Phosphatidylinositol and inositolphosphatide metabolism in hypertrophied rat heart
H. Saito, Y. Yamori, M. Minami, S.H. Parvez in New Advances in SHR Research –, 2020
Chemicals. D-[inositol-2-3H]-(l,4)-bisphosphate (2-10 Ci/mmol), D- [inositol-1-3H] (1, 4, 5)-trisphosphate (17 Ci/mmol), [inositol-l-3H] (1, 3, 4, 5)-tetrakisphosphate (17 Ci/mmol), and myo[2-3H] inositol (14.6 Ci/mmol) were obtained from New England Nuclear (Boston, MA, USA). [5,6, 8,9, 11,12, 14, 15-3H] arachidonic acid (163 Ci/mmol) was purchased from Amersham International (Amersham, UK). Ham F-10 medium was obtained from Flow Laboratories, Inc. (McLean, VA, USA). IP3 and IP4 were purchased from Dojindo Laboratories (Kumamoto, Japan). (2 3)-Diphospho-D-glyceric acid (2,3-DPG) was obtained from Sigma (St. Louis, MO, USA). AG 1x8 was obtained from BIO-RAD Laboratories (Richmond, CA, USA). Protein kinase assay system was purchased from Amersham International (Amersham, UK).
Boron, Manganese, Molybdenum, Nickel, Silicon and Vanadium
Judy A. Driskell, Ira Wolinsky in Sports Nutrition, 2005
Boron status apparently has an impact on energy metabolism during exercise training. Sedentary rats responded differently to changes in dietary boron than rats exercised on a powered running wheel.20,21 Exercise-trained rats, but not sedentary rats, had higher body weights, serum lactate dehydrogenase activity and serum creatinine concentrations when fed supplemental boron (2.0 mg B/kg diet) than when fed a low-boron diet (0.2 mg B/kg). In humans not involved in exercise training, blood urea nitrogen and creatinine concentrations were higher during boron depletion than during boron repletion.22 Boron deprivation increased serum glucose and decreased serum triglyceride concentrations.22 Dietary boron may affect glycolysis. In chicks, boron deprivation decreased the hepatic concentrations of fructose-1,6-biphosphate, glycerate-2-phosphate and dihydroxyace-tone phosphate23 and exacerbated the cholecalciferol deficiency-induced elevation in plasma glucose and decrease in serum triglycerides.23,24 These findings suggest that the utilization of energy from carbohydrate for exercise and the body’s intermediary metabolism response to exercise training are changed by boron deprivation.
Nutritional Ergogenic Aids: Introduction, Definitions and Regulatory Issues
Ira Wolinsky, Judy A. Driskell in Nutritional Ergogenic Aids, 2004
Relative to the data available for sodium bicarbonate and sodium citrate, fewer studies have investigated the effects of phosphate salts on exercise performance. The rationale for the effectiveness of phosphate salts is somewhat different from that of previously discussed blood buffers (sodium bicarbonate and sodium citrate). Additional effects of phosphate loading may occur due to an increased capacity to store intracellular inorganic phosphate, which may permit a greater quantity of creatine phosphate to be stored for use during short-duration bursts of exercise. With regard to aerobic activity, phosphate loading has been suggested to increase 2,3 diphospho-glycerate (2,3-DPG).44 Increased levels of 2,3-DPG may yield increased dissociation or release of oxygen from hemoglobin,45 thereby theoretically creating an opportunity to provide more oxygen to working tissues.
Mass spectrometry-based untargeted metabolomics study of non-obese individuals with non-alcoholic fatty liver disease
Published in Scandinavian Journal of Gastroenterology, 2023
Metin Demirel, Fatmanur Köktaşoğlu, Esin Özkan, Halime Dulun Ağaç, Ayşe Zehra Gül, Rasul Sharifov, Ufuk Sarıkaya, Metin Başaranoğlu, Şahabettin Selek
After processing the raw data obtained by mass spectrometry, metabolite annotation was performed, and the fold change analysis results of the metabolites showing significant differences between the groups were visualized. In individuals with NAFLD who were not obese, it was determined that the metabolites D-pantothenic acid, hypoxanthine, citric acid, citramalic acid, L-phenylalanine, glutamine, tramadol, 1,4-butynediol, DL-pyroglutamic acid, dehydroisoandrosterone sulfate (DHEA-S), 5-androsten-3-β,17-β-diol-3-sulfate, glyceric acid, D-ribose, and 5-αpregnan-3-α-,17-diol-20-one 3-sulfate were significantly higher compared to the non-obese healthy control group. On the other hand, it was found that the metabolites β-hydroxymyristic acid, histamine-trifluoromethyl-toluidide, DL-Lactic acid, and 3-methyl-2-oxopentanoic acid were significantly lower (Figure 1 and Table 2).
Prognostic value of neuron-specific enolase (NSE) for prediction of post-concussion symptoms following a mild traumatic brain injury: a systematic review
Published in Brain Injury, 2018
Eric Mercier, Pier-Alexandre Tardif, Peter A. Cameron, Marcel Émond, Lynne Moore, Biswadev Mitra, Marie-Christine Ouellet, Jérôme Frenette, Elaine de Guise, Natalie Le Sage
In humans, NSE is a major protein of the brain, constituting between 0.4% and 2.2% of its total soluble protein (16) and experimental data suggest that it reaches peripheral blood through the lymphatic system (18). More precisely, NSE is a 78 kDa dimeric enzyme with a half-life of approximately 24 hours (16). It is the dominant enolase isoenzyme found mostly in neuronal (γγ-dimer) and peripheral neuroendocrine tissues (a mixture of γ and α units) (15,16,19). NSE plays an essential role in the glycolytic pathway by catalysing the dehydration of 2-phospho-D-glycerate (PGA) to phosphoenolpyruvate (PEP) and conversely the hydration of PEP to PGA (16). Its relevance as a biomarker of differential diagnosis is well acknowledged in small cell lung cancer and suggested in neuroendocrine tumours and neuroblastoma (16). In addition, NSE seems to be a marker of injury in patients with a TBI (20–25), including mild TBI (15,26). After a TBI, its peak value seems to be reached within 6–12 hours of injury (15,18,20,27). More recently, elevated serum and cerebrospinal fluid levels of NSE were shown to be associated with death and life-long neurologic disabilities in patients who incurred a moderate or severe TBI (28). However, its predictive value for prediction of post-concussion symptoms in patients with a mild TBI remains unclear.
From pathogenesis to novel therapies in primary hyperoxaluria
Published in Expert Opinion on Orphan Drugs, 2019
Gill Rumsby, Sally-Anne Hulton
This disorder accounts for approximately 10% of primary hyperoxaluria and is caused by a deficiency of glyoxylate reductase/hydroxypyruvate enzyme (GR/HPR), a cytosolic enzyme that is present in most tissues but with highest expression and activity in the liver [7,8]. Under normal metabolic conditions, the higher levels of the cofactor NADPH in the cytosol favor glyoxylate reduction by GR/HPR rather than oxidation by LDH [9]. The enzyme can also reduce hydroxypyruvate to D-glycerate in the gluconeogenic pathway from serine (Figure 1). GR/HPR deficiency is manifested by an accumulation of cytosolic glyoxylate and hydroxypyruvate which are metabolized to oxalate and L-glycerate, respectively, by LDH and excreted in the urine.
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