Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ENERGY METABOLISM”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2001

Metabolic energy metabolism in diabetes: therapeutic implications.

Diabetic alterations of myocardial metabolism result mainly from malfunctions of acetyl-coenzyme A carboxylase, carnitine-palmitoyl-transferase-I and pyruvate-dehydrogenase inducing an overshoot of fatty acid oxidation that inhibits glucose oxidation. Gene expression of pyruvate-dehydrogenase and glucose transporters and depression of the third step of the mitochondrial respiratory chain also contribute to the diabetic alterations of myocardial metabolism. Ischaemic cardiovascular alterations are common and treatment is rarely successful in cases of diabetes since fatty acid oxidation is the costliest metabolic pathway for oxygen. Thus, in diabetes, aerobic glycolysis gradually shifts to anaerobic glycolysis under ischaemia, with accumulation of lactate and acid metabolites that in turn induce myocardial deterioration, Animal experiments have demonstrated that elective depression of activity of carnitine-palmitoyl-transferase-I enzyme-activity promotes glucose oxidation and early rapid recovery of myocardial contractility, especially under diabetic conditions. To reduce diabetic alterations of myocardial metabolism, anti-diabetic treatment must be switched to insulin during the acute ischaemic and post-ischaemic period of coronary diseases. Trimetazidine optimizes energy metabolism by selectively inhibiting action of the 3-ketoacyl-coenzyme A thiolase enzyme involved in beta-oxidation and inhibiting the overshoot of fatty oxidation. Trimetazidine, as the first 3-ketoacyl-coenzyme A thiolase inhibitor, therefore provides permanent myocardial cytoprotection in stable angina pectoris. However, in our experience, this beneficial anti-anginal effect is only observed in well-controlled situations.

Angina Pectoris↗
PubMed2002

[The concept of pathogenic therapy of epilepsy with medications restoring energy metabolism].

Energy metabolism state was studied in experiment and in epileptic patients with reference to the disease clinical course and antiepileptic drugs. Adjuvant pathogenetic treatment was validated. The use of drugs activating energy metabolism facilitate a long-term clinical and electroencephalographic compensation of epilepsy that is confirmed by positive histological dynamics in experiment. The compensation is accompanied by significant intensification of energy metabolism. According to experimental findings, such treatment prevents destructive and degenerative changes in neurons and epileptic encephalopathy development.

Adult↗
PubMed1978

[Energy metabolism and energy requirements of growing boars].

The nitrogen and energy metabolism and the energy consumption of growing boars were measured in 2 metabolic and feeding trials using 8 parallel animals each. The studies covered the 30 to 150 kg live weight range. The growth intensity of the boars was found strongly influenced by the protein level of the ration. At a crude protein level of 18% in the ration, the boars gained, on the average, 780 g per day during the fattening period under study. Energy conversion was found to decline as the protein amount went up. The energy expediture for protein deposition was estimated at 1.8 to 2.0 kcal metabolizable energy per kg deposited. The energy and feed expenditures were calculated to be 7.1 Mcal net energy--fat retention for the whole development period or 3.0 kg dry matter per kg live weight. Boars proved to have an energy requirement differing from that of barrows and gilts; equations are presented for derivation.

Animals↗
PubMed1995

Deterioration of platelet energy metabolism following energy crisis of liver after hepatectomy.

The aim of this study is to investigate the relationship in energy metabolism between the platelet and the liver. The adenylate energy charge of human platelets and arterial ketone body ratio (AKBR:acetoacetate/3-hydroxybutyrate) were measured in 11 patients after hepatectomy. Hepatic energy crisis was defined as the decrease of AKBR below 0.7. The platelet energy charge was measured on the first (Day 1), the second (Day 2), third (Day 3) and sixth (Day 6) day during AKBR decreased and remained under 0.7. The values before AKBR decreased were employed as the control. The values of the platelet energy charge were 0.917 +/- 0.008 in the control (n = 11) and 0.896 +/- 0.009 in all samples after AKBR decreased under 0.7 (n = 30). There was no significant difference between them. The values of energy charge were divided into four groups according to the periods of time after AKBR decreased and remained under 0.7 and compared. The energy charge was 0.923 +/- 0.006 (Day 1, n = 11), 0.907 +/- 0.008 (Day 2, n = 10), 0.890 +/- 0.005 (Day 3, n = 5), and 0.815 +/- 0.012 (Day 6, n = 4). The energy charge of Day 3 was significantly lower than that of Day 1 (p < 0.01). The energy charge of Day 6 was significantly lower than that of Day 1, 2, 3 (p < 0.001, p < 0.001, and p < 0.01, respectively). The 4 patients whose AKBR remained under 0.7 for more than 6 days had hemostatic disorder. The deterioration of the platelet energy charge metabolism lags behind that of the liver.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMedDate not supplied

