Biomedical subjects

A Palou

Publications and source records attributed to A Palou.

At least 91 records · Page 5Linked to original sources

PubMed1992

Regulation of rat erythrocyte L-glutamine, L-glutamate and L-lysine uptake by short term starvation.

1. The kinetic parameters (Km, Vmax and Kd) of L-glutamine, L-glutamate and L-lysine uptake by isolated red blood cells in fed and 24 hr starved rats have been determined. 2. L-Lysine and L-glutamine uptake was best fitted by a two transport component: a saturable component and a diffusion one. 3. Starvation brought about important decreases in the Km and Vmax for both L-lysine and L-glutamine uptake. 4. The Kd for L-glutamine showed a significant increase whereas that corresponding to L-lysine did not change by starvation. 5. L-Glutamate uptake adjusted to diffusion kinetics, with a Kd which did not change due to starvation. 6. It is concluded that the amino acid uptake showed specific regulation by starvation. 7. The mechanism involved is not dependent on protein synthesis--given the unnucleated nature of mammal red cells. 8. The magnitude of the changes observed in the uptake kinetic parameters may account for the extent of the blood amino acid pool changes as those produced in vivo over physiological limits.

Animals↗

PubMed1992

Impaired starvation-induced loss of mitochondrial protein in the brown adipose tissue of dietary obese rats.

The effects of fasting and refeeding on interscapular brown adipose tissue (IBAT) in normal rats and in those made obese by cafeteria feeding was investigated in order to evaluate the sequential feeding responses relating to the IBAT facultative thermogenesis. The thermogenic activity (GDP binding) and related parameters such as IBAT mass, tissue protein, mitochondrial protein and cytochrome c oxidase (COX) activity were compared in fed, fasted and refed situations in controls and in rats made obese by cafeteria feeding. The IBAT mass, tissue protein content, mitochondrial protein content, total COX activity and specific GDP binding were significantly increased by the cafeteria diet. The thermogenic response to fasting and refeeding was different between control and cafeteria obese rats. Thus, in control rats, the loss of mitochondrial protein as well as total COX activity are probably the main responses to fasting, whereas in cafeteria obese rats no changes in mitochondrial protein and total COX activity occur during fasting. Furthermore mitochondrial protein and total COX activity were not recovered during refeeding in control rats, and no changes occurred in cafeteria fed rats. However, the proton conductance pathway (measured by GDP binding) is inactivated in control and cafeteria fed rats on fasting. In conclusion, these results indicate different responses during fasting in the mitochondrial protein between control and dietary obese rats, suggesting a possible activated mitochondrial proteolysis in the control rats only.

Adipose Tissue, Brown↗

PubMed1992

Dietary regulation of fasting-induced mitochondrial protein degradation in adult rat brown adipose tissue.

Mitochondrial protein, cytochrome-c-oxidase and mitochondrial ATPase activities, which can participate in brown adipose tissue thermogenesis, were measured in the present study in order to evaluate mitochondrial activity, oxidative capacity and ATP synthesis in dietary obese rats compared to control rats. Cafeteria-diet induced increase of cytochrome-c-oxidase and ATPase activities of 54% and 37% respectively, but mitochondrial protein content remained unchanged. Fasting induced active mitochondrial protein degradation (about 50%) only in control rats, but in both cafeteria fed and post-cafeteria obese rats fasting-induced loss of mitochondrial protein was impaired. It was concluded that cafeteria diet is able to induce specifically both the oxidative capacity and the ATP synthesis in adult rat brown adipose tissue without affecting the mitochondrial protein. Furthermore, during fasting the obese (or overweight) status 'per se' regulates the overall mitochondrial protein degradation which was impaired or inactivated in overweight dietary rats compared with controls.

Adenosine Triphosphatases↗

PubMed1992

Effect of diet-induced obesity on kinetic parameters of amino acid uptake by rat erythrocytes.

