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X Remesar

Publications and source records attributed to X Remesar.

At least 91 records · Page 5Linked to original sources
PubMed1994

L-alanine transport in small intestine brush-border membrane vesicles of obese rats.

Membrane vesicles from the small intestine brush border were obtained and used to determine the possible effects of genetic or nutritional obesity on L-alanine uptake. Membrane vesicles from Zucker fa/fa obese rats and cafeteria diet-fed Zucker Fa/? rats showed the same characteristics as those of standard diet-fed lean animals. All preparations showed sodium-dependent transport as the main pathway for L-alanine uptake within the substrate concentration range tested. The apparent substrate affinity constant (Km) values and the pattern of inhibition of Na(+)-dependent L-alanine uptake by other amino acids (L-leucine and L-glutamine), suggests that system B involved in the transport of dipolar amino acids (formerly named Neutral Brush Border System) participates in the Na(+)-dependent transport of L-alanine. The affinity constant (Km) for L-alanine was essentially the same for all the groups studied (in the range of 10 mM). However, there was a higher (P < 0.05) maximal capacity (Vmax) in preparations from diet-induced obese animals (cafeteria diet) than that of genetically obese rats. These results indicate that either nutritional or genetic obesity may modify the capacity but not the affinity of transport systems for L-alanine uptake in the brush border of rat small intestine.

Alanine↗
PubMed1994

Hind leg muscle amino acid balances in cold-exposed rats.

The changes in hind leg tissue (muscle and skin) amino acid pool size and arteriovenous balance were measured in rats subjected to 0-90 min of cold exposure (4 degrees C). Tissue free amino acid pools presented a different composition pattern from protein amino acids. Muscle rapidly reacted to cold exposure by releasing small amounts of some amino acids (alanine, aspartate), with only small changes in pool size during the first 30 min. Amino acid oxidation was very limited during the whole period of cold exposure, since at all times tested there was either nil ammonia efflux or net absorption of ammonia and glutamine; i.e. the muscle was in positive nitrogen balance throughout the period studied. Thus most of the amino acid nitrogen taken up from the blood and not found in the free amino acid pools must have been incorporated into protein, since it was not oxidized, as shown by the glutamine and ammonia balance. The data on amino acid incorporation into proteins indicate that hind leg protein turnover is rapidly and widely modulated from a low initial setting upon cold exposure to a higher protein synthesis rate immediately afterwards, suggesting that protein turnover may have an important role in short-term events in cold-exposed muscle, in addition to its influence in long-term adaptation.

Amino Acids↗
PubMed1994

Management of dietary essential metals (iron, copper, zinc, chromium and manganese) by Wistar and Zucker obese rats fed a self-selected high-energy diet.

The balances and content of essential elements (iron, copper, zinc, chromium and manganese) in the body of Wistar, Zucker lean and Zucker obese rats fed a reference or cafeteria diet from day 30 to 60 after birth have been studied. Intestinal iron absorption compensated for low iron content of the cafeteria diet and the extra needs of growth and fat deposition. It can be assumed that the altered energy regulation processes that afflict the genetically obese rat are not directly related to altered iron metabolism. Obese Zucker rats had lower copper tissue concentrations than lean rats, but when fed a cafeteria diet the differences between Zucker rats strains disappear. This cannot be traced to large differences in diet copper concentration. A low diet availability of zinc--such as that of cafeteria-fed fa/fa rats--is easily compensated for by increasing absorption. So, as a consequence, we can conclude that genetic obesity did not impair zinc absorption. There was no deficit of zinc in any of the groups studied; the rats have enough capacity to extract zinc within a wide range of dietary concentrations. The absorption of dietary chromium was inversely proportional to its concentration. The ability to extract chromium from the diet and the very low urinary losses are a consequence of its scarcity in most dietary items. Despite wide variations in the manganese of the diets, the absorption rates were practically unchanged except for obese rats fed the cafeteria diet. It seems that this low absorptive capacity is enough to supply the rat with the manganese it needs, since a sizeable--but subjected to 8-fold-span variations--proportion is lost in the urine. This alone points towards a considerable excess of manganese in both diets studied. Obesity does not have a significant effect on the abilities to absorb and retain minerals, since these processes were more related to dietary availability. Management of essential metals by obese rats depends whether this condition is genetic or induced by diet. Most of the differences observed can be related to differences in diet concentration, to the excess fat content or different metabolic attitude to use substrates of obese animals. The data presented show that the cafeteria diet used adequately serves the mineral needs of the rat, since the rat adapts its absorbing and retaining strategies to match the dietary availability of these minerals.