Ischemia and aging brain. Studies on glucose and energy metabolism in rat cerebral cortex.

Age has been considered to be a crucial risk factor for brain ischemic insults and their mortality. Brain ischemia has been found to cause severe abnormalities in glucose metabolism, energy metabolism and related metabolism, thus damaging the structure and function of brain cells. To study the effect of age and ischemia on brain glucose and energy metabolism, investigations were performed on one-and two-year-old male Wistar rats, the latter of which can be designated as aged. In both age groups, ischemia resulted in a depletion of glucose, OAA, ATP AND CRP, a diminution of Pyr, Citr and alpha-Keto and an accumulation of FDP, Lact, Succ, ADP and AMP in brain cortex. During ischemia, differences between the two age groups became most obvious in the concentrations of Glu, FDP, DHAP, Lact, Succ, Mal, ADP and AMP. In general, the metabolic changes in both age groups point to an increased glycolytic flux which may be less accelerated in the aged group, to an inhibition of the starting reactions of the tricarboxylic acid cycle more severe in aged animals, to a preponderance of anaplerotic reactions in this oxidative system more pronounced in the two-year-old group and to a loss of AMP in the same age group. The age-related metabolic variations measured may indicate that with age the biological plasticity of the brain may be reduced to meet emergency conditions.

Adenine Nucleotides↗
PubMed1983

[Behavior of various parameters of lipid and energy metabolism. 6. Energy turnover in various lengths of time in rats fed a low- and high-fat diet].

Weanling Wistar rats were fed a high-fat diet (HFD) or a low-fat diet (LFD) over 3 and 5-6 weeks. In both comparable groups the absorption of energy was almost the same. In the HFD animals glucose-6-phosphate dehydrogenase (G-6-PDH, E.C. 1.1.1.49) showed its well-known restrictive behaviour in the liver and also in the fatty tissues. After 3 weeks on the respective diet, the body fat content of the LFD animals was lower than that of the HFD animals. After 6 weeks on the respective diet, the body fat contents were nearly the same in the animals of both groups. The energy turnover was greater after 3 weeks on the diet than after 6 weeks, the significantly highest values being found in animals fed over 3 weeks. After 5 weeks on the respective diet, all the energy turnover values were at a lower level, but this was the same in both animal groups. It may be concluded that the fatty-acid synthesis de novo indicated by the G-6-PDH activity does not depend upon the experimental time, and is determined only by the amount of dietary fat. In contrast to this, the establishment of the energy turnover during the experimental time is subject to relatively great changes which might be correlated with the regulation of total fat retention in the body.

Animals↗
PubMed1989

A review of energy metabolism in producing ruminants. Part 1: Metabolism of energy substrates.

The efficiency of metabolisable energy utilisation, for growth and fattening, is dependent upon the relative VFA proportions produced in the rumen. Sufficient propionate is required to meet glucose demand for producing NADPH, glycerol and nucleic acid synthesis. Since diet has the greatest effect on the pattern of VFA fermentation, it will play a major role in controlling the supply of VFA to the animal. Magnitude of the acetate supply determines the proportion of acetate supplied to oxidation or to fatty acid synthesis, which is also dependent upon the extracellular supply of glucose, NADPH and ATP. Since the optimal levels of acetate and glucose for lipogenesis appear to vary with glucose concentration, a diet that decreases the supply of glucogenic precursors, but increases the acetate supply, may suppress fatty acid synthesis. An increased supply of propionate may suppress glucose synthesis from other sources. The isoenergetic replacement of roughage by concentrate, appears to increase the glucose entry rate, due to both an increase in propionate, and glucose absorbed from the small intestine. Dietary nitrogen source also affects the rate of gluconeogenesis. An optimum dietary energy-protein ratio exists for maximum efficiency of utilisation of both dietary energy and protein. In dairy cows, for example, the energy is most effectively metabolised when protein content of the diet is 15-25% of net energy.

