Factors affecting the free fatty acids in rat brain cortex

Tang, Wilson; Sun, Grace Y.

doi:10.1016/0197-0186(82)90063-8

Cited by 44 publications

(17 citation statements)

References 16 publications

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“…Results of this study confirm the earlier observations indicating the biphasic mode of FFA release in brain as a result of global cerebral ischemia (Tang and Sun, 1982;Yasuda et al, 1985;Ikeda et al, 1986) and that 18:0 and 20:4 are preferentially released during the initial period (Aveldano and Bazan, 1975a;Bazan et al, 1981). Furthermore, it is also clear that FFA are continuously released during the 30 min whereas DG release can only be observed during the initial period (1.5 min).…”

Section: Discussionsupporting

confidence: 81%

Section: Is ^1mentioning

confidence: 99%

“…An interesting aspect of the FFA release resulting from the decapitation ischemia is the preferential release of 18:0 and 20:4, especially during the initial time period (Aveldano and Bazan, 1975a;Bazan et al, 1981;Tang and Sun, 1982). The biphasic mode of FFA release during decapitation ischemia suggests that more than one biochemical pathway is responsible for this event (Tang and Sun, 1982;Yasuda et al, 1985;Ikeda et al, 1986). Although the exact mechanism(s) contributing to the FFA release has not yet been clearly elucidated, there is the notion that FFA release may involve both activation of the phospholipase A2 pathway and sequential hydrolysis of poly-PI and DG by phospholipase C and DG-lipase (see reviews by Bazan, 1975;Sun, 1990Sun, , 1991.…”

Section: Is ^1mentioning

confidence: 99%

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Decapitation ischemia-induced release of free fatty acids in mouse brain

Sun

Lin

et al. 1992

Molecular and Chemical Neuropathology

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In this study, the release of lysophospholipids (to depict phospholipase A2 activity) and diacylglycerols (DG) (to depict stimulated hydrolysis of polyphosphoinositides) was related to the decapitation-induced release of free fatty acid (FFA) in the mouse brain. To assay for lysophospholipids, Balb/c mice were injected intracerebrally with either [3H]choline or [3H]inositol for 16 h in order to label their respective phospholipids. These lipids were examined at various times (30 s to 30.5 min) after decapitation. Between 30 s and 1.5 min after decapitation, the rate of FFA release (3 micrograms FA/mg FA in phospholipids/min) was three times more rapid than that between 10 and 15 min (0.8 microgram FA/mg FA in phospholipids/min). FFA released during the initial phase were enriched in 20:4 and 18:0 whereas those released during the latter phase were nonspecific. The DG fatty acids are enriched in 18:0 and 20:4. Ischemia induced a rapid release of DG as measured by its fatty acid content (3.2 micrograms FA/mg FA in phospholipids/min). Unlike FFA, the level of DG reached a plateau after 1.5 min and remained elevated for the entire 30.5 min. In agreement with previous notions indicating the involvement of phospholipase A2 in ischemic insult, steady increases in radioactivity of both lysophosphatidylcholines and lysophosphatidylinositols were observed with time after decapitation. Based on the preferential increase in both 18:0 and 20:4 during the initial time period, the results suggest that poly-PI hydrolysis coupled to DG-lipase may contribute to the initial release of FFA, whereas the FFA released subsequent to the initial phase may be mainly a result of activation of phospholipase A2 acting on phosphatidylcholines and phosphatidylinositols.

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Section: Discussionsupporting

confidence: 81%

Section: Is ^1mentioning

confidence: 99%

Section: Is ^1mentioning

confidence: 99%

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Decapitation ischemia-induced release of free fatty acids in mouse brain

Sun

Lin

et al. 1992

Molecular and Chemical Neuropathology

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“…It is generally accepted that free fatty acids (FFA) increase in the brain under ischemic conditions (Bazan, 1970;Bazan et al, 1971;Galli and Spagnuolo, 1976;De Medio et al, 1980;Tang and Sun, 1982;Yoshida et al, 1982) and that FFA is released from membrane phospholipids by phospholipases C and A. Phosphatidylinositol (PI), phosphatidylinositol 4-phosphate (PIP), and phosphatidylinositol 4, 5-bisphosphate (PIP 2) are closely linked to cellular signal transduction mechanism. The above phospholipids are rich in arachidonic acid and stearic acid (Baker and Thompson, 1972;Michell, 1975;Berridge, 1984).…”

