Diacylglycerol accumulation

Koenderman, L., Tool, A., Roos, D., Verhoeven, A. J. (1989). 1,2-Diacylglycerol accumulation in human neutrophils does not correlate with respiratory burst activation. FEBSLett. 243, 399-403. 

Diacetylpyridine, template synthesis, 21 14 Diacylglycerol, accumulation, lithium and, 36 58... 

Reddy TS, Bazan NG. Arachidonic acid, stearic acid, and diacylglycerol accumulation correlates with the loss of phosphatidylinositol 4,5-bisphosphate in cerebrum 2 seconds after electroconvulsive shock complete reversion of changes 5 minutes after stimulation. J Neurosci Res 1987 18 449 55. 

PKC0 also activates IkB kinase and c-Jun N-terminal kinase in adipocytes. Both of these protein kinases have been shown to phosphorylate a serine residue of IRS-1. In contrast to PKC0, PKC5 leads to phosphorylation of p47, activating NADPH oxidase. These molecular mechanisms that result from increased diacylglycerol accumulation in adipocytes may at least in part, explain the insulin resistance associated with obesity. 

Chavez JA, Summers SA. Characterizing the effects of saturated fatty acids on insulin signaling and ceramide and diacylglycerol accumulation in 3T3-L1 adipocytes and C2C12 myotubes. Arch Biochem Biophys. 2003, 419 101-9. 

Bocckino, SB, Blackmore, PE and Exton, JH (1985) Stimulation of 1,2-diacylglycerol accumulation in hepatocytes by vasopressin, epinephrine, and angiotensin II. Journal of Biological Chemistry, 260, 14201-14207. 

Martin, TF, Hsieh, KP and Porter, BW (1990) The sustained second phase of hormone-stimulated diacylglycerol accumulation does not activate protein kinase C in GH3 cells. Journal of Biological Chemistry, 265, 7623-7631. 

Less explored is the role and metabolic fate of 2-AG. It is possible that in many tissues, 2-AG is only an intermediate of a signaling pathway that generates 1,2-diacylglycerol and arachidonic acid, two well-known signaling molecules. In the brain however, 2-AG may have regulatory roles, since it escapes immediate metabolism and accumulates in response to stimuli-generated Ca2+ surges (Stella, 1997). These differences may arise... 

Free arachidonic acid, along with diacylglycerols and free docosahexaenoic acid, is a product of membrane lipid breakdown at the onset of cerebral ischemia, seizures and other forms of brain trauma. Because polyunsaturated fatty acids are the predominant FFA pool components that accumulate under these conditions, this further supports the notion that fatty acids released from the C2 position of membrane phospholipids are major contributors to the FFA pool, implicating PLA2 activation as the critical step in FFA release [1,2] (Fig. 33-6). 

The physiological functions of carboxylesterases are still partly obscure but these enzymes are probably essential, since their genetic codes have been preserved throughout evolution [84] [96], There is some evidence that microsomal carboxylesterases play an important role in lipid metabolism in the endoplasmic reticulum. Indeed, they are able to hydrolyze acylcamitines, pal-mitoyl-CoA, and mono- and diacylglycerols [74a] [77] [97]. It has been speculated that these hydrolytic activities may facilitate the transfer of fatty acids across the endoplasmic reticulum and/or prevent the accumulation of mem-branolytic natural detergents such as carnitine esters and lysophospholipids. Plasma esterases are possibly also involved in fat absorption. In the rat, an increase in dietary fats was associated with a pronounced increase in the activity of ESI. In the mouse, the infusion of lipids into the duodenum decreased ESI levels in both lymph and serum, whereas an increase in ES2 levels was observed. In the lymph, the levels of ES2 paralleled triglyceride concentrations [92] [98],... 

