Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “metabolic efficiency”

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
PubMed1976

[Absorption and metabolic efficiency of iron in nickel deficiency].

Absorption and Metabolic Efficiency of Iron During Ni Deficiency. Ni deficiency leads to reduced iron contents in organs and to greatly reduced Hb levels and erythrocyte counts. Using models it was studied whether this Ni-dependent Fe anemia can be attributed to an impaired absorption of iron or to its metabolic efficiency. An experiment with seven 30-day-old rats from each of two generations were used for this. In Ni deficiency (0.015 ppm dietary nickel) iron absorption was clearly impaired at both 50 ppm and 100 ppm iron in the diet. Compared to the groups given 20 ppm nickel, the amount of iron absorbed fell two-thirds and one-third, respectively. By comparison, the influence on the metabolic efficiency of the iron was relatively small; at high iron supply, however, it was reduced by 8% in the Ni-deficient animals. Therefore, the reduced levels of hemoglobin, erythrocytes and hematocrit must essentially be caused by the impared absorption.

Animals↗
PubMed1976

[Technic and dosage of zinc injections for studies on metabolic efficiency].

When rats are supplied with zinc by the diet, absorption interferes with the determination of the efficiency of utilization of zinc in metabolism. In studies on the metabolic efficiency of zinc it was therefore attempted to by-pass the step of absorption by i.m. or i.v. injection and, at the same time, to determine the appropriate dosage for these zinc injections. For that reason, young male rats, after 20 days of zinc depletion were injected i.m. or i.v. in five different dosages of ZnCl2 solutions and their gains in live weight were followed. It was found that higher zinc doses given i.v. were lethal to rats, whereas they were tolerated when given i.m. The better metabolic efficiency of zinc, indicated by comparatively higher live weights of the i.v. injected groups, could be seen even at the lower i.v. zinc dosages. Therefore, based on the results of the present experiment, a dose of 0.4 mg zinc is proposed for the i.v. injection to study the metabolic efficiency of zinc in rats.

Animals↗
PubMed1991

Relative metabolic efficiency of concentric and eccentric exercise determined by 31P magnetic resonance spectroscopy.

To determine the relative metabolic efficiency (metabolic energy used per unit of mechanical energy output) of negative to positive muscular power, we used 31P magnetic resonance spectroscopy to monitor the cellular energy metabolism of limb muscles in eight healthy subjects during a nonfatiguing, mixed concentric-eccentric activity and during its concentric and eccentric components. We also studied isometric contractions. We found that in terms of the flow of metabolic energy through the muscle cells, the cost of concentric exercise at this intensity was proportional to the mechanical power generated, but the cost of eccentric and isometric exercise did not increase significantly as the apparent intensity of the exercise increased over the range studied. Although the pattern was similar in all subjects, the quantitative relationship between metabolic cost and mechanical output was different in subjects with different muscular strength. The qualitative results can be explained in the context of the known biochemistry and biophysics of the cellular contractile apparatus (sliding filament theory, with independent force generators).

Adult↗
PubMed1979

The application of microcalorimetry to the assessment of metabolic efficiency in isolated rat hepatocytes.