Section: Introductionmentioning

confidence: 99%

Changes of polyphosphoinositides, lysophospholipid, and free fatty acids in transient cerebral ischemia of rat brain

Kinouchi

Imaizumi

Yoshimoto

et al. 1990

Molecular and Chemical Neuropathology

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Phosphatidylinositol (PI), phosphatidylinositol 4-phosphate (PIP), phosphatidylinositol 4, 5-bisphosphate (PIP2), 1, 2-diglyceride (DG), lysophosphatidylcholine (LPC), and free fatty acids (FFA) contents, as well as their fatty acid composition, were measured in transient global cerebral ischemia. ATP and CTP were also studied. Male Wistar rats were subjected to 1, 5, and 30 min of ischemia and 10, 30, and 60 min of recirculation following 30 min of ischemia. In addition, for the quantification of PI, PIP, and PIP2, rats were also subjected to 30 and 60 min of recirculation following 5 min of ischemia. PIP2 and PIP decreased rapidly during 5 min of ischemia and recovered completely after recirculation. DG increased almost at the same rate during ischemia and returned to normal after recirculation. PI showed almost no changes throughout entire course. LPC increased during 5 min of ischemia and returned to normal after recirculation. Stearic acid and arachidonic acid contained in DG increased during 5 min of ischemia, whereas saturated fatty acids increased in LPC. Among the FFA accumulated during ischemia, stearic acid and arachidonic acid increased rapidly and were followed by increases of other FFA. From these results, the pathways for the increase of FFA during ischemia and the fate of FFA after recirculation are discussed. In addition, the importance of the changes of PIP, PIP2, and LPC is also discussed.

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“…During the initial phase, in a onefold increase in the DG level. The decapitative arachidonic and stearic acids are preferentially released model resulted in a one-and fivefold increase in FFA [Tang and Sun, 1982; Yasuda et al, 19851. The biphasic level (with respect to 1 and 5 min, respectively), mode suggests that more than one biochemical mechawhereas ligation for 1 min resulted in an increase of nism is responsible for the FFA release owing to decap-42% of the FFA.…”

mentioning

confidence: 99%

Acidic phospholipids, diacylglycerols, and free fatty acids in gerbil brain: A comparison of ischemic changes resulting from carotid ligation and decapitation

Huang

Sun

1987

J of Neuroscience Research

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The levels of brain acidic phospholipids (poly-PI, PI, PA, and PS), DG, and FFA and their acyl group profiles were determined after induction of ischemia in gerbils by ligation of the common carotid arteries and decapitation. Ischemia induced by both procedures resulted in a significant decrease in poly-PI (20% for 1-min decapitation and 1-min ligation). Except for a 16% increase in PI in the 5-min decapitation group, no apparent change was found in other phospholipids after either ischemic condition. The level of DG was increased one- and three-fold after 1 and 5 min, respectively, of decapitative ischemic treatment. Ligation of the carotid arteries for 1 min resulted also in a one-fold increase in the DG level. The decapitative model resulted in a one- and five-fold increase in FFA level (with respect to 1 and 5 min, respectively), whereas ligation for 1 min resulted in an increase of 42% of the FFA. The acyl groups of poly-PI and PI in the control gerbil brain are enriched in 18:0 and 20:4, but those of DG, FFA, and PA have a higher proportion of 16:0 besides 18:0 and 20:4. However, a preferential increase in the proportion of 18:0 and 20:4 was shown for the DG and FFA in both types of ischemic treatments. It is concluded from the results that both models of ischemic treatment elicit a similar decrease in poly-PI and increase in DG, but differ in the amount of FFA release. The higher level of FFA release in the decapitative model suggests that other biochemical mechanisms may be activated to cause the additional release.

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Factors affecting the free fatty acids in rat brain cortex

Cited by 44 publications

References 16 publications

Decapitation ischemia-induced release of free fatty acids in mouse brain

Decapitation ischemia-induced release of free fatty acids in mouse brain

Changes of polyphosphoinositides, lysophospholipid, and free fatty acids in transient cerebral ischemia of rat brain

Acidic phospholipids, diacylglycerols, and free fatty acids in gerbil brain: A comparison of ischemic changes resulting from carotid ligation and decapitation

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