Animals↗
PubMed1994

Effect of a cafeteria diet on energy intake and balance in Wistar rats.

The energy balance and nutrient selection strategies of 30-day-old Wistar rats offered a reference pellet and a seven-item cafeteria diet were studied in two consecutive 15-day periods: 30-45 and 45-60 days after birth. Cafeteria-fed rats grew faster, incorporating more fat and water, but a similar amount of protein to reference-fed animals. In the second 15 days all rats ate less and produced less heat than in the first 15 days. Reference-fed rats also deposited less energy in their bodies, in contrast to the tendency towards higher carcass energy deposition in cafeteria-fed rats. Cafeteria-fed rats selected much more fat and sugars than controls, with similar protein and less starch; in the second period studied, cafeteria-fed rats significantly increased their sugar consumption, with no change in fat or protein. It is suggested that the switch to selecting more sugars may be an essential factor in the shift towards increased fat deposition at the expense of heat production in cafeteria-fed rats.

Animals↗
PubMed1994

Whole-rat protein content estimation: applicability of the N x 6.25 factor.

The amino acid composition of the protein from three strains of rat (Wistar, Zucker lean and Zucker obese), subjected to reference and high-fat diets has been used to determine the mean empirical formula, molecular weight and N content of whole-rat protein. The combined whole protein of the rat was uniform for the six experimental groups, containing an estimate of 17.3% N and a mean aminoacyl residue molecular weight of 103.7. This suggests that the appropriate protein factor for the calculation of rat protein from its N content should be 5.77 instead of the classical 6.25. In addition, an estimate of the size of the non-protein N mass in the whole rat gave a figure in the range of 5.5% of all N. The combination of the two calculations gives a protein factor of 5.5 for the conversion of total N into rat protein.

Amino Acids↗
PubMed1994

Changes in alanine turnover rate due to nutritional and genetic obesity in the rat.

The changes in alanine turnover were determined in Zucker rats, which were either genetically obese (fa/fa) or rendered obese by dietary treatment (cafeteria fed). The whole body rate of alanine turnover was higher in genetically obese rats than in rats in which obesity was induced by diet (cafeteria). This is possibly due to variations in the rate of the amino acid incorporation into proteins, since the rate of whole body alanine degradation is the same for both groups. Thus, the different pattern followed by alanine turnover rate in these types of obese animals reflects the differences in the nitrogen economy of these animals, pointing to a higher alanine utilization in the genetically obese animals and a conservative management of alanine in the cafeteria-fed animals.

Alanine↗
PubMed1994

Splanchnic ammonia management in genetic and dietary obesity in the rat.

Three groups of 60-day-old Zucker rats: lean (Fa/Fa), obese by diet (Fa/Fa diet-obese) and genetically-obese (fa/fa) were fed ad libitum in order to study their splanchnic ammonia management. The study was also performed in 12 h food-deprived diet-obese and lean rats, to exclude a possible effect of diet composition on the parameters studied. Ammonia concentration was higher in the hepatic, portal and arterial plasma of diet-obese rats. The intestine did not contribute to a rise in the blood ammonia levels. This increase of ammonia in the blood of diet-obese rats coincides with higher alanine levels in plasma and a net glutamine production by liver. In fa/fa rats, ammonia levels were similar to those of lean rats, except for portal ammonia, which was lower. Hepatic availability of ammonia increased dramatically in diet-obese rats, but ammonia uptake by the liver was similar to that of lean rats. Conversely, hepatic availability of ammonia in fa/fa rats was similar to that of lean animals, whereas ammonia uptake by the liver was reduced to 50% of either lean or diet-obese values. Fasting for 12 h reduced plasma ammonia concentration in diet-obese rats: ammonia levels in the hepatic vein and aorta were similar to those of lean rats fasted for 12 h, whereas they were lower in the portal vein. Furthermore, ammonia hepatic availability was in the same range as that of lean animals, whereas ammonia uptake by the liver was reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine↗
PubMed1993

Distribution of oleyl-anilide hydrolysing activity in rat and human tissues.