The effects of cafeteria diet-induced obesity upon in vitro uptake of L-Alanine, Glycine, L-Lysine, L-Glutamine, L-Glutamic acid, L-Phenylalanine and L-Leucine by isolated rat erythrocytes have been studied. The total Phe and Leu uptakes followed Michaelis-Menten kinetics. The Glu uptake was fitted to diffusion kinetics. The uptakes of Ala, Gly, Lys and Gln were best explained by a two-component transport: one saturable and one diffusion. Obesity increased the Km value for Ala, Gln and Leu, and the Vmax value for Ala, but decreased the Vmax for Lys. Kinetic parameters of Phe uptake were unaffected by obesity. In addition, the pseudo-first order rate constant (Vmax/Km) for Ala, Gly, Gln, Lys and Leu uptake decreased as a result of cafeteria diet-induced obesity. The Kd value for Ala, Gly, Gln and Glu decreased and that of Lys increased as result of obesity. These adaptations could, at least in part, explain alterations in amino acid distribution between blood cells and plasma related to overfeeding or obesity.

Amino Acids↗

PubMed1991

Altered blood amino acid distribution in genetically obese mice.

The present study was undertaken to determine whether the alteration in amino acid distribution between the plasma and cellular compartment of the blood, previously described in dietary-obese rats, also occurs in genetically obese mice. The blood concentration of individual amino acids and its distribution between plasma and cells of lean and genetically obese mice (ob/ob) have been measured. The results demonstrated that genetically obese mice showed a decrease (55%, P = 0.0489) of free amino acids in the blood cells. Most amino acids were affected and among the most noteworthy characteristics was the observation that the reduction in concentration was more pronounced for the total concentration of the essential amino acids which was reduced by 76% (P = 0.0112) compared to cells of lean mice. These results suggest that an altered amino acid distribution between plasma and blood cells is a consequence of both diet-induced and genetic obesities.

Amino Acids↗

PubMed1991

Evidence for masking of brown adipose tissue mitochondrial GDP-binding sites in response to fasting in rats made obese by dietary manipulation. Effects of reversion to standard diet.

A specific immunoassay of uncoupling protein (UCP) and measurement of GDP binding were used to study the chronic responses of brown adipose tissue (BAT) mitochondria from rats made obese by dietary means (cafeteria rats) and from obese rats subsequently fed a standard diet (post-cafeteria rats). We studied the response to fasting in order to assess the masking/unmasking responses in these groups. These studies have shown the following. (1) In the obese rats (cafeteria and post-cafeteria) the chronic increase in mitochondrial UCP concentration compared with controls parallels the increase in GDP binding. (2) In 24 h-fasted control rats the decrease in GDP binding is associated with a change in UCP concentration, but in fasting cafeteria and post-cafeteria obese rats the decrease in GDP binding is not associated with any change in UCP concentration. (3) Post-cafeteria obese rats showed increased GDP binding and higher UCP concentrations than the controls, but these values were less than in cafeteria obese rats. (4) Control rats at 8 months old showed greater GDP binding and had a higher UCP concentration than 11-month-old control rats. (5) The responses of GDP binding and UCP concentration to fasting in post-cafeteria obese rats were similar to those in cafeteria obese rats, suggesting that such abbreviations are related to the obese status itself rather than to the composition of the cafeteria diet. The evidence supports the hypothesis that the response of the cafeteria and post-cafeteria obese rats to fasting is associated with a masking of UCP, whereas with chronic manipulation of diet changes in UCP concentration predominate.

Adipose Tissue, Brown↗

PubMed1991

A significant pool of amino acids is adsorbed on blood cell membranes.

It is well known that the amino acids in the blood are distributed between the plasma and inside the cells. This study was conducted to determine whether amino acids can be located adsorbed on blood cell membranes. The amino acid concentration in the deproteinized haemolysed blood was higher than that in the fraction of blood after removal of the blood cell membranes by centrifugation. These results showed that a pool of amino acids representing 21.1% of the whole blood cell amino acids was adsorbed on the blood cell membranes of adult Wistar rats. The non-polar amino acids showed high adsorption on the membrane, whereas out of the polar amino acid group, only the non-ionic amino acids did adsorb.

Adsorption↗

PubMed1991

Sustained changes in blood alpha amino nitrogen compartmentation during recovery from cafeteria feeding in rats.

We have previously reported that blood urea and blood cell amino acids levels are reduced in rats obese by feeding a palatable cafeteria diet. In order to distinguish whether these changes result from the altered diet, or from the obesity per se, we have studied cafeteria fed rats after returning to standard diet. As in previous studies, obesity induced by cafeteria feeding (for 90 days) was maintained when the cafeteria diet was removed and rats were fed standard diet only. After removal of the cafeteria diet, blood urea levels of 24 h starved obese rats were lower (23%) than those of starved control rats. Blood cell amino acid levels of obese were lower than control ones from day 50 onwards, during and after cafeteria feeding (21% lower on day 100 of life), and thus coincided with divergence of body weights; these differences were maintained despite removal of cafeteria diet. The effects of starvation on plasma amino acid levels were more marked in obese than control rats, during and after cafeteria feeding. Thus the effects on blood amino acids and urea levels in cafeteria diet induced obese rats are related to the obese status rather than to the diet composition.

