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L Arola

Publications and source records attributed to L Arola.

At least 37 records · Page 2Linked to original sources
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

Long-term effects of cafeteria diet feeding on young Wistar rats.

The long-term effects of cafeteria diet feeding were studied by comparing the circulating levels of glucose, lactate, glycerol, 3-hydroxybutyrate and urea, and liver glycogen in female Wistar rats offered the diet from birth (CB) or from 30 days (C30) after birth, compared with controls fed on a standard reference diet. Body weight was maximal for CB, distinctly higher than that of C30, which in turn were heavier than controls. Growth rates, however, were similar for most of the period studied. Plasma glucose homeostasis was maintained fully in all three groups, with a remarkable lack of changes in liver glycogen concentration. The patterns of lactate and glycerol concentration changed with age. Different initial settings converged to adult values in all groups. The higher ability of cafeteria rats to use lipids as energy fuel is in agreement with their higher circulating levels of 3-hydroxybutyrate, a factor that may be essential in the shift to increased fat deposition that characterizes prolonged cafeteria feeding. Urea levels were highest in controls, and lowest in cafeteria rats fed from day 30, a consequence of the different setting of nitrogen sparing induced by the timing of initiation of cafeteria feeding. From the results presented it can be postulated that the type of diet onto which the rats are weaned may significantly affect their weight and metabolic correlations much later in life.

3-Hydroxybutyric Acid↗
PubMed1994

Effects of glucose, ethanol, Hg(II) and Cu(II) on almond beta-glucosidase.

The kinetic parameters of almond beta-glucosidase (beta-D-glucoside glucohydrolase; EC 3.2.1.21), using pNGP as substrate were kM = 2.24 +/- 0.11 mM and Vmax 588 +/- 25.1 U/mg protein. Only Hg(II) and Cu(II) showed irreversible inactivation of the enzyme. However, when these metals were present in the reaction system the inhibition effects were consistent with a mixed-type inhibition pattern (Cu(II) ki: 5.08 mM and Hg(II) ki: 0.07 mM). The glucose kinetic effect was also consistent with a mixed-type inhibition (ki = 406 mM) pattern with pNGP as varied substrate. Ethanol displayed the kinetic pattern of competitive inhibition (ki = 640 mM).

Amino Acid Sequence↗
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

Changes in plasma copper and zinc during rat development.

The association of copper and zinc to plasma ligands was studied during the rat perinatal period. Analysis was carried out by means of column chromatography (Sephadex G-150) and atomic absorption spectrophotometry. Levels of copper were low at birth and showed a sharp increase after day 10. This increase was similar to that of ceruloplasmin activity as well as its association with copper. Zinc levels, instead, showed higher levels before birth and decreased slowly toward the adult values. Association of zinc to albumin and associated proteins showed a pattern similar to the decrease in plasma zinc levels.

Aging↗
PubMed1993

The plasma amino acid response to cafeteria feeding and essential-amino acid gavage in weaning rats.

The plasma amino acid concentrations of cafeteria-fed and standard-fed rats gavaged either an essential amino acid mixture or saline solution have been studied from 14 to 30 days after birth. The consumption of a cafeteria diet caused higher levels in many amino acids. The amino acid-gavaged cafeteria-fed rats showed the highest cysteine levels. The amino acid gavage produced lower concentrations of alanine, glutamate+glutamine, hydroxyproline, proline and ornithine, in both cafeteria-fed and standard-fed animals. The results show that the supply of amino acids has a positive effect on nitrogen retention and amino acid availability in cafeteria-fed pups.

Alanine↗
PubMed1993

Nickel effects on hepatic amino acids.

Female Wistar rats were treated with nickel (single i.p. injection of 6 mg Ni(II)/kg body weight) and twenty amino acids and glutathione (GSH) concentrations were determined in liver 90 minutes later. Hepatic GSH content dramatically diminished after nickel injection. Glycine and glutamate levels, precursor amino acids of GSH, were not affected by nickel treatment, whereas cysteine level, the third precursor, was drastically increased in comparison with control rats. These findings showed that hepatic GSH depletion, caused by acute nickel exposure, was not due to a reduction in the availability of precursor amino acids. Nickel treatment also induced a 2-fold increase in phenylalanine and a decrease in taurine to one fifth. Therefore, the role of taurine in protecting membranes was clearly jeopardized in liver after nickel exposure, which could account for some of the toxicologic actions of this metal. However, further research is needed to explore such suggestion.

Amino Acids↗
PubMed1992

Nickel-induced hyperglycaemia: the role of insulin and glucagon.