A method has been developed and tested for the measurement of anilide hydrolysing activity in rat tissues. A concentrated solution of labelled oleyl anilide in isopropanol is added to the tissue homogenates and after incubation, the chloroform/methanol extract of the samples is chromatographed on Silicagel TLC plates and the oleic acid radioactivity is measured. The activity is time-, homogenate- and temperature-dependent, the optimal pH for measurement is 8 and there is no significant spontaneous anilide degradation. In the rat, the activity is widely distributed, with highest protein specific activity in the adipose tissues. The tissue activities of a same animal are fairly well inter-correlated, with rats showing very low activity in all tissues compared with others presenting high overall activity. The levels of activity found can easily explain the fast elimination of anilides administered to rats and their scant toxic effects. Human adipose tissue samples showed a wide range of anilide hydrolase activities per gram of protein, in general lower than in rats and with some values very low. It is postulated that this lack of anilide-hydrolising capability in some humans may be related to the incidence of the toxic oil syndrome.

Adipose Tissue↗
PubMed1993

Individual amino acid balances in young lean and obese Zucker rats fed a cafeteria diet.

The amino acid composition of the diet ingested by reference and cafeteria diet-fed lean and obese Zucker rats has been analyzed from day 30 to 60 after birth. Their body protein amino acid composition was measured, as well as the urinary and faecal losses incurred during the period studied. The protein actually selected by the rats fed the cafeteria diet had essentially the same amino acid composition as the reference diet. The mean protein amino acid composition of the rat showed only small changes with breed, age or diet. Cafeteria-fed rats had a higher dietary protein digestion/absorption efficiency than reference diet-fed rats. Obese rats wasted a high proportion of dietary amino acids when given the reference diet, but not on the cafeteria diet. In all cases, the amino acids lost as such in the urine were a minimal portion of available amino acids. In addition to breed, the rates of protein accretion are deeply influenced by diet, but even more by the age-or size-of the animals: cafeteria-fed rats grew faster, to higher body protein settings, but later protein accrual decreased considerably; this is probably due to a limitation in the 'blueprint for growth' which restricts net protein deposition when a certain body size is attained. Obese rats, however, kept accruing protein with high rates throughout. Diet composition--and not protein availability or quality--induced deep changes in amino acid metabolism. Since the differences in the absolute levels of dietary protein or carbohydrate energy ingested by rats fed the reference or cafeteria diets were small, it can be assumed that high (lipid) energy elicits the changes observed in amino acid metabolism by the cafeteria diet. The effects induced in the fate of the nitrogen ingested were more related to the fractional protein energy proportion than to its absolute values. Cafeteria-fed rats tended to absorb more amino acids and preserve them more efficiently; these effects were shown even under conditions of genetic obesity. There were deep differences in handling of dietary amino acids by dietary or genetically obese rats. The former manage to extract and accrue larger proportions of their dietary amino acids than the latter. The effects of both 'models' of amino acid management were largely additive, suggesting that the mechanisms underlying the development of obesity did not run in parallel to those affecting the control of amino acid utilization. Obesity may be developed in both cases despite a completely different strategy of amino acid assimilation, accrual and utilization.

Amino Acids↗
PubMed1993

Alanine uptake by liver of mid-lactating rats.

