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Biomedical subjects

F Sánchez-Medina

Publications and source records attributed to F Sánchez-Medina.

At least 19 recordsLinked to original sources

Antihypercholesterolemic effect of dipyridamole in chickens.

The administration of a 4 mg/kg dose of dipyridamole daily in chickens fed a diet supplemented with 2% cholesterol reversed the hypercholesterolemic effects of the diet. In particular, it reduced the plasma cholesterol concentration in approximately 18%; the levels of very-low-density lipoproteins and intermediate-density lipoproteins and the liver cholesterol content. Although the mechanism was not fully elucidated, the increased excretion of cholesterol seemed to be responsible for the lipid lowering effect. When dipyridamole was administered in chickens fed the same diet without cholesterol no significant changes were observed. Inasmuch as the chicken lipoprotein metabolism differs in several aspects to human, the extrapolation of the hypocholesterolemic effect of dipyridamole to man must be made with care.

Animals↗

Plasma fatty acid profile in advanced cirrhosis: unsaturation deficit of lipid fractions.

Fatty acid (FA) profile of plasma total lipids, phospholipids (PL), cholesteryl esters (CE), and triglycerides (TG) were measured in 101 patients with advanced liver cirrhosis and in 44 age- and sex-matched healthy controls. Plasma levels of lipidic phosphorus, esterified cholesterol, and TG also were measured, and the unsaturation index (UI) was calculated for each fraction. Total plasma concentrations of saturated FA, linoleate, and polyunsaturated FA (PUFA) were lower in cirrhotics than in controls. This profile was also found in plasma levels of PL- and CE-associated FA. No detectable amounts of C20:3n9 were found in cirrhotic patients. Percent FA distribution of lipid fractions showed a lower percentage of linoleate and PUFA and a higher relative amount of saturated and monoenoic FA in cirrhotics than in controls. As a consequence, the UI of PL and CE was diminished in liver cirrhosis. Linoleate and PUFA deficiency was more marked in CE than in PL, as shown by the number of patients with values below the 5th percentile of the control group, suggesting an attempt to maintain the unsaturation of PL as the most important component of cell membranes. Hepatic failure, poor essential FA intake, and malnutrition are some of the possible etiologic factors for PUFA deficiency in cirrhosis. Their relative contribution to plasma FA abnormalities, as well as the clinical and pathophysiological consequences of PUFA deficit in cirrhotic patients, requires further investigation.

Adult↗

Metabolic changes induced by urethane-anesthesia in rats.

1. Fasting hyperglycemia was observed in urethane-anesthetized rats. No significant changes had been observed in fed animals. The effect is dose-dependent, being ineffective doses lesser than 1.4 g/kg of body weight. 2. Urethane originates a rise in glycemia during the first 10 min of anesthesia followed by control values at 30 min, and a latter hyperglycemic phase for more than 60 min that remain at 2 hr. 3. The negative correlationship between plasma glucose, lactate and amino acid levels suggest that gluconeogenesis may be the main responsibility of the observed hyperglycemia during the first phase, but it is possible that during the second phase a decrease in the consumption of glucose may take place as a consequence of the competitive effects of ketone bodies increased during the first 30 min of anesthesia. 4. We postulate that the mechanism of the hyperglycemic response to urethane is a sympathetic response with release of catecholamines both in the liver and in the adrenal gland which enhances gluconeogenesis and lipolysis.

Amino Acids↗

[Lipid profile in low birth weight neonates, small for gestational age].

Serum triglycerides, cholesterol, lipoproteins and fatty acids has been determined in 11 normal infants (RN) and 20 small for date newborn infants (SFD) at birth, before feeding, and at one week of life. All infants were bed with a milk formula (Maseda adaptado ) according with ESPGAN recommendations. Serum triglycerides are significantly increased in SFD after one week of feeding (p less than 0.01). Serum cholesterol in SFD show no differences in relation to normal infants. VLDL are significantly increased in SFD ab birth (p less than 0.01) reaching normal values after one week of feeding. After delivery SFD infants show a low serum level of linoleate (C18:2 omega 6) (p less than 0.05), linolenate (C18:3 omega 3) (p less than 0.02) and eicosadienoate (C20:2 omega 6) (p less than 0.02). No differences are observed in arachidonate (C20:4 omega 6). At one week after feeding no differences are observed in serum fatty acids between SFD and normal infants.

