Anxiety disturbs the blood plasma metabolome in acute coronary syndrome patients
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Abstract Coronary heart disease (CHD) is the result of a complex metabolic disorder caused by various environmental and genetic factors, and often has anxiety as a comorbidity. Rupture of atherosclerotic plaque in CHD patients can lead to acute coronary syndrome (ACS). Anxiety is a known independent risk factor for the adverse cardiovascular events and mortality in ACS, but it remains unclear how stress-induced anxiety behavior impacts their blood plasma metabolome and contributes to worsening of CHD. The present study aimed to determine the effect of anxiety on the plasma metabolome in ACS patients. After receiving ethical approval 26 ACS patients comorbid anxiety were recruited and matched 26 ACS patients. Blood plasma samples were collected from the patients and stored at − 80 °C until metabolome profiling. Metabolome analysis was performed by liquid chromatography mass spectrometry (LC–MS), and the data were subjected to multivariate analysis. Disturbance of 39 plasma metabolites was noted in the ACS with comorbid anxiety group compared to the ACS group. These disturbed metabolites were mainly involved in tryptophan metabolism, pyrimidine metabolism, glycerophospholipid metabolism, pentose phosphate pathway, and pentose and glucuronate interconversions. The most significantly affected pathway was tryptophan metabolism including the down-regulation of tryptophan and serotonin. Glycerophospholipids metabolism, pentose and glucuronate interconversions, and pentose phosphate pathway were also greatly affected. These results suggest that anxiety can disturb three translation of material in ACS patients. Besides the above metabolism pathways pyrimidine metabolism was significantly disturbed. Based on the present findings the plasma metabolites monitoring can be recommended and may be conducive to early biomarkers detection for personalized treatment anxiety in CHD patients in future.Keywords:
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Abstract Under physiological conditions, erythrocytes of the horse metabolized 638 ± 37 (± SE) nmoles glucose/ml cells/hr at 37°C compared to 942 ± 31 for the cat, 1,329 ± 44 for the dog, and 1,485 ± 43 for man. On an absolute basis, pentose phosphate metabolism was similar between species, with species differences in erythrocyte glucose utilization attributable to differences in Embden‐Meyerhof pathway metabolism. By examining pentose phosphate pathway recycling, it appears that some functional compartmentation exists within erythrocytes.
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Abstract Coronary heart disease (CHD) is the result of a complex metabolic disorder caused by various environmental and genetic factors, and often has anxiety as a comorbidity. Rupture of atherosclerotic plaque in CHD patients can lead to acute coronary syndrome (ACS). Anxiety is a known independent risk factor for the adverse cardiovascular events and mortality in ACS, but it remains unclear how stress-induced anxiety behavior impacts their blood plasma metabolome and contributes to worsening of CHD. The present study aimed to determine the effect of anxiety on the plasma metabolome in ACS patients. After receiving ethical approval 26 ACS patients comorbid anxiety were recruited and matched 26 ACS patients. Blood plasma samples were collected from the patients and stored at − 80 °C until metabolome profiling. Metabolome analysis was performed by liquid chromatography mass spectrometry (LC–MS), and the data were subjected to multivariate analysis. Disturbance of 39 plasma metabolites was noted in the ACS with comorbid anxiety group compared to the ACS group. These disturbed metabolites were mainly involved in tryptophan metabolism, pyrimidine metabolism, glycerophospholipid metabolism, pentose phosphate pathway, and pentose and glucuronate interconversions. The most significantly affected pathway was tryptophan metabolism including the down-regulation of tryptophan and serotonin. Glycerophospholipids metabolism, pentose and glucuronate interconversions, and pentose phosphate pathway were also greatly affected. These results suggest that anxiety can disturb three translation of material in ACS patients. Besides the above metabolism pathways pyrimidine metabolism was significantly disturbed. Based on the present findings the plasma metabolites monitoring can be recommended and may be conducive to early biomarkers detection for personalized treatment anxiety in CHD patients in future.