L-Alanine transport in liver plasma membrane vesicle preparations from fed virgin and 15-day-lactating rats was studied. Lactation was found to induce a decrease of the maximal rate (Vmax) of a high-capacity-low-affinity component of the Na(+)-dependent L-alanine uptake. However, a high-affinity-low-capacity agency was significantly induced in lactating-rat livers. L-Alanine uptake was differentially inhibited by other amino acids in those preparations from lactating rats, and showed different sensitivity to Li+ as a cosubstrate instead of Na+ and to inhibition by sulfhydryl modifying reagents (N-ethylmaleimide [NEM] and p-chloromercuribenzosulfonate [PCMBS]). All of these observations taken together suggest that system A is upregulated in lactating-rat livers, thus resulting in a different contribution of both agencies A and ASC to the total Na(+)-dependent alanine transport into liver plasma membrane vesicles. This was demonstrated using the analogue alpha-methyl-aminoisobutyric acid (MeAIB), a specific system A substrate. L-Alanine uptake rates, as calculated from plasma membrane enzyme marker recoveries, were also enhanced in the physiologic range of alanine concentrations in blood. Our results prove that the physiologic adaptation to lactation involves modulation of system A activity in the liver.

4-Chloromercuribenzenesulfonate↗
PubMed1993

A radio-enzymatic method for the estimation of L-leucine-specific radioactivity.

A method is presented for the estimation of L-leucine concentration and radioactivity in biological samples. The sample L-leucine is specifically bound to tRNA and its radioactivity estimated in the presence of either added labelled L-leucine or cold L-leucine (in the same proportion), as well as in the presence of a large excess of cold L-leucine. The latter gave the measurement of non-leucine radioactivity present in the sample. The measurements in the presence and absence of labelled/cold L-leucine allowed the estimation of L-leucine levels and radioactivity by using a simple set of calculations and a standard curve built with known cold L-leucine concentrations in the presence of a fixed known amount of [14C]L-leucine.

Alanine↗
PubMed1993

Cooling rates of tissue samples during freezing with liquid nitrogen.

The time-course of temperature changes undergone by tissue samples during freezing in liquid nitrogen has been studied with small thermocouple probes. The specific heat of liver, muscle, adipose tissue and blood has been measured with a calorimeter. Most tissues have lower specific heat values than water. The lower thermal conductance of adipose tissue and fat muscle result in much longer freezing times. It may take an inordinate amount of time for tissue samples to freeze when immersed in liquid nitrogen; in addition, not all tissues behave in the same way, so it takes longer for a muscle sample to freeze than for a piece of liver. These differences between tissues are considerable and may affect the outcome of experiments if not taken into account.

Adipose Tissue↗
PubMed1993

Rates of utilization of intravenous oleylanilide administered chronically to the rat.

The constant injection of [14C]oleylanilide into the vena cava of Wistar rats for 7 days with osmotic minipumps was used to estimate tissue distribution of chronically administered anilides. The largest concentrations of the anilide were found in the brown adipose tissue; all other tissues showed much lower proportions. When anilide distribution was expressed as nmol/g lipid, the high concentration of the compound in the brown adipose tissue contrasted with its very low presence in the white adipose tissue; all other tissues showed intermediate concentrations. Anilide-treated rats consumed more food and lost more weight than did controls; their energy balance showed higher energy inefficiency. The results suggest a possible effect of anilides on the thermogenic pathway of the rat brown adipose tissue. In addition, there was a large individual variability in the proportions of anilide present in all tissues, from as little as 0.3% of the total anilide injected in some animals to 6% in others.

Adipose Tissue↗
PubMed1993

Water balance in Zucker obese rats.

The water balance in Wistar, Zucker obese and Zucker lean rats, aged 60 days, was measured by determining the amount of water they drank, that contained in the solid food eaten, the water lost through urine and droppings, the net water accrued (estimated from the composition of the body and the daily increase in body weight), the measurement of the water vapour lost and the calculation of metabolic water production by means of the measurement of oxygen consumption, carbon dioxide production and protein oxidation in a 24 hr period. 1. Despite widely different body weights, all three groups of animals accrued a similar proportion of their daily water budget (4.3-4.9%, i.e. 1.2-1.4% of the total rat water mass). 2. Wistar and Zucker obese rats had a similar daily water budget despite very different body weights, lean Zucker rats had lower water budgets. 3. Obese and lean Zucker rats produced a more concentrated, and excreted much less urine (the highest urea concentration was found in obese rats) than Wistar rats. 4. The water lost in the droppings was in the same range as that in urine for obese rats, slightly less for lean Zucker rats and much less in Wistar rats. Obese rats produced a higher amount of stool with respect to the amount of food eaten than the lean animals studied. 5. The contribution of metabolic water to the daily water budget was a 23.6% for Zucker obese, 22.5% for Zucker lean and 15.9% for Wistar rats.