Cholesterol↗

Urinary 3-methylhistidine derivative as indicator of nutrients intake in low-birth-weight infants.

Urinary excretion levels of N-methylhistidine derivatives and N-methylhistidine/creatinine ratios were studied in a group of 20 small for date newborns, 10 premature infants and 8 normal infants, at birth and at one week of life. All infants were fed with an adapted milk formula supplying 2.8 g protein/kg body weight. 1-methyl and 3-methylhistidine urinary excretion were increased in all groups of infants from birth to the 7th day of life. Creatinine and N-methyl derivatives/creatinine ratios were also significantly increased at one week of life. The two ratios showed a higher level in small for date and premature infants than in normal infants at birth which continued relatively increased at one week of life. 3-methyl-histidine/creatinine ratio appears as a useful indicator of the turnover rate of muscular proteins in low-birth-weight infants.

Body Weight↗

Changes in serum albumin, transferrin and amino acid indices during the first month of life in small-for-date infants.

Total serum proteins, albumin, albumin/globulin ratio, and plasma-free amino acids have been determined in 12 small-for-date infants and in 14 normal infants at birth, at 1 week and at 1 month after birth. All infants were fed ad libitum with an adapted infant formula providing 1.9 g protein and 74 kcal/100 ml. Total serum proteins and albumin but not transferrin were low at birth in small-for-date infants, reaching normal values after 1 week of feeding. Serum globulins were low from birth to 1 week in small-for-date infants but they were normal after 1 month. Values for classical amino acid malnutrition indices suggest a state of protein-energy malnutrition which disappeared after 1 week of feeding.

Amino Acids↗

Serum and urine amino acid patterns during the first month of life in small-for-date infants.

Prenatal nutrition is impaired in small-for-gestational-age infants. Serum amino acids may show some biochemical features related to the nutritional state of these children. We have carried out a study on serum and urine amino acids in 12 small-for-date infants (SFD) and 14 healthy newborns from birth to 1 month of life. SFD infants showed a high serum level of alanine and decreased concentrations of branched chain amino acids, aspartate, cystine and tryptophan at birth. The results are compatible with a protein malnutrition state. Levels of serum amino acids in SFD infants showed no differences in relation to normal infants after 1 month of rehabilitation with a diet consisting of an adapted milk formula.

Amino Acids↗

Role of renal gluconeogenesis in the maintenance of glycaemia after L-tryptophan administration to rats.

The time-course of liver and kidney gluconeogenesis after L-tryptophan administration has been studied. Two and half hours after injection of L-tryptophan (0.5 g/kg body wt) a 97% inhibition of hepatic gluconeogenesis in starved rats was observed. Twelve hours later, the inhibition remained 35%. Hepatic glycogen was almost completely depleted (97%) in fed rats after 5 hours. At this time there was a severe hypoglycaemia in fed and 48 h starved rats which gradually disappeared with time, the values going back to normal after 12 hours. Tryptophan treatment was associated with a significant increase in renal gluconeogenesis in fed and 48 h starved rats with a maximum at 5 h (165% and 190% respectively). When hepatic gluconeogenesis was constantly inhibited in fed rats by periodic injection (every 4 h) of L-tryptophan, renal gluconeogenic ability remained increased throughout the experiment while blood glucose concentrations did not change. These observations suggest that kidney contributes to maintain glycaemic homeostasis under these conditions of liver gluconeogenesis impairment.

Animals↗

Evolution of gluconeogenic enzyme activities during starvation in liver and kidney of the rainbow trout (Salmo gairdneri).

1. There was a general increase in the activities of enzymes involved in gluconeogenesis in liver and kidney of rainbow trout, Salmo gairdneri, during the second month of starvation. 2. The need of gluconeogenesis during the first month of the starvation period was probably minimal because of the utilization of liver glycogen as a source of blood glucose. 3. The decline of fat was more pronounced than that of protein total content in absolute values, suggesting that lipid reserved were the main sources of energy during starvation.