Animals↗
PubMed1984

[Energy metabolism and energy consumption of intensive care patients on respirators].

There are two main reasons for assessing energy turnover individually and as accurately as possible; firstly, the marked variation in available data on the degree to which energy turnover increases after severe trauma, and secondly accumulating evidence of the potential dangers of an inappropriately high so-called "hypercaloric" substrate dosage, which exceeds energy requirements. The energy turnover of 50 polytraumatized intensive care patients was therefore measured by indirect calorimetry and compared with norm values. Comparison of the median values revealed an approximately 50% higher energy turnover in the polytraumatized cases than calculated basal levels. The median values of our patients all lay within a similar range, but for each individual case we found marked differences between the energy turnover as measured by indirect calorimetry, and that estimated from norm tables. The oxygen consumption and CO2 production rates of 10 polytraumatized ventilated patients, measured at short time intervals, showed only minimal variations during the course of 24 h. The separate measurements carried out at hourly intervals varied by less than 10% when compared to an 1-h period of observation between 11 and 12 a.m. The oxygen consumption of a group of 40 polytraumatized, ventilated intensive care patients receiving various different i.v. infusions and parenteral nutrition regimens was, with an average of 382 +/- 47 ml/min, much higher than physiologically normal values. The energy turnover rate of these patients was correspondingly much higher than that of a fit person at rest, despite the fact that the rates measured were relatively low when compared to values found in the older literature.(ABSTRACT TRUNCATED AT 250 WORDS)

Calorimetry, Indirect↗
PubMed1982

Partition of energy metabolism and energy cost of growth in the very low-birth-weight infant.

Energy requirements are partitioned between needs for maintenance (including resting metabolism, thermoregulation, and muscular activity) and needs for synthesis and storage of new tissue. The partition of energy utilization was evaluated by 22 metabolic and nutritional balance studies in 13 formula-fed (SMA 20/24), growing, appropriate-for-gestational age, very low-birth-weight infants (mean +/- SE birth weight, 1,155 +/- 39 gm; study weight, 1,271 +/- 60 gm; age at study, 21 +/- 2 days; weight gain, 16.8 +/- 1 gm/kg/day). Continuous open-circuit, indirect calorimetry was performed for periods of 6 +/- 0.25 hours in a thermoneutral environment. Results expressed as mean kilocalories per kilogram per day (+/- SE) were: energy intake, 148.6 (+/- 3.9); stool and urine losses, 18.2 (+/- 1.5); metabolizable energy, 130.4 (+/- 3.5); "basal" metabolic rate, 47.0 (+/- 0.75); energy cost of activity, 4.3 (+/- 0.9); thermic effect of food, 11.3 (+/- 0.65); energy stored in new tissue, 67.8 (+/- 3.0). These results provide a partition of energy utilization in very low-birth-weight infants under thermoneutral conditions. Increased activity and a thermal environment outside the neutral range will augment maintenance energy requirements, thus decreasing the amount of energy available for growth if metabolizable energy intake remains constant. The energy cost of growth (ie, for synthesis of, and storage in, new tissue) was determined as 4.9 kcal/gm of weight gain. To attain the equivalent rate of intrauterine weight gain, a metabolizable energy intake of approximately 60 kcal/kg/day in excess of maintenance requirements of 51.3 kcal/dk/day must be provided.

Anthropometry↗
PubMed1986

Relation of actin fibrils to energy metabolism of endothelial cells.

The physiological significance of the association of glycolytic enzymes with actin fibrils was investigated in cell culture. Cytochalasin D (CD) was used to induce the known actin-based sequence of events in a culture of an endothelial-cell line (XTH-2) derived from hearts from tadpoles of Xenopus laevis. 1 min following addition of CD, ruptures in the cortical fibrillar meshwork and in stress fibres are seen. At the same time the cellular ATP level decreases by ca. 25%. This and the following reactions resulting in a kind of arborization depend on a continuous supply with metabolic energy. As shown by measurements of oxygen consumption, cells with intact energy metabolism provide the ATP needed from glycolysis; ATP produced by oxidative phosphorylation is not utilized as long as lactate dehydrogenase (LDH) reoxidizes NADH2. After inhibition of LDH, respiration in XTH-2 cells doubles. CD treatment induces a transient increase in oxygen consumption, indicating an increased energy supply by respiration. From these results we conclude: The energy needed by the actomyosin system is - under normal metabolic conditions -supplied from ATP phosphorylated in glycolysis. The processes of energy metabolism seem to be highly compartmentalized; ATP is not a parameter that is kept constant in time intervals of minutes up to one hour.

