[Effect of vitamin E deficiency on creatine phosphokinase activity and creatine phosphate levels in the heart muscle].
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Vitamin E deficient diet of rats developed impairments in energy metabolism of myocardium, involving a decrease in content of creatine phosphate and in the activity of creatine phosphokinase by 20-35%. Concentration of adenine nucleotides was not altered in myocardium and the content of glycogen was only slightly changed. The impairments in activity of creatine phosphokinase and in the content of creatine phosphate might be among the factors responsible for deterioration of the heart muscle contractile functions in avitaminosis E.Keywords:
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ABSTRACT Purine nucleotides (ATP, ADP, AMP, IMP), creatine, phosphocreatine, lactate, pyruvate and glycogen were measured in rainbow trout (Oncorhynchus my kiss) white muscle following exercise to exhaustion. Estimates of intracellular pH permitted calculation of free concentrations of nucleotides ([nucleotide]f) required for most models of control of energy metabolism. Creatine charge, [PCr]/([PCr]+[Cr]), fell from 0.49±0.05 (mean±S.E.M.) to 0.08±0.02 with exercise but recovered completely by the first sample (2h). Although [ATP] declined to 24% of resting levels and recovered very slowly, RATP, [ATP]/ ([ATP] + [ADP]f+[AMP]f), and energy charge, EC, ([ATP]+0.5[ADP]f)/ ([ATP] + [ADP]f+[AMP]f), recovered as quickly as creatine charge. Changes in [IMP] mirrored those in [ATP], suggesting that AMP deaminase is responsible for maintaining RATP and EC. Recovery of carbon status was much slower than recovery of energy status. Lactate increased from 4 μmol g−1 at rest to 40 μmol g−1 at exhaustion and did not recover for more than 8h. Glycogen depletion and resynthesis followed a similar time course. During the early stages of recovery, calculated [ADP]f declined by more than 10-fold relative to the resting values. The resulting high [ATP]/[ADP]f ratios may limit the rate at which white muscle mitochondria can produce ATP to fuel glycogenesis in situ. It is postulated that the high [ATP]/[ADP]f ratios are required to drive pyruvate kinase in the reverse direction for glyconeogenesis in recovery.
Energy charge
Creatine
Adenine nucleotide
Creatine kinase
Adenosine triphosphate
Adenosine diphosphate
AMP deaminase
Gluconeogenesis
Inosine monophosphate
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Our objective was to investigate whether improved in vivo mitochondrial function in skeletal muscle and intramyocellular lipids (IMCLs) contribute to the insulin-sensitizing effect of rosiglitazone.Eight overweight type 2 diabetic patients (body mass index = 29.3 +/- 1.1 kg/m(2)) were treated with rosiglitazone for 8 wk. Before and after treatment, insulin sensitivity was determined by a hyperinsulinemic euglycemic clamp. Muscular mitochondrial function (half-time of phosphocreatine recovery after exercise) and IMCL content were measured by magnetic resonance spectroscopy.Insulin sensitivity improved after rosiglitazone (glucose infusion rate: 19.9 +/- 2.8 to 24.8 +/- 2.1 micromol/kg.min; P < 0.05). In vivo mitochondrial function (phosphocreatine recovery half-time: 23.8 +/- 3.5 to 20.0 +/- 1.7 sec; P = 0.23) and IMCL content (0.93 +/- 0.18% to 1.37 +/- 0.40%; P = 0.34) did not change. Interestingly, the changes in PCr half-time correlated/tended to correlate with changes in fasting insulin (R(2) = 0.50; P = 0.05) and glucose (R(2) = 0.43; P = 0.08) levels. Changes in PCr half-time did not correlate with changes in glucose infusion rate (R(2) = 0.08; P = 0.49).The rosiglitazone-enhanced insulin sensitivity does not require improved muscular mitochondrial function.