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Repeated supercoolings down to rectal temperatures (19-20 degrees C) results in the different changes in the dehydrogenase activity of pentose and glucuronate pathways in the rat brain: the activity of the pentose cycle oxidative enzymes (glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase) lowers considerably and that of VDP-glucose dehydrogenase rises. The dehydrogenase activity in the pentose cycle is found to be inhibited in rats cooled for the first time, the UDP-glucose dehydrogenase activity being preserved at the control level. In the adapted rats the cooling causes mobilization of the pentose cycle, the UDP-glucose dehydrogenase activity remains unchanged.
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The pentose phosphate pathway operates at an elevated level in rat kidney following induction of diabetes and in the compensatory hypertrophy following unilateral nephrectomy in control and alloxan‐diabetic rats, as shown by the yields of 14 Co 2 from [1‐ 14 C]glucose, [6‐ 14 C]glucose and 3 H 2 O yields from [2‐ 3 H]glucose. The elevated flux through the pentose phosphate pathway is correlated with the increased RNA content and weight of the kidney. The direct utilization of NADPH for reductive synthetic reactions and the potential for indirect utilization via the sorbitol route and the linked transhydrogenase reactions of the glucuronate‐xylulose pathway, for NADH and ATP generation, are also discussed.
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Studies in this laboratory designed to elucidate the metabolism of L-xylulose, the characteristic urinary sugar of essential pentosuria, have shown that n-glucuronolactone is a precursor of the ketopentose in guinea pigs and in humans (1, 2) and that there are enzymes in guinea pig liver which can interconvert L-xylulose and xylitol as well as xylitol and D-xylulose (3, 4). The discovery that n-xylulose 5-phosphate is an intermediate in the pentose phosphate shunt (6-phosphogluconate oxidation pathway) (5, 6) suggested that glucuronate and the xyluloses might be ultimately metabolized via this pathway (4, 7). A kinase has indeed been found in calf liver which can convert n-xylulose to n-xylulose 5-phosphate (8). These findings suggest that the following sequence of reactions occurs in mammals: n-glucuronate --) L-xylulose G= xylitol ti n-xylulose + D-xylulose 5-phosphate. Since the formulation of this sequence is based upon work done on different species and partly on enzymatic studies performed in vitro, it seemed desirable to obtain evidence in tivo regarding its physiological occurrence. The tracer experiments reported elsewhere (2) have demonstrated the conversion of n-glucuronolactone to L-xylulose in a pentosuric human through reactions involving loss of the carboxyl carbon of the former compound, with the aldehydic carbon becoming the fifth carbon of the pentose. The present paper reports a study of the metabolic fate of a compound which is intermediate in the reaction sequence shown above. Xylitol-l-Cl4 was chosen because it can be conveniently prepared from the readily available n-xylose-1-CY4. n-Ribose, known to be metabolized via the pentose phosphate shunt (9), and n-xylose were tested for comparative purposes. A recent report has shown that the latter is also metabolized via this pathway (10). It was first demonstrated that xylitol is oxidized in vivo to carbon dioxide. A study was then undertaken to determine whether the distribution of
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Phosphoribosyl pyrophosphate (PPRibP), required in nucleotide synthesis, increases 2-fold in rat kidney from 1 day post partum to adult stage; there is no accompanying increase in PPRibP synthetase activity measured in vitro. Ribose 5-phosphate is a key factor in the regulation of PPRibP synthesis. The activity and regulation of 3 routes of ribose 5-phosphate formation have been measured in renal growth: (i) the flux through the oxidative pentose phosphate pathway was high in the neonatal period but increased only +50% thereafter; (ii) the non-oxidative pentose phosphate pathway, including transketolase, increased by +145%; (iii) the rate-limiting enzymes of the glucuronate-xylulose route increased +200% from 1 day to the adult stage. The importance of systems reoxidizing NADPH was shown by: (i) the stimulation of renal PPRibP formation from glucose by phenazine methosulphate; (ii) the early involvement of the oxidative pentose phosphate pathway at the stage where NADPH is used for biosynthetic routes; (iii) the increasing involvement of the glucuronate-xylulose route, which acts as a transhydrogenase producing NADP+ in addition to pentose phosphate formation and (iv) the correlation between renal PPRibP content and the activity of aldose reductase, which, by utilization of NADPH, stimulates ribose 5-phosphate formation via the oxidative pentose phosphate pathway. Evidence is adduced that the contribution of the 3 routes of ribose 5-phosphate formation in the kidney varies at different stages of development.
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