Actins↗
PubMed1986

Uptake of iron from transferrin by isolated hepatocytes. Relationship to cellular energy metabolism.

The mechanism by which utilization of transferrin-bound iron is linked with cellular metabolism has been studied in isolated rat hepatocytes. The initial binding of transferrin to the hepatocyte is not dependent on metabolic energy, but the subsequent progressive binding of transferrin and uptake of iron depend on metabolic energy and the drainage of reducing equivalents from the respiratory chain. When respiration is completely blocked with cyanide a limiting energy level for the uptake of iron is found at an intracellular concentration of ATP of approximately 0.2 mmol/l. The iron uptake process utilizes ATP hydrolysis, substrate oxidation and dissipation of ionic gradients as energy sources interchangeably.

Adenosine Triphosphate↗
PubMed1995

Energy metabolism in muscle approaching maximal rates of oxygen utilization.

Muscle is capable of operating over a wide range of metabolic rates. Most of the metabolic energy for work (ATP), and essentially all of the oxygen consumption of muscle, is due to mitochondrial oxidative phosphorylation. The rate of mitochondrial oxidative phosphorylation is determined by the rate of ATP consumption by the cells (demand) while the metabolic energy level at each metabolic rate is determined by the supply of oxidizable substrate and oxygen (supply). The maximal rate of metabolism is limited by several factors, including the supply of oxidizable substrates (mitochondrial dehydrogenases), of oxygen (blood supply and oxygen diffusion) and the respiratory enzyme capacity (tissue content of mitochondria).

Adenosine Triphosphate↗
PubMed1980

A symbiotic relationship of energy metabolism between a 'non-glycolytic' mammalian red cell and the liver.

The red cell of newborn pig loses the ability to carry out glycolysis within a month after birth. The metabolic energy source for this 'non-glycolytic' mammalian red cell is unknown. Hepatectomy of an adult pig results in the loss of red cell ATP with a characteristic half-time of 7--8 h which is identical to the rate with which ATP disappears in the pig cells under in vitro substrate-free incubation. Exposure of pig red cells with either normal or depleted levels of ATP to isolated hepatocytes causes a net synthesis of red cell ATP during a 12 h incubation. These findings suggest that a symbiotic relationship of energy metabolism may exist between the red cell and the liver of the pig.

Adenosine Triphosphate↗
PubMed1995

Acetazolamide-induced inhibition of carbonic anhydrase influences energy metabolism and respiratory work in healthy subjects.

To assess the usefulness of acetazolamide in weaning a patient from a respirator, we monitored the changes in the respiratory quotient ratio (RQ ratio), the ventilation volume (VE; l/min.), carbon dioxide elimination (VCO2; ml/min.), the oxygen consumption (VO2; ml/min.) and the metabolic energy expenditure (EE; Cal/day) for 6 hours before (baseline) and after the intravenous administration of acetazolamide, 6 mg/kg, in 12 healthy adult volunteers. The RQ ratio decreased significantly from 0.88 to 0.82 after the injection of acetazolamide, 6 mg/kg, and remained below baseline throughout the 6 hours of observation. VCO2 decreased significantly and VE increased significantly after acetazolamide administration. There were no significant changes in VO2 or EE. The RQ ratio increased only slightly, from 0.85 to 0.87, in the control group (no acetazolamide). No significant changes in VCO2 or VE were observed in the control group. Findings suggest that acetazolamide may alter the main pathway of energy metabolism from being carbohydrate-dominant to being fat-dominant, with a resulting fall in CO2 production to maintain the adequate work of ventilation. The inhibition of carbonic anhydrase by acetazolamide may be useful in reducing respiratory work in a patient who is weaned from a respirator.

Acetazolamide↗