1. Heat output by suspensions of isolated rat hepatocytes was determined by using a modified batch-type microcalorimeter. 2. The ratio of O(2) uptake (determined polarographically) to heat output was used to assess the metabolic efficiency of isolated hepatocytes. 3. Cells from starved or fed rats incubated in either bicarbonate-buffered physiological saline containing gelatin, or bicarbonate-buffered physiological saline containing amino acids, serum albumin and glucose showed no significant difference with respect to the ratio of O(2) uptake to heat output. 4. For liver cells from 24h-starved rats, the addition of 10mm-dihydroxyacetone and 2.5mm-fructose significantly decreased the ratio of O(2) uptake to heat output from 1.94+/-0.05 in the controls to 1.52+/-0.04 and 1.54+/-0.01mumol/J respectively. 5. Glucagon (1mum), which slightly increased both O(2) uptake and heat output, did not significantly alter the ratio. 6. The addition of extracellular 10mm-NH(4)Cl and urease to provide an energetically wasteful cycle by ensuring hydrolysis of newly synthesized urea, lowered the ratio of O(2) uptake to heat output from 1.81+/-0.08 to 1.47+/-0.06mumol/J, indicating a reduced metabolic efficiency. 7. Metabolic efficiency in rats of different dietary regimen, age and genetically based obesity was also assessed. No differences in the ratio of O(2) uptake to heat output were found between liver cell suspensions prepared from rats maintained on colony diet and high-fat diet or sucrose-rich diet nor between animals ranging from 38 to 179 days of age. Comparison of the ratio of liver cell O(2) uptake to heat output between homozygote Zucker fa/fa obese rats and their lean littermates showed no significant difference. 8. It is concluded that the ratio of O(2) uptake to heat output for isolated hepatocytes is relatively constant unless perturbed by conditions that markedly enhance substrate cycling.

Animals↗
PubMed1985

Increased metabolic efficiency in obese mutant mice.

Several different single gene mutations are known to cause similar diabetes-obesity syndromes in mice. Our studies with two mutations, obese (ob) and diabetes (db) have shown that each syndrome develops similarly. Symptoms include hyperinsulinemia, hyperglycemia, hyperphagia, diabetes, and obesity coupled with similar, and large increases, in the efficiency of food utilization. Even when maintained on 50 percent of normal food intake, mutants still become obese. This increase in metabolic efficiency has been suggested to be due to a failure of mutant mice to thermoregulate. Our studies indicate that any defect in thermoregulation is not severe enough to conserve sufficient calories to account for the large increase in metabolic efficiency observed in each mutant and the increased efficiency seen in mutants must be a result of other mechanisms. More critical studies in both normal and obese mice should lead to information defining the contribution of the many different potential energy saving mechanisms available.

Animals↗
PubMed1990

Comparison of the pharmacokinetics of moclobemide in poor and efficient metabolizers of debrisoquine.

A number of pharmacokinetics studies in which patients had been phenotyped and poor metabolizers for moclobemide found were analysed retrospectively. There were 27 subjects in all, aged between 19 and 75 years, and 5 of these were classified as poor debrisoquine metabolizers. Although there was a wide variability in the pharmacokinetic parameters observed, no consistent relationship was found between these and debrisoquine phenotype. Poor debrisoquine metabolizers all had values within the extremes for the efficient metabolism. This was true for both single and multiple dosing. This analysis is limited by the small number of subjects as well as its retrospective nature. Nevertheless, the data suggest that no deviations of moclobemide pharmacokinetics should be expected in poor metabolizers of debrisoquine compared with normal metabolizers.

Adult↗
PubMed1986

Insulin and metabolic efficiency in rats. II. Effects of NE and cold exposure.

The role of insulin in metabolic efficiency (ME, i.e., efficiency of body wt gain) was examined under conditions of maximal energy expenditure in control and diabetic rats. Long-lasting insulin was administered using a protocol that did not affect food intake and increased ME in both groups. Half the animals were injected chronically with norepinephrine (NE). NE alone in controls decreased body weight and ME and increased brown adipose tissue (BAT) growth, thermogenic potential [cytochrome c oxidase activity (COA)], and lipoprotein lipases (LPL) activity; however, in diabetics, body weight, ME, and food intake all decreased and only BAT LPL activity and DNA content increased. The combination of NE and insulin increased BAT protein and COA in diabetics; in controls, all BAT measures were further increased and ME was intermediate to that of either treatment alone. Cold exposure decreased body weight and ME, increased food intake and qualitatively produced similar increases in BAT growth, COA, and LPL activity in both controls and diabetics. In diabetics, combined cold exposure and insulin did not affect the increase in BAT growth or LPL activity resulting from either treatment alone, but in controls this combination decreased BAT growth and COA. It is concluded that, even under conditions of maximal energy expenditure, both extremes of basal insulin status result in decreased BAT growth and thermogenic potential, but have opposite effects on ME.