Amino Acids↗

PubMed1991

Dietary obesity shows adaptations of amino-acid metabolism on enzyme activities to save amino nitrogen.

An increased aspartate transaminase in the liver of dietary (post-cafeteria) obese rats was found. It was consistent with the functionality of the malate-aspartate shuttle, that could be responsible for enhancement of metabolic efficiency. The muscle and intestine of obese rats showed a greater capacity for alanine and glutamine synthesis than the controls. Furthermore, enterocyte adaptations in the obese rats indicated higher capabilities for the intake of nitrogen than in the controls. In conclusion, the pattern of amino-acid enzyme activities reflected adaptations to keep from amino nitrogen depletion in dietary obesity which were compatible with an enhancement of the metabolic efficiency.

AMP Deaminase↗

PubMed1991

Short term starvation-induced changes in the kinetic parameters of rat red cell L-alanine and glycine uptake.

Na(+)-dependent L-Alanine and Glycine uptake by rat red blood cells were best fit to a common model of two transport components, saturable transport and diffusion. 24 hours of food deprivation provoked statistically significant increases of the Km and Vmax red cells L-Alanine uptake, whereas the diffusion constant did not change in response to starvation. The Glycine uptake kinetics poorly follows the L-Alanine pattern and no significant response to starvation can be outlined. The physiological meaning of these adaptations has to be related to short term food deprivation regulation, independent of protein synthesis in the erythrocytes. Such mechanisms could be important to account for the previously described changes in the distribution patterns of amino acids between the blood plasma and blood cell compartments in response to short term starvation.

Alanine↗

PubMed1991

Dietary-induced permanent changes in brown and white adipose tissue composition in rats.

We have previously observed that feeding rats a cafeteria diet causes excess weight gain and changes in tissue composition. The object of this study was to assess whether these alterations were sustained after withdrawal of the palatable diet in the rat. The results showed that the obesity was not reversed by feeding a standard diet ad libitum for five months after withdrawal of the cafeteria diet. Body weight was 26 per cent greater than in control rats and tissue composition showed permanent alterations. The excess weight of lumbar white adipose tissue was due mainly to lipid content (86 per cent) and this was also true, but to a less extent, for interscapular brown fat (59 per cent). Increased brown fat mass was a result of hyperplasia and hypertrophy, whereas increased lumbar white fat was mainly a result of hyperplasia alone. In conclusion, changes in tissue composition, particularly in fat depots, were permanent and could be ascribed to the obesity per se, and not to the diet composition.

Adipose Tissue↗

PubMed1990

The effects of cafeteria diet induced obesity on rat blood amino acid compartmentation.

In female virgin Wistar rats, the effects of a cafeteria-diet induced obesity on blood amino acid levels and their distribution between plasma and blood cells have been studied in fed and 24-hour starved states. Cafeteria diet induced obesity provoked a decrease in total blood cell amino acid content, both in fed and starved situations when compared with controls. Whether is a causal factor for developing obesity due to imbalance in tissue amino acid supply for protein biosynthesis processes, or represents some signal related to hypothalamic control of feeding, or is a consequence of the obesity remains to be established.

Amino Acids↗

PubMed1990

Influence of diet and obesity on placental amino acid enzyme activities in the rat.

The objective of this study was to assess the impact of dietary obesity and acute starvation on the activity of placental enzymes involved in amino acid metabolism. Twenty-four hours starvation caused a significant fall (10%) in the foetal weight in rats fed standard diet, and this was associated with only modest changes in amino acid enzyme activities. In contrast, in obese rats, foetal weight was unaffected by acute starvation, and was accompanied by a reduced adenylate deaminase activity (24%) and lower ammonia concentrations (50%) in placentae of obese rats after 24h starvation. Thus obesity may confer a protective effect on the foetus growth during acute starvation of diminishing amino acid utilization.

AMP Deaminase↗

PubMed1990

In vivo alanine metabolism in late pregnant rats.

