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Synaptosomal phosphoglycerides were labeled after incubation with [1-14C]arachidonic acid, ATP, Mg2+, CoASH, and a small amount of 1-acylglycerophosphocholines. Under this incubation system, radioactivity was directed largely to diaclyglycerophosphocholines but diacylglycerophosphoinositols were also labeled to a lesser extent. Synaptosomes obtained after a(More)
Type 2 diabetes (T2D) is characterized by insulin resistance and pancreatic β-cell dysfunction, the latter possibly caused by a defect in insulin signaling in β-cells. We hypothesized that insulin's effect to potentiate glucose-stimulated insulin secretion (GSIS) would be diminished in insulin-resistant persons. To evaluate the effect of insulin to modulate(More)
In the presence of Ca2+ (2.5 mM) and using [14C]arachidonoyl phosphatidylinositol (PI) membrane as substrate, phosphatidylinositol-specific phospholipase C (PI-PLC) (EC in rat brain synaptosomes was activated by deoxycholate but not taurocholate. Calcium stimulated enzymic hydrolysis by both detergents, but the stimulatory effect of taurocholate(More)
The hydrolysis of acyl-CoA by acyl-CoA hydrolase (EC in brain synaptosomes was inhibited by calcium. This inhibition was partly due to interaction of Ca2+ with the acyl-CoA, which was present in the soluble form, and partly due to complex formation among acyl-CoA, Ca2+ and membrane phospholipids. The inhibition of acyl-CoA hydrolase activity, as(More)
Rats subjected to mild hypoxic and postdecapitative ischemic treatments indicated a decrease (8-16%) in the proportion of polyunsaturated acyl groups of diacyl glycerophosphocholines (diacyl-GPC), diacyl glycerophosphoethanolamines (diacyl-GPE), and alkenylacyl glycerophosphoethanolamines (alkenylacyl-GPE) in brain synaptosomes. In general, the acyl group(More)
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