Animals↗
PubMed1993

Lipid synthesis: a thermogenic mechanism in cold-exposed Zucker fa/fa rats.

1. The oxygen consumption and carbon dioxide production of Wistar and Zucker lean (Fa/?) and obese (fa/fa) rats was measured at 4, 10, 20 and 30 degrees C. 2. There was a net synthesis of lipid at the expense of carbohydrate in Wistar rats at 20 degrees C, with active lipid oxidation at 4 degrees C, and increasing heat production at lower temperature. Zucker lean rats also showed this trend. 3. Zucker fa/fa rats synthesized lipid at 4, 10 and 20 degrees C, showing a less marked increase in heat production with lowering temperature. 4. It is postulated that Zucker obese rats synthesize lipids as a way to obtain residual metabolic heat to maintain their body temperature. This is part of a process--fully functional in Wistar and Zucker lean rats, and truncated in Zucker obese rats--in which liver lipogenesis can combine with brown adipose tissue lipolysis to generate enough heat to maintain body functions under a cold environment.

Animals↗
PubMed1993

Intestinal and hepatic nitrogen balance in the rat after the administration of an oral protein load.

The fate of a small oral dose of protein given to overnight-starved rats was studied. After 3 h, 62% of the protein amino acids had been absorbed. Most of the absorbed N went into the bloodstream through the portal in the form of amino acids, but urea and ammonia were also present. About one-quarter of all absorbed N was carried as lymph amino acids. The liver was able to take all portal free ammonia and a large proportion of portal amino acids, releasing urea. The hepatic N balance was negative, indicating active proteolysis and net loss of liver protein.

Amino Acids↗
PubMed1993

Methodological evaluation of indirect calorimetry data in lean and obese rats.

1. The applicability of current indirect calorimetry formulae to the study of energy and substrate balances on obese rats has been evaluated. The energy consumption of series of 60-day rats of Wistar, lean and obese Zucker stock were studied by means of direct and indirect calorimetry, and by establishing their energy balance through measurement of food intake and retention. Calorimetric studies encompassed a 24 h period, with gas and heat output measurements every 2 or 5 min, respectively, for direct and indirect calorimetry. 2. The analysis of fat composition (diet, whole rat, and synthesized and oxidized fat) showed only small variations that had only a limited effect on the overall energy equation parameters. 3. A gap in the nitrogen balance, which represents a urinary N excretion lower than the actual protein oxidized, resulted in significant deviations in the estimation of carbohydrate and lipid oxidized when using the equations currently available for indirect calorimetry. 4. Analysis of the amino acid composition of diet and rat protein as well as of the portion actually oxidized, and correcting for the nitrogen gap allowed the establishment of a set of equations that gave better coincidence of the calculated data with the measured substrate balance. 5. The measured heat output of all rats was lower than the estimated values calculated by means of either indirect calorimetry of direct energy balance measurement; the difference corresponded to the energy lost in water evaporation, and was in the range of one-fifth of total energy produced in the three rat stocks. 6. Wistar rats showed a biphasic circadian rhythm of substrate utilization, with alternate lipid synthesis/degradation that reversed that of carbohydrate, concordant with nocturnal feeding habits. Zucker rats did not show this rhythm; obese rats synthesized large amounts of fat during most of the light period, consuming fat at the end of the dark period, which suggests more diurnal feeding habits. Lean Zucker rats showed a similar, but less marked pattern. 7. The results obtained indicate that lean and obese rats can be studied using the same indirect calorimetry formulae provided that there is an adequate measure of protein oxidation and the composition of diet does not differ.

Amino Acids↗