Alanine metabolism in 24 hour starved 20-day pregnant rats, following intravenously administered C14-alanine, in trace dose that does not affect the normal availability of this amino acid, has been studied. The steady state levels of alanine and glucose in blood, liver and skeletal muscle, together with the tissue glycogen, metabolites and amino acid composition pools, are given in both the maternal and foetal compartments compared with the virgin control rats. The utilization of alanine as a gluconeogenetic precursor is not increased in late pregnancy under 24-hour starvation and it depends on the lower blood substrate availability.

Administration, Oral↗

PubMed1990

In vivo C14-L-alanine metabolism in rat dietary obesity induced by cafeteria diet.

The "in vivo" handling of L-alanine in 24 hours starved rats, in which obesity was induced by feeding with cafeteria diet, was compared with that of starved control rats. 14C-alanine was administered in trace amounts in order not to affect the normal handling of this amino acid. The results obtained in blood and liver support a lowered glucose formation from alanine. The specific radioactivities corresponding to lactate, glutamate + glutamine and asparagine as well as total protein and total lipid, were all lowered in the obese group. This strongly suggests that glucose formation from alanine in the liver was impaired. The specific radioactivity of the metabolites studied in the striated muscle are compatible with the above suggestion. It can be concluded that the glucose alanine cycle operation is inhibited in the cafeteria diet starved obese rats.

Alanine↗

PubMed1989

Investigation of GAGS on 24-hour and 2-hour urines from calcium oxalate stone formers and healthy subjects.

The role of urinary glycosaminoglycans (GAGS) in calcium oxalate lithiasis is of great interest in urologic research. It has been claimed that GAGS are important inhibitors of calcium oxalate crystal growth and aggregation. The aim of this paper is to evaluate GAGS excretion and concentration in two groups of patients, calcium stone formers (with or without metabolic alteration) and a control group, to detect possible differences. The findings of this study show that significant differences exist not only in the 24-hour average excretion between stone formers without alteration and healthy subjects but also in the mean concentration values between the stone former and control groups. The same results are obtained from the 2-hour urine analysis. It is concluded that 2-h urine analyses of GAGS have the same or more practical value than a 24-h urine analysis and that the results must be expressed in terms of concentration.

Calcium Oxalate↗

PubMed1989

Metabolic response to short term starvation in non-pregnant and late pregnant cafeteria-obese rats.

We have determined the blood metabolite responses to a 24-h starvation period of cafeteria obese rats, in both non-pregnant and late pregnant states. In the fed condition the concentrations of glucose, lactate, pyruvate, glycerol and urea do not differ when compared in control and obese rats, but acetoacetate and 3-hydroxybutyrate levels are higher in the obese group. The overall response of the cafeteria-obese rats to starving seems characterized by decreased rates of glucose and amino-acids utilization, substituted by a more intense utilization of lipid fuels, with excess ketone bodies production and increased utilization of the mobilized glycerol. What we observed in the obese pregnant response to starvation can be summarized as the additional or superimposed effects of excess fat reserves. In the obese pregnant starved rats a less severe hypoglycaemia, lower levels of glycerol (as a consequence of increased utilization), reduced urea levels, and increased acetoacetate and 3-hydroxybutyrate levels were observed. It can be assumed that the pregnant obese rat response to starvation is related to the size of the fat deposits: the more obese, the more hyperketonaemia and less hypoglycaemia, and even diminished rates of amino-acid utilization, as indicated by a lower levels, when compared to the lean pregnant.

3-Hydroxybutyric Acid↗

PubMed1988

Body weight and tissue composition in rats made obese by a cafeteria diet. Effect of 24 hours starvation.

Rat body size and tissue composition changes from pre-weaning to three months age resulted from voluntary hyperphagia triggered by offering a cafeteria diet. The effects of a 24 hour starvation period in both cafeteria and chow fed controls were compared. Obesity develops earlier in females than in males. This difference is related to the growth patterns in both sexes. Obesity occurs at the stages of development when growth rate decreases. Cafeteria fed female rats attained a 32% greater weight than their controls, with lumbar adipose cords that were 4 times heavier and brown interscapular adipose tissue 2 times heavier than controls. The overall cafeteria fed versus chow fed rat differences in the effects of a 24 hour starvation, were minor but less liver glycogen and much more skeletal muscle lipids were mobilized in the cafeteria fed rats than in controls.

Adipose Tissue↗