A spectrophotometric method for the determination of free fatty acid in serum using acyl-coenzyme A synthetase and acyl-coenzyme A oxidase

Matsubara, Chiyo; Nishikawa, Yuji; Yoshida, Yasushi; Takamura, Kiyoko

doi:10.1016/0003-2697(83)90659-0

Cited by 94 publications

(50 citation statements)

References 18 publications

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“…We determined via HPLC analysis that greater than 80% of the radioactivity released into the extracellular space by NMDA stimulation was AA and not a metabolite. 2 …”

Section: Methodsmentioning

confidence: 99%

“…AMPA is not an effective stimulus for AA release in cortical cell cultures either (53). 2 Finally, a recent report demonstrated that activation of group I mGluRs augments injury-induced AA release from rat cortical cultures, a process presumably mediated via NMDA receptors (59), lending further support to this idea of functional synergy.…”

Section: Fig 6 Astrocytes Do Not Contribute To Stimulated [mentioning

confidence: 95%

“…Although many of the cellular and molecular mechanisms that lead to ischemic cell death have been described, efficacious methods of intervention remain elusive. Brain levels of free fatty acids, specifically arachidonic acid (AA), 1 can be released rapidly during cerebral ischemia and can reach up to 10-fold higher concentrations than levels estimated during normal physiological conditions (1,2). Thus, it is perhaps not surprising that pharmacological inhibition of AA metabolism has proven to be an effective strategy for ameliorating cerebral ischemic damage in animal models (3)(4)(5)(6)(7), perhaps through inhibition of deleterious metabolite (8 -11) and/or oxygen-derived free radical formation (8,(12)(13)(14)(15).…”

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confidence: 99%

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Potassium-evoked Glutamate Release Liberates Arachidonic Acid from Cortical Neurons

Taylor

Hewett

2002

Journal of Biological Chemistry

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Ischemic cell death in the brain accompanies any condition characterized by a significant interruption in cerebral blood flow, including stroke and head trauma. Although many of the cellular and molecular mechanisms that lead to ischemic cell death have been described, efficacious methods of intervention remain elusive. Brain levels of free fatty acids, specifically arachidonic acid (AA), 1 can be released rapidly during cerebral ischemia and can reach up to 10-fold higher concentrations than levels estimated during normal physiological conditions (1, 2). Thus, it is perhaps not surprising that pharmacological inhibition of AA metabolism has proven to be an effective strategy for ameliorating cerebral ischemic damage in animal models (3-7), perhaps through inhibition of deleterious metabolite (8 -11) and/or oxygen-derived free radical formation (8,(12)(13)(14)(15). However, AA itself can have effects independent from its metabolites, some of which can have deleterious consequences for a cell. For instance, AA may directly decrease membrane integrity by acting as a detergent, thereby altering membrane fluidity (16). Further, AA directly enhances NMDA receptor currents (17) and may enhance the concentration of glutamate in the synaptic cleft by increasing its release (18,19) and/or blocking its reuptake (20 -22). These effects could potentiate excitotoxicity, a major contributor to ischemic cell death (23). In addition, unesterified AA has been reported to inhibit mitochondrial respiration (24, 25) and may directly signal apoptosis through the concomitant activation of caspase 3 (26) and down-regulation of bcl-2 (27). Given this, inhibition of AA release from cellular membranes may be a more effective neuroprotective strategy than inhibition of its metabolism alone. Thus, it is of great import to understand the mechanism by which AA is released following cerebral ischemia.Since a large rise in extracellular [K ϩ ] (up to 60 mM) has been measured during cerebral ischemia (16, 28), we questioned whether this might be a trigger for AA release. Studies addressing this question are discrepant. Rat cortical synaptosomes (i.e. isolated nerve terminals) or isolated cerebellar glomeruli release AA when bathed in a depolarizing K ϩ buffer (29 -31), but primary cultures of striatal or hippocampal neurons do not (32-34). The ability of elevated [K ϩ ] o to stimulate AA release from intact cortical cells, which are highly susceptible to cerebral ischemic damage, has not been explored. Thus, the aim of the present study was to determine whether a rise in extracellular [K ϩ ] was a sufficient stimulus for AA release in a murine mixed cortical cell culture system, and if so, by what mechanism. Part of this work has appeared in abstract form (35). EXPERIMENTAL PROCEDURESMaterials-MK-801 (dizocilpine maleate) and CNQX (6-cyano-7-nitroquinoxaline-2,3-dione) were purchased from Research Biochemicals Inc. (Natick, MA). DL-threo-␤-benzyloxyaspartate was purchased from Tocris (Ellisville, MO). CdCl 2 , iodoacetamide, and triethanolami...