Ginkgo alters lipid metabolism created by electroconvulsive shock treatments. EGb 761 reduced accumulation of free fatty acids and removal of diacylglycerol, which is more pronounced in the hippocampus than cerebral cortex (Rodriguez de Turco et al. 1993). Ginkgo also has protective effects on lipid membranes under hypoxic conditions. Bilobalide, but not ginkgolides, suppressed hydrolysis of choline induced... 

Rodriguez de Turco EB, Droy-Lefaix MT, Bazan NG. (1993). Decreased electroconvulsive shock-induced diacylglycerols and free fatty acid accumulation in the rat brain by Ginkgo biloba extract (EGb 761) selective effect in hippocampus as compared with cerebral cortex. J Neurochem. 61(4) 1438-44. 

Electroconvulsive shock (ECS), as well as ischemia, induces increases in free fatty add (FFA) and diacylglycerol (DAG) in the rat brain, probably due to the breakdown of membrane phospholipids through the activation of phospholipases (PLC, PLAj/A,). EGb treatment (100 mg/kg/day, p.o. for 14 days) selectively decreases endogenous FFA levels and increases endogenous DAG levels in the hippocampus. Therefore, ECS-induced accumulation of FFAis prevented in the hippocampus of EGb-treated rats during clonic seizures (30 sec to 2 min after... 

The mechanisms by which antitumor-promoters suppress the tumor promotion are not known, but may be due to the following effects (i) inhibition of polyamine metabolism (ii) inhibition of arachidonic acid metabolism (iii) protease inhibition (iv) induction of differentiation (v) inhibition of oncogene expression (vi) inhibition of PKC and (vii) inhibition of oxidative DNA damage [3,6,91]. The polyamine content of cells is correlated to their proliferative, and often, their neoplastic capabilities. A key enzyme in the polyamine biosynthetic pathway, ornithine decarboxylase (ODC), catalyzes the convertion of ornithine to putrescine. Phorbol ester promoters such as TPA cause increased ODC activity and accumulation of polyamines in affected tissues. Diacylglycerol activated PKC, and the potent tumor promoter, TPA, binds to, and activates PKC, in competition with diacylglycerol. PKC stimulation results in phosphorylation of regulatory proteins that affect cell proliferation. Some chemopreventive agents have inhibitory activity towards PKC. Refer to recent review articles for further discussion [3,6,91]. 

Epileptic seizures also stimulate CPLA2 activity and expression with accumulation of arachidonic acid (Visioli et al., 1994 Kajiwara et al., 1996). Levels of free fatty acids and diacylglycerols in rat brain rise rapidly with the onset of epileptic... 

Yen, C.L., Mar, M.H., and Zeisel, S.H., 1999, Chohne deficiency-induced apoptosis in PC12 cells is associated with diminished membrane phosphatidylcholine and sphingomyelin, accumulation of ceramide and diacylglycerol, and activation of a caspase. FASEB. J. 13 135-142... 

The de novo synthesis of phosphatidylcholine requires choline. In liver, phosphatidylcholine is synthesized and enters the membranes and lipoproteins. The dc novo synthesis of phosphatidylcholine also requires 1,2-diacylglycerol. If there is insufficient choline available, phosphatidylcholine production by the de novo pathway cannot occur. The 1,2-diacylglycerol is then converted to triacylglycerol. which accumulates, as it is not secreted in lipoproteins, by the liver. Therefore, the liver cells fill with triacylglycerol. 

Properties of Component Phases The composition and physicochemical properties of both the oil and aqueous phases influence the size of the droplets produced during homogenization (52). Variations in the type of oil or aqueous phase will alter the viscosity ratio, ri ,/ri(-, which determines the minimum size that can be produced under steady-state conditions. The interfacial tension of the oil-water interface depends on the chemical characteristics of the lipid phase, e.g., molecular structure or presence of surface-active impurities, such as free fatty acids, monoacylglycerols, or diacylglycerols. These surface-active hpid components tend to accumulate at the oil-water interface and lower the interfacial tension, thus lowering the amount of energy required to disrupt a droplet. 

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