Acclimatization↗
PubMed1986

Insulin and metabolic efficiency in rats. I. Effects of sucrose feeding and BAT axotomy.

The role of insulin and brown adipose tissue (BAT) thermogenesis in metabolic efficiency (ME, the efficiency of body wt gain) was examined in rats with varied basal insulin status. Long-lasting insulin was administered using a protocol that did not alter food intake, yet increased ME in both groups. Half the rats were fed sucrose to stimulate BAT growth and thermogenesis. Insulin overrode the exaggerated decrease in ME in sucrose-fed diabetics, with only partial attenuation in controls. Interscapular BAT (IBAT) lipoprotein lipase activity was decreased in diabetic rats, restored by insulin treatment, and not affected in controls. Sucrose-fed diabetics and controls had their IBAT sham or bilaterally surgically denervated. Insulin decreased the thermogenic potential of BAT [cytochrome oxidase activity (COA)] in intact controls and diabetics; in the latter, insulin restored COA independent of BAT innervation. We conclude that insulin can increase ME without an associated increase in energy intake, regardless of basal insulin status, both insulin deficiency and excess decrease BAT thermogenic potential (COA), and hyperinsulinemia-induced increases in ME may result from decreased BAT mitochondrial proliferation.

Adipose Tissue, Brown↗
PubMed1982

Efficient metabolism of benzo(a)pyrene at nanomolar concentrations by intact murine hepatoma cells.

We have studied the metabolism of benzo(a)pyrene (BP) by intact mouse hepatoma cells, at nM concentrations of the carcinogen, using an assay in which we directly measure the rate of BP fluorescence disappearance. The rate of BP metabolism is half-maximal, at limiting cell dilution, when the concentration of BP is about 4 nM. This apparent Km for BP metabolism is much lower than those reported previously for several reasons. (a) Partitioning of BP into cells markedly influences kinetic measurements, and we account for these effects. (b) Enzyme inducers can competitively inhibit BP metabolism and thus may introduce artifacts into kinetic measurements. (c) Under the conditions of this assay, phenolic BP metabolites are produced but do not accumulate, due to their further metabolism; therefore, assays of BP metabolism which measure the production of phenols, such as the commonly used aryl hydrocarbon hydroxylase assay, may markedly underestimate the rate of BP metabolism when intact cells and low substrate concentrations are used. Our results show that cells can efficiently metabolize BP when exposed to BP concentrations similar to those present in the environment.

Animals↗
PubMed1989

Reduced aerobic metabolic efficiency in globally "stunned" myocardium.

Post-ischemic "stunned" myocardium appears to be metabolically inefficient, since oxygen consumption is preserved, while mechanical work is depressed. The present study investigated whether this metabolic inefficiency represents a basal functional abnormality present in the quiescent myocardium (e.g. abnormal mitochondrial coupling) or is specifically related to muscle contraction. Isolated perfused rabbit hearts (n = 7) were exposed to 20 min zero-flow ischemia to produce post-ischemic myocardial stunning. After 10 min of reperfusion, mean rate-pressure product (mmHg/min), was reduced to 56.1% of baseline in stunned hearts, while mean oxygen consumption (mumol O2/min/g LV) was reduced to only 71.8% of baseline. The ratio of oxygen consumption to rate-pressure product remained significantly elevated throughout 40 min of reperfusion when compared with non-ischemic controls (P less than 0.01). Despite inappropriately high oxygen consumption in the beating stunned heart, basal oxygen consumption measured after KCl arrest was not significantly different from controls (1.07 +/- 0.07 vs. 1.03 +/- 0.04, respectively). These results indicate that the metabolic inefficiency found in stunned myocardium is not a basal abnormality, but rather is related specifically to abnormalities in contraction or electromechanical coupling.

Animals↗
PubMedDate not supplied

[Evaluation of metabolic efficiency of the liver in patients with psoriasis by the antipyrine test].