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“…We determined via HPLC analysis that greater than 80% of the radioactivity released into the extracellular space by NMDA stimulation was AA and not a metabolite. 2 …”

Section: Methodsmentioning

confidence: 99%

Section: Fig 6 Astrocytes Do Not Contribute To Stimulated [mentioning

confidence: 95%

mentioning

confidence: 99%

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Potassium-evoked Glutamate Release Liberates Arachidonic Acid from Cortical Neurons

Taylor

Hewett

2002

Journal of Biological Chemistry

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“…Nonesterified fatty acid (NEFA) and glucose concentrations were determined by automated analysis, with sensitivity and intra-and inter-assay CV values of 0·04 mmol/l, 2·0 and 4·0% respectively for NEFA (Matsubara et al 1983), and 0·34 mmol/l, 0·35 and 2·3% respectively for glucose (Peterson & Young 1968). Leptin concentrations were determined by homologous RIA (Marie et al 2001) in a single assay with a sensitivity of 0·45 ng/ml and intra-assay CV of 12·0%.…”

Section: Hormone and Metabolite Analysesmentioning

confidence: 99%

Contrasting effects of different levels of food intake and adiposity on LH secretion and hypothalamic gene expression in sheep

Archer¹,

Rhind²,

Findlay³

et al. 2002

Journal of Endocrinology

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Body reserves (long-term) and food intake (short-term) both contribute nutritional feedback to the hypothalamus. Reproductive neuroendocrine output (GnRH/LH) is stimulated by increased food intake and not by high adiposity in sheep, but it is unknown whether appetiteregulating hypothalamic neurons show this differential response. Castrated male sheep (Scottish Blackface) with oestradiol implants were studied in two 4 week experiments. In Experiment 1, sheep were fed to maintain the initial body condition (BC) score of 2·0 0·00 (lower BC (LBC), n=7) or 2·9 0·09 (higher BC (HBC), n=9), and liveweight of 43 1·1 and 59 1·6 kg respectively. LBC and HBC sheep had similar mean plasma LH concentration, pulse frequency and amplitude, but HBC animals had higher mean plasma concentrations of insulin (P<0·01), leptin (P<0·01) and glucose (P<0·01). Gene expression (measured by in situ hybridisation) in the hypothalamic arcuate nucleus (ARC) was higher in LBC than HBC sheep for neuropeptide Y (NPY; 486% of HBC, P<0·01), agouti-related peptide (AGRP; 467%, P<0·05) and leptin receptor (OB-Rb; 141%, P<0·05), but lower for cocaine-and amphetamine-regulated transcript (CART; 92%, P<0·05) and similar between groups for pro-opiomelanocortin (POMC). In Experiment 2, sheep with initial mean BC score 2·4 0·03 and liveweight 55 0·8 kg were fed a liveweight-maintenance ration (low intake, LI, n=7) while sheep with initial mean BC score 2·0 0·03 and liveweight 43 1·4 kg were fed freely so that BC score increased to 2·5 0·00 and liveweight increased to 54 1·4 kg (high intake, HI, n=9). Compared with LI, HI sheep had higher mean plasma LH (P<0·05), baseline LH (P<0·01) and pulse amplitude (P<0·01) and showed a trend towards higher pulse frequency. Although there were no differences in final mean plasma concentrations, there were significant increases over time in mean concentrations of insulin (P<0·001), leptin (P<0·05) and glucose (P<0·001) in HI sheep. Gene expression for AGRP in the ARC was higher in HI than LI animals (453% of LI; P<0·05), but expression levels were similar for NPY, OB-Rb, CART and POMC. Thus, the hypothalamus shows differential responses to steady-state adiposity as opposed to an increase in food intake, in terms of both reproductive neuroendocrine activity and hypothalamic appetiteregulating pathways. Differences in hypothalamic gene expression were largely consistent with contemporary levels of systemic leptin and insulin feedback; however, increased nutritional feedback was stimulatory to GnRH/LH whereas constant high feedback was not. The hypothalamus therefore has the ability to retain a nutritional memory that can influence subsequent responses.

