Simultaneously quantitative measurement of comprehensive profiles of esterified and non-esterified fatty acid in plasma of type 2 diabetic patients

Yi, Lunzhao; He, Jun; Liang, Yi‐Zeng; Yuan, Dian; Gao, Haiyan; Zhou, Hong‐Hao

doi:10.1016/j.chemphyslip.2007.08.002

Cited by 64 publications

(46 citation statements)

References 24 publications

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“…Although the majority of studies examining the deleterious effects of FA have been performed using saturated FA, LA is a major component of NEFA, and its concentration is significantly elevated in diabetes (29). The PIMCE response to LA and other PUFA may account for a portion of the adverse effects of NEFA, especially at the mitochondrial level, whereas saturated and monounsaturated FA may exert their effects via other pathways.…”

Section: Discussionmentioning

confidence: 99%

“…NEFA in animal and human plasma and tissues are composed of saturated FA, monounsaturated FA, and PUFA (29), and there is evidence that the deleterious effects of these different types of FA may be mediated by distinct cellular pathways. For example, a recent study indicates that saturated and monounsaturated FA, but not PUFA, are effective in increasing cellular levels of diacylglycerol and thus causing stimulation of protein kinase C (30).…”

Section: Discussionmentioning

confidence: 99%

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Heat Shock Protein 90β1 Is Essential for Polyunsaturated Fatty Acid-induced Mitochondrial Ca2+ Efflux

Zhang

et al. 2008

Journal of Biological Chemistry

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Defective mitochondrial function has been observed in type 2 diabetes and is proposed to be a major contributing factor in the pathogenesis and progression of the disease (1, 2). Although the mechanism leading to mitochondrial dysfunction in diabetes remains under intensive investigation, a critical role for nonesterified fatty acids (NEFA) 2 and/or fatty acid metabolites is emphasized by an increasing body of evidence (3-5). NEFA may influence mitochondrial function by alterations in gene expression (6), metabolism (7), and/or mitochondrial Ca 2ϩ homeostasis (8, 9). Ionic Ca 2ϩ in the mitochondria regulates substrate oxidation by activation of mitochondrial dehydrogenases (9). Deficiency of pyruvate dehydrogenase (PDH) activity in pancreatic islet ␤-cells (10), cardiomyocytes (11), and skeletal muscles (7, 12, 13) has been demonstrated in diabetes. The degree to which PDH is dephosphorylated (i.e. the balance between phosphorylation and dephosphorylation) determines the level of enzyme activity. The concentration of mitochondrial Ca 2ϩ ([Ca 2ϩ ] m ) is an important activator of PDH phosphatase, which dephosphorylates and activates PDH. Additionally, [Ca 2ϩ ] m has been shown to activate at least three other mitochondrial dehydrogenases (i.e. glycerol 3-phosphate dehydrogenase, NAD-linked isocitrate dehydrogenase, and 2-oxoglutarate dehydrogenase), all of which play important roles in substrate oxidation (9). NEFA, which are chronically elevated in type 2 diabetes, inhibit PDH by mechanisms thought to involve FA oxidation and elevation of acetyl-CoA. We have previously reported that polyunsaturated fatty acids (PUFA) induce Ca 2ϩ efflux from mitochondria (8), an action that could deplete [Ca 2ϩ ] m and thus contribute to NEFA-responsive reduction of PDH activity and mitochondrial dysfunction. The PUFA-induced mitochondrial Ca 2ϩ efflux (PIMCE) cannot be blocked with cyclosporine A and bongkrekic acid, two inhibitors of the mitochondrial permeability transition pore. However, the pathway(s) underlying PIMCE has not previously been defined.In the current work, we have used proteomic analysis to demonstrate a parallel reduction in PIMCE and the level of heat shock protein 90␤1 (hsp90␤1) in NT2 cells treated with retinoic acid (RA). Further studies with pharmacological inhibitors and RNA interference (RNAi) indicate that hsp90␤1 plays an essential role in PIMCE in NT2 cells.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Heat Shock Protein 90β1 Is Essential for Polyunsaturated Fatty Acid-induced Mitochondrial Ca2+ Efflux

Zhang

et al. 2008

Journal of Biological Chemistry

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“…Рассмотренные дериватизирующие агенты, такие как гидроксид триметилсулфония [8,9], BF 3 в MeOH [10,11], HCl в MeOH [12,13], NaOH + BF 3 [14,15], AcCl в MeOH [7] -способны с различной эффективно-стью этерифицировать СЖК, в то время как обра-ботка пробы раствором KOH в MeOH [7] -это спо-соб селективной дериватизации ЭЖК. В работе [16] предложено поэтапное метилирование СЖК и ЭЖК. Для этого сначала метилировали ЭЖК с помощью раствора NaOH в MeOH и извлекали из плазмы об-разовавшиеся метиловые эфиры.…”

Section: Introductionunclassified

GС-MS quantification of free and esterified fatty acids in blood plasma

Орлова¹,

Ukolov²,

Savel’eva³

et al. 2015

АиК

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“…Various analytical approaches like enzymatic, spectrophotometric and chromatographic based procedures, such as high performance liquid chromatography (HPLC) and gas chromatography (GC), have been employed for the analysis of fatty acids [7,8,[19][20][21][22]. GC coupled to mass spectrometer (MS) is the mostly employed technique for the evaluation of fatty acids in samples [7][8]23,24]. In order to develop fatty acid profile through GC, it is required that the fatty acids must be gaseous phase.…”

Section: Introductionmentioning

confidence: 99%

Quantification of methyl esters of fatty acids in the oil of Physalis minima by GC-MS

Qureshi¹,

Wajid²,

Inayat-ur-Rahman³

2015

JCLM

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Simultaneously quantitative measurement of comprehensive profiles of esterified and non-esterified fatty acid in plasma of type 2 diabetic patients

Cited by 64 publications

References 24 publications

Heat Shock Protein 90β1 Is Essential for Polyunsaturated Fatty Acid-induced Mitochondrial Ca2+ Efflux

Heat Shock Protein 90β1 Is Essential for Polyunsaturated Fatty Acid-induced Mitochondrial Ca2+ Efflux

GС-MS quantification of free and esterified fatty acids in blood plasma

Quantification of methyl esters of fatty acids in the oil of Physalis minima by GC-MS

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