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The content of adenylic system components and creatine phosphate was determined in skeletal muscles and myocardium after intraperitoneal injection and short-term action of myorelaxin and arduan. The injected myorelaxin causes no significant changes in macroergic phosphates in skeletal muscles, whereas arduan lowers the ATP amount by 39%. The both myorelaxants have the same effect on the adenylic system components of the myocardium: they lower significantly the level of ATP and enhance that of ADP and AMP. Different variational tendences of variation in the content of creatine phosphate in skeletal muscles (a certain rise) and in the myocardium (a decrease more than by 30%) are observed.
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The creatine kinase-adenylate kinase equilibria equations are given a dimensionless form by normalizing to total creatine concentration. Analysis with appropriate equilibrium and cation-binding constants identified two sharply separated phases of energy depletion. In the "buffering" phase, energy is derived from phosphocreatine. In the "depleting" phase, adenine nucleotides are the source of energy. Defining the state of the adenine nucleotide pool requires only pH, phosphocreatine, and creatine concentrations. Analysis of data from skeletal muscle, heart, brain, and smooth muscle demonstrated that the [free adenine nucleotide]/[total creatine] and [total phosphate]/[total creatine] are essentially constant over the greater than 20-fold concentration range among tissues and species. This result permits quantitative evaluation of cell energetics with data scaled to the total phosphate, as obtained with nuclear magnetic resonance studies, or to total creatine, as obtained in chemical analysis of freeze-trapped tissue. By applying the stability of the tissue parameters to the equations, it is demonstrated that unique identification of a hypothesis describing the recruitment of O2 uptake requires testing at several pH values.
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The effects of high-energy phosphate contents in muscles on glucose tolerance and glucose uptake into tissues were studied in rats and mice. Enhanced glucose tolerance associated with depleted high-energy phosphates and elevated glycogen content in muscles and liver was observed in animals fed creatine analogue beta-guanidinopropionic acid (beta-GPA). Distribution of infused 2-[1-14C]deoxy-D-glucose in tissues especially in the soleus muscle, kidney, and brain was greater in mice fed beta-GPA than controls. The glucose uptake was decreased when the contents of ATP and glycogen were normalized following creatine supplementation. Plasma insulin in animals at rest was lower and its concentration after intraperitoneal glucose infusion tended to be less in animals fed beta-GPA than controls (p > 0.05), although the pattern of insulin response to glucose loading was similar to the control. The daily voluntary activity in beta-GPA fed mice was also less than controls. These results suggest that improved glucose tolerance is not related to elevated insulin concentration and/or decreased glycogen following exercise. Such improvement may be due to an increased mitochondrial energy metabolism caused by depletion of high-energy phosphates.
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Carbohydrate Metabolism
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The effects of phosphate depletion (PD) of 4, 8, and 12 wk duration on myocardial energy metabolism were studied in rats fed a phosphate-deficient diet and compared with rats pair-fed a normal phosphate diet. Myocardial biopsies were examined for high-energy phosphate bonds. The results show that PD causes a significant reduction in myocardial concentration of inorganic phosphorus at 4 wk of PD and creatine phosphate at 8 wk of PD, while adenine nucleotides were significantly reduced only after 12 wk of PD. The changes in cellular inorganic phosphorus and creatine phosphate displayed a significant correlation with serum phosphorus levels. Mitochondrial respiration was impaired early in PD. Total cellular, mitochondrial, and myofibrillar creatine kinase activities were significantly reduced at 4 wk of PD and fell further at 8 and 12 wk. These data show that chronic PD is associated with reduced mitochondrial capacity to produce ATP, impaired transport via the creatine phosphate shuttle, and reduced myofibrillar ability to utilize ATP. These abnormalities indicate that all steps of myocardial energetics are impaired in PD and provide the molecular basis for the altered myocardial function seen in PD.
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Creatine
Creatine kinase
Adenosine triphosphate
High-energy phosphate
Adenine nucleotide
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Creatine
High-energy phosphate
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Adenine nucleotide
Creatine kinase
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