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“…progestérone / métabolite fécal de progestérone / vache laitière Australia); blood NEFAs using the Acyl CoA synthetase coupled enzymatic system (Randox, Australia) with Randox reagents [15]; blood BHB using 3HBDeOH enzymatic system [17]; and blood urea was measured using an enzymatic reaction (Trace Scientific, Australia) [40].…”

Section: Animals and Experimental Protocolmentioning

confidence: 99%

Excretion rate of progesterone in milk and faeces in lactating dairy cows with two levels of milk yield

2001

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-This study was conducted to measure the effect of the level of daily milk yield on the excretion rate of progesterone (P4) in milk and faeces in high-producing (HP) and low-producing (LP) lactating dairy cows. A GnRH-agonist was implanted to block endogenous production of P4. A CIDR device was inserted into the vagina and left in place for 11 days. The average and peak milk yields were greater in HP cows (P < 0.0001). Mean plasma concentrations of P4 were also similar in both groups (P = 0.44), even though the average mass of P4 delivered from a CIDR device was higher with HP cows (P = 0.02). Average milk P4 concentration was similar in both groups (P = 0.81), so that average daily excretion of P4 in the milk was greater with HP cows (P = 0.05). The concentrations (P = 0.83) and daily yields (P = 0.4) of total faecal progesterone metabolites were not affected by level of milk yield. These data show that the concentrations of plasma and milk P4, and the concentration and yield of P4 metabolites are not affected by the levels of daily milk yield.progesterone / faecal progesterone metabolite / dairy cow Résumé -Taux d'élimination de la progestérone dans le lait et les fèces des vaches laitières selon leur production de lait. Cette étude a pour but de mesurer le taux d'élimination de la progestérone (P4) dans le lait et les fèces chez des vaches à haute (HP) ou basse (LP) production laitière quotidienne. Un agoniste de GnRH a été implanté pour bloquer la production endogène de P4. Un dispositif CIDR a été inséré dans le vagin et laissé en place pendant 11 jours. Les productions laitières moyennes ou maximum ont été plus élevées (P < 0,0001) chez les vaches HP que chez les LP. Dans le plasma, les concentrations moyennes de P4 ont été similaires dans les deux lots (P = 0,44) bien que la quantité moyenne de P4 libérée par le CIDR ait été plus élevée chez les vaches HP (P = 0,02). Dans le lait, la concentration moyenne de P4 a été équivalente dans les deux lots (P = 0,81). Ceci signifie que l'excrétion moyenne de P4 dans le lait a été supérieure chez les vaches HP par comparaison aux LP (P = 0,05). Les concentrations (P = 0,83) et les excrétions journalières (P = 0,40) des métabolites fécaux Reprod. Nutr. Dev. 41 (2001) [309][310][311][312][313][314][315][316][317][318][319] 309

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A spectrophotometric method for the determination of free fatty acid in serum using acyl-coenzyme A synthetase and acyl-coenzyme A oxidase

Cited by 94 publications

References 18 publications

Potassium-evoked Glutamate Release Liberates Arachidonic Acid from Cortical Neurons

Potassium-evoked Glutamate Release Liberates Arachidonic Acid from Cortical Neurons

Contrasting effects of different levels of food intake and adiposity on LH secretion and hypothalamic gene expression in sheep

Excretion rate of progesterone in milk and faeces in lactating dairy cows with two levels of milk yield

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