Glucagon and insulin changes were measured in acute nickel-treated rats. Also, several parameters related to glucose homeostasis were evaluated. Nickel treatment caused an important and transitory rise in plasma glucose levels. These changes occurred simultaneously to hyperglucagonemia and hypoinsulinemia, leading to a drastic drop in the insulin/glucagon plasma ratio. In such a catabolic situation, hepatic and muscular glycogen levels remained almost unaltered. Hepatic fructose-2,6-bisphosphate (an indicator of gluconeogenic/glycolytic state) was drastically reduced a short time after nickel injection. Such events suggested that it was mainly gluconeogenesis and not glycogenolysis, which contributes to enhanced plasma glucose. Animals treated with large doses of glucagon did not mimic the hyperglycaemic responses induced by nickel, due to counteracting effects of insulin on plasma glucose. When diabetic rats were treated with nickel, the hyperglucagonemic response still remained, but plasma glucose levels did not increase at the same extent as when nickel was applied to control animals. Overall results suggest that both, glucagon and insulin changes are essential in the development of nickel-induced hyperglycaemia. Also, the lack of glycogenolytic response insinuates a direct or indirect inhibition of this process mediated by nickel and will need further investigation.

Animals↗
PubMed1992

Effect of diet and essential amino acids gavage on young rat amino acid metabolism enzymes.

1. The effects of a high-fat, high-energy diet and essential plus semi-essential amino acid gavage on pup rats have been studied (60-65 animals). 2. The activities of alanine transaminase, adenylate deaminase, glutamine synthetase and serine dehydratase have been tested in liver and muscle. 3. Plasma was used for the estimation of proteins, urea, amino acids, glucose, lactate, 3-hydroxybutyrate and acetoacetate. 4. Liver and muscle glutamine synthetase activities are increased by diet and gavage administered. Hepatic serine dehydratase is inhibited by a cafeteria diet but activated by amino acid gavage. Adenylate deaminase is inhibited by diet and gavage in the liver, but gavage does not affect this enzyme activity in muscle. Liver alanine transaminase is increased by the diet; in the muscle, cafeteria diet and amino acid gavage showed the highest values for this enzyme. 5. In the plasma, the increase in lactate produced by the diet is inhibited by the amino acids provided. Cafeteria-fed pups showed lower urea levels and higher 3-hydroxybutyrate concentrations in the plasma. 6. Intracellular glucose is diminished by cafeteria diet. In contrast, the blood cell amino acid concentration increases with diet and gavage supplied.

AMP Deaminase↗
PubMed1992

Effects of copper, cadmium and nickel on liver and kidney glutathione redox cycle of rats (Rattus sp.).

1. Glutathione redox cycle alterations induced by acute treatment of nickel, cadmium and copper, have been investigated in liver and kidney of adult male rats. 2. In liver, nickel treatment decreased GSH and GSSG levels, followed by a significant rebound in GSH content. Copper produced drastic reduction in the GSH/GSSG ratio, while cadmium treatment altered GSSG concentrations. 3. In kidney, the glutathione redox cycle remained unaltered after cadmium or nickel exposure, whereas copper caused similar changes to those observed in liver. 4. Hepatic glucose-6-P dehydrogenase and GSSG-reductase activities decreased after copper or nickel injection. GSH-S-transferase activity was altered in various ways, depending on the organ and the metal.

Animals↗
PubMed1991

Response to acute nickel toxicity in rats as a function of sex.

The effects of different nickel chloride doses upon blood and plasma glucose and essential metal homeostasis were studied in male and female rats. A definite sex-dependent response to injections of nickel has been observed for both the increase in plasma and blood glucose levels and the time at which these levels peak. Males showed a fast recovery from the rise in glucose levels and were much less affected by changes in the other parameters studied. In females, an extended rise in glucose levels was observed. All these effects are clearly nickel dose-dependent. Plasma, liver and kidney copper levels rose significantly in females while only a small decrease was observed in male kidneys. Zinc levels rose in all organs studied but males recovered to basal levels after the study period, whereas females maintained maximum levels at the end of the same period. An increase in urinary excretion of iron was observed. The present results show that the sex differences to acute nickel toxicity can be a helpful way to study metal interaction and discriminate between specific toxicity due to nickel or that induced by the associated hyperglucagonemia.

Animals↗
PubMed1991

Metabolic adaptations to nitrogen excess in late gestation in rat.

Pregnant rats of 19th and 21st days were given an acute nitrogen overload produced by an infusion of either 0.2 M ammonium acetate or 0.2 M glutamine. Metabolic adaptations to nitrogen excess were studied measuring--in fetomaternal unit--non-protein nitrogen content and the activities of enzymes related with ammonia metabolism. Maternal and fetal plasma urea levels were increased by ammonium acetate treatment. Glutamine overload increased more the amino acid content in the mothers than in conceptus. As response to ammonium acetate treatment, glutamate dehydrogenase activity in liver was more sensitive in pregnant than in nonpregnant rats, suggesting more nitrogen incorporation into amino acids in pregnancy. Regarding glutamine synthetase activity, both treatments had an opposite effect except in kidney. The adenylate deaminase activity of pregnant rats was inhibited similarly to nonpregnant rats by nitrogen overloads, but stronger after glutamine infusion. Placenta and fetal metabolism were adjusted, as the dams, to lack of ammonia production by nitrogen overloads and to glutamine synthesis by ammonium acetate infusion.

AMP Deaminase↗
PubMed1991

Postnatal development of plasma amino acids in hyperphagic rats.