Animals↗

Hormonal effects on the liver glucose metabolism in rainbow trout (Salmo gairdneri).

1. Glucagon, adrenaline and dibutyril cyclic AMP increased the release of glucose to the medium during incubation of liver slices from rainbow trout (Salmo gairdneri) while insulin had no effect. 2. Glycogen content decreased only slightly after cyclic AMP addition and even increased in the presence of glucagon and adrenaline. Consequently, the release of glucose was due mainly to gluconeogenesis. 3. This is corroborated by the reduction of glucose liberation in presence of alpha-cyanocinnamate, an inhibitor of gluconeogenesis.

Animals↗

Dissociation between renal gluconeogenesis and ammoniagenesis after acute liver intoxication.

Renal glucose and ammonia production as well as phosphoenolpyruvate carboxykinase and phosphate-dependent glutaminase activities were measured for acute liver intoxication. Gluconeogenesis and phosphoenolpyruvate carboxykinase activity increased, whereas ammonia production and phosphate-dependent glutaminase showed no changes with respect to the controls. The dissociation between gluconeogenesis and ammoniagenesis may be explained by the differential effect on the enzymes in these conditions.

Acidosis↗

[Stimulation of gluconeogenic capacity in partially hepatectomized rats (author's transl)].

Renal gluconeogenic capacity was enhanced to 150% 24 h after partial hepatectomy, remained increased at 48 h (144%) and returned to normal values at 72 h. Glucose production by renal cortical slices from hepatectomized rats was also enhanced 48 h after surgery when pyruvate, alpha-ketoglutarate and fructose were used as gluconeogenic precursors. The stimulation of renal gluconeogenic capacity seems to be due to the increase of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase activities which behaved similarly to glucose production after hepatectomy. The renal metabolic response may be partially due to starvation in the first 24 h. Afterwards food intake became normalized and the acceleration of glucose production should be attributed to hepatectomy. Since there was no metabolic acidosis in our experimental conditions the involvement of glucocorticoids in the stimulation of renal phosphoenolpyruvate carboxykinase and glucose-6-phosphatase activities is suggested.

Animals↗

[Biochemical indicators of malnutrition in children with intrauterine growth retardation].

The evolution of plasma and urine amino acids in "small for dates" newborns from the first hours of life to 30 days has been studied. The results obtained point out the occurrence of malnutrition in these newborns who have lower levels of plasma albumin than controls, high indexes of malnutrition from plasma aminograms and lower urinary excretion of histidine and its N-methyl derivatives. All indexes are normalized at 7 days of life with the used diet.

Amino Acids↗

[Selective inhibition of hepatic gluconeogenesis gy tryptophan administration].

The levels of quinolinic acid in liver and kidney and the gluconeogenic capacity in these tissues were determined in rats treated with tryptophan. The administration of this aminoacid produced a high increase in the hepatic quinolinic acid concentrations fed and 48 h. starved rats. On the contrary, only slight variations in the concentrations of renal quinolinic acid were observed. The highest value raised in these conditions was three times lower than Ki of the quinolinic acid for the phosphoenolpyruvate carboxykinase. These results suggest that tryptophan administration originates a selective inhibition of hepatic gluconeogenesis.

Animals↗

[Evolution of the content of gluconeogenic metabolites in rat liver and kidney during exercise (author's transl)].

The evolving concentration of metabolite intermediates for gluconeogenesis in liver and kidney has been studied in rats after varying periods of exercise (swimming in water at 22 degrees C). Lactate consumption by liver, according to the results, does not take place by gluconeogenesis primarily, since the values for malate, aspartate and PEP show a low in vivo activity for phosphoenolpyruvate carboxykinase. The PEP/aspartate ratio, on the contrary, gradually rises in kidney, suggesting a gradual increase in the in vivo activity of phosphoenolpyruvate carboxykinase, which agree quite well with the results of previously obtained in vitro. The prevention of metabolic acidosis by bicarbonate administration affects the metabolite profile in liver during exercise only very slightly. Renal phosphoenol-pyruvate carboxykinase activity in vivo decreases in relation to previously untreated rats, as well as gluconeogenesis, although to a lesser extent.

Animals↗