In 47 patients with generalized psoriasis vulgaris and 23 healthy subjects the effectiveness of the hepatic metabolism reflected by drug biotransformation was assessed with the antipyrine elimination test. In the group of psoriatic patients there were 25 men and 22 women and in the control group--age-matched 12 men and 11 women. The half-time of antipyrine was longer and the clearance index was lower in the patients than those in the control group. The differences were statistically significant. After 2 weeks of PUVA or SUP-therapy the differences were more significant. The findings indicate an impairment of the liver metabolic effectiveness reflected by drug biotransformation in psoriatic patients.

Adult↗
PubMed1987

Metabolic efficiency of the liver in patients with breast cancer as determined by pharmacokinetics of phenazone.

Phenazone pharmacokinetics was determined in 24 healthy women and in 39 women with breast cancer; in the latter before and after antineoplastic treatment. The mean phenazone half-life time (t0.5) was significantly shorter in patients with breast cancer (8.880 +/- 2.5585 h) than in healthy persons (12.024 +/- 3.8486 h, P less than 0.001). Mean elimination rate constant (K, 0.063 +/- 0.0197 h-1) and mean metabolic clearance rate (MCR, 54.968 +/- 20.3476 ml/min) differed statistically (P less than 0.01) from the same parameters in control group, where K was 0.063 +/- 0.0197 h-1, MCR was 41.832 +/- 14.7153 ml/min. In patients receiving antineoplastic drugs, pharmacokinetic parameters of phenazone did not differ significantly in comparison with the initial values. Our results obtained with phenazone as a model substance suggest that in breast cancer elimination of other drugs metabolized by the pathway similar to phenazone also may be changed. This should be considered in selection of their dosage.

Adult↗
PubMed1988

Phenazone pharmacokinetics as an index of hepatic metabolic efficiency.

Phenazone pharmacokinetics as an index of hepatic microsomal enzyme activity was studied in 31 patients with Hodgkin's disease, 11 patients with non-Hodgkin's lymphoma and 52 healthy volunteers. The mean phenazone half-life (t0.5) was significantly shorter in patients with Hodgkin's disease (8.002 +/- 2.775 h) and in patients with non-Hodgkin's lymphoma (8.775 +/- 2.440 h) than in healthy persons (11.351 +/- 3.706 h). In patients with Hodgkin's disease and in patients with non-Hodgkin's lymphoma mean elimination rate constant (Kel) (0.101 +/- 0.050 h-1; 0.086 +/- 0.028 h-1) and mean metabolic clearance rate (MCR) (70.464 +/- 50.347 ml/min; 71.621 +/- 21.448 ml/min) differed statistically significantly from the same parameters in control group, where K was 0.067 +/- 0.021 h-1 and MCR 49.361 +/- 18.167 ml/min. Treatment with antineoplastic drugs inhibited phenazone elimination. No correlations were found between the phenazone pharmacokinetics parameters and routine laboratory tests of liver function. Since many drugs are metabolized by cytochrome P-450, similar to phenazone, it is likely that their elimination in patients with Hodgkin's disease and in patients with non-Hodgkin's lymphoma will be also changed. This should be considered in selection of their dosage.

Adult↗
PubMedDate not supplied

[The metabolic efficiency of baker's yeast in an atherogenic diet].

The effect of bakery compressed yeasts in the amounts of 6 and 12 g/100 g of the ration was studied in rats. It was revealed that 12 g of yeasts per 100 g of the atherogenic ration produced a hypocholesterolemic effect. A negative effect of this amount of the yeasts was manifest in the slow growth of the rats' body mass and in an increased ratio of the kidney/body mass. The yeasts amounts used did not protect the test animals from the kidney infiltration with lipids and cholesterol; 12 g of yeasts per 100 g of the ration promoted elevation of sialic acid content in the blood plasma. Morphologic changes were observed only in the aortal wall, they were characteristic of the prelipid stage of atherosclerosis and did not depend on the yeasts amount.

Animals↗