The effect of feeding a highly palatable high-energy cafeteria diet on individual amino acid levels in plasma during postnatal development of the rat has been evaluated and compared to chow-fed controls. The cafeteria diet selected by the rats was hypercaloric and hyperlipidic, with practically the same amount of carbohydrate as the control diet, and slightly hyperproteic. In response to cafeteria feeding, significant decreases were observed in plasma serine and cysteine along the period studied. Significant changes with age during the growth period were shown by cafeteria-fed animals, which were not observed in control rats. Citrulline levels were lower on days 10 and 14 in cafeteria pups than in chow pups. Methionine was highest on day 30. Threonine was also higher at days 20 and 30, as was valine but with a nadir at day 10. Lysine showed maximal values on days 14 and 30.

Amino Acids↗
PubMed1991

Glutathione and related enzyme activity in the 11-day rat embryo, placenta and perinatal rat liver.

Glutathione reductase (EC 1.6.4.2; GSSG-R), glutathione peroxidase (EC.1.11.1.9; GSHpx) and glutathione transferase (EC 2.5.1.18; GST) enzymatic activities and glutathione status were investigated in 11-day embryos and the yolk sac, placenta and perinatal liver in rats. It is observed that: (a) levels of GSSG differ between the embryo (lower) and yolk sac (higher); (b) GSH concentrations increased significantly in fetal livers with respect to the days of gestation; in contrast, GSSG hepatic concentrations showed a significant rise with respect to time only during lactation; (c) the specific enzymatic activity of both GSHpx and GSSG-R were higher in the visceral yolk sac than in the embryo; (d) hepatic GSSG-R activity increased significantly during gestation. In addition, hepatic GSHpx and GST activities showed statistically significant increases over the period studied.

Aging↗
PubMed1991

Parallel modulation of brown adipose tissue GDP-binding, substrate uptake and (Na(+)-K+)-ATPase activity in the rat.

Brown adipose tissue (Na(+)-K+)-ATPase activity, in vitro glucose uptake and 2-aminoisobutyric acid uptake, as well as mitochondrial GDP-binding and succinate dehydrogenase activity were determined in order to study the relationship between these parameters in control, cold acclimated and cafeteria-fed rats. GDP-binding, (Na(+)-K+)-ATPase and glucose uptake were increased in interscapular brown adipose tissue from cold-acclimated and cafeteria-fed rats, whereas 2-aminoisobutyric acid uptake was only increased in cafeteria-fed rats. GDP-binding and (Na(+)-K+)-ATPase activity showed a high correlation coefficient suggesting a parallel modulation of both systems, which would probably share a common regulation mechanism.

Adipose Tissue, Brown↗
PubMed1991

Effects of acute nickel toxicity upon plasma and liver metal homeostasis as a function of sex.

The effects of an acute dose of nickel chloride (4 mg Ni/kg body wt) upon liver and plasma essential metal homoeostasis were studied in male and female rats. Total levels of copper and zinc in the tissues and in the fractions of chromatographic profiles (Sephadex G-100 and G-150) were determined. Plasma and liver levels of both metals rose significantly. The higher levels of copper in plasma are associated with increased ceruloplasmin activity and the initial increase of zinc in plasma is due to higher zinc content in the plasma albumin fraction. In the liver, the higher levels of both metals similarly affected all the metal-containing chromatographic fractions, although a significant increase is only observed in metallothionein-containing fractions, which agrees with previous reports on increased levels of metallothionein after nickel treatment. Regarding the sex-dependent changes, both sexes showed the same alterations, yet males recovered faster than females from all the nickel-induced changes in metal homoeostasis.

Animals↗
PubMed1990

Cytosolic copper-binding proteins in rat and mouse hepatocytes incubated continuously with Cu(II).

The proteins that bind copper when it first enters cells are likely to play roles in its intracellular distribution and utilization. When hepatocytes were incubated with 64Cu(II), the time-dependence of the subcellular distribution of 64Cu was consistent with one or more cytosolic proteins distributing copper to the mitochondrial and nuclear fractions. Cytosolic copper was reproducibly distributed among four protein fractions from Sephadex G-150 columns at the earliest time (1 min) and at the lowest concentration used [2 microM-64Cu(II)] with both rat and mouse hepatocytes. Copper binding to proteins in these functions was sensitive to copper metabolic status. Hepatocytes from nutritionally copper-deficient rats or neonatal (9-30 days old) developing rats showed an inverse correlation between copper binding to metallothionein and copper binding to proteins in fraction I (approximately 88 kDa apparent) and fraction II (approximately 38 kDa apparent). The distribution of cytosolic 64Cu from the brindled-mouse model of Menkes disease indicated decreased binding by a protein in fraction I. Brindled-mouse hepatocytes also contain decreased levels of a approximately 55 kDa protein or subunit, which most likely represents a liver-specific secondary response to the primary defect. The results are consistent with one or more copper-binding proteins in fractions I and II having significant functions in intracellular copper metabolism.

Animals↗