽  
Sciatic Nerve ◽  
Essential Fatty Acids ◽  
Diabetic Rats ◽  
Anti Oxidant ◽  
Streptozotocin Diabetic Rats ◽  
Nerve Dysfunction

scholarly journals Anti-oxidant treatment prevents the development of peripheral nerve dysfunction in streptozotocin-diabetic rats

Diabetologia ◽  
1993 ◽  
Vol 36 (4) ◽  
pp. 299-304 ◽  
Author(s):  
N. E. Cameron ◽  
M. A. Cotter ◽  
E. K. Maxfield
Keyword(s):  
Peripheral Nerve ◽  
Diabetic Rats ◽  
Anti Oxidant ◽  
Streptozotocin Diabetic Rats ◽  
Nerve Dysfunction

scholarly journals Inhibitory effects of some long-chain unsaturated fatty acids on mitochondrial β-oxidation. Effects of streptozotocin-induced diabetes on mitochondrial β-oxidation of polyunsaturated fatty acids

1985 ◽  
Vol 230 (2) ◽  
pp. 329-337 ◽  
Author(s):  
H Osmundsen ◽  
K Bjørnstad
Keyword(s):  
Fatty Acids ◽  
Unsaturated Fatty Acids ◽  
Reductase Activity ◽  
Liver Mitochondria ◽  
Inhibitory Effect ◽  
Diabetic Rats ◽  
Inhibitory Property ◽  
Streptozotocin Induced Diabetes ◽  
Streptozotocin Diabetic Rats ◽  
Coa Reductase

Evidence showing that some unsaturated fatty acids, and in particular docosahexaenoic acid, can be powerful inhibitors of mitochondrial β-oxidation is presented. This inhibitory property is, however, also observed with the cis- and trans-isomers of the C18:1(16) acid. Hence it is probably the position of the double bond(s), and not the degree of unsaturation, which confers the inhibitory property. It is suggested that the inhibitory effect is caused by accumulation of 2,4-di- or 2,4,7-tri-enoyl-CoA esters in the mitochondrial matrix. This has previously been shown to occur with these fatty acids, in particular when the supply of NADPH was limiting 2,4-dienoyl-CoA reductase (EC 1.3.1.-) activity [Hiltunen, Osmundsen & Bremer (1983) Biochim. Biophys. Acta 752, 223-232]. Liver mitochondria from streptozotocin-diabetic rats showed an increased ability to β-oxidize 2,4-dienoyl-CoA-requiring acylcarnitines. Docosahexaenoylcarnitine was also found to be less inhibitory at lower concentrations with incubation under coupled conditions. With uncoupling conditions there was little difference between mitochondria from normal and diabetic rats in these respects. This correlates with a 5-fold stimulation of 2,4-dienoyl-CoA reductase activity found in mitochondria from streptozotocin-diabetic rats.

scholarly journals Transport of myo-inositol into endoneurial preparations of sciatic nerve from normal and streptozotocin-diabetic rats

1983 ◽  
Vol 210 (3) ◽  
pp. 775-781 ◽  
Author(s):  
K R W Gillon ◽  
J N Hawthorne
Keyword(s):  
Sciatic Nerve ◽  
Glucose Concentration ◽  
Reductase Inhibitor ◽  
Streptozotocin Diabetes ◽  
Diabetic Rats ◽  
Aldose Reductase Inhibitor ◽  
Similar Extent ◽  
Elevated Glucose ◽  
Streptozotocin Diabetic Rats ◽  
Energy Dependent

myo-Inositol transport by a viable rat sciatic-nerve preparation is described. Such ‘endoneurial’ nerve preparations accumulated myo-inositol by an energy-dependent saturable system. Streptozotocin-diabetes reduced myo-inositol transport into sciatic nerve by approx. 40%. Elevated medium glucose concentration reduced myo-inositol transport into control nerves to a similar extent. Fructose and sorbitol did not inhibit myo-inositol transport. Inclusion of an aldose reductase inhibitor in the medium counteracted the reduced myo-inositol transport caused by elevated glucose concentration. The importance of these results to the problem of diabetic neuropathy is discussed.

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