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Biomedical subjects

R A Wapnir

Publications and source records attributed to R A Wapnir.

At least 91 records · Page 5Linked to original sources
PubMed1983

In vivo intestinal absorption of manganese in the rat.

The mechanisms of intestinal absorption of Mn in rats and the effects of low-molecular-weight ligands in this process were investigated using an in vivo perfusion system. Segments of either jejunum or ileum were perfused with isotonic solutions containing 0.0125 to 0.1 mM MnSO4 X 7H2O, in the presence or absence of double its concentration of either L-histidine (His) or citrate (Cit). In all cases the absorption of Mn declined with time; for example, in the absence of ligand Mn absorption fell from (means +/- SEM) 16.0 +/- 2.2 at 30 minutes to 2.3 +/- 4.1 pmol/(minute X cm) after 90 minutes of perfusion. Comparable declines occurred both in the jejunum and in the ileum in the presence of His or Cit. The initial absorption rates of Mn, obtained by extrapolation, were higher in the jejunum when His or Cit were present than when no ligands were included in the perfusate [means +/- SD, with His, 66.4 +/- 11.9; with Cit, 79.5 +/- 6.2; none = 17.8 +/- 3.3 pmol/(minute X cm)]. In the ileum, optimum absorption with His was observed between pH 7 and 8. The kinetics of in vivo Mn ileal absorption in the presence of His yielded a Kt of 0.056 mM and an estimated Vmax of 158 pmol/(minute X cm). The coefficient of diffusion was calculated to be 1.5 X 10(-3) cm2/minute. These data are compatible with a high affinity, low capacity, active transport mechanism for Mn in the rat intestine and suggest a limited role for small-molecular-weight ligands associated with both diffusional or active translocation processes.

Animals↗
PubMed1983

Absorption of zinc by the rat ileum: effects of histidine and other low-molecular-weight ligands.

The role of certain amino acids, dipeptides and organic acids as ligands to facilitate the intestinal absorption of zinc was investigated by using an in vivo procedure on ileal segments of adult rats. Ligand:zinc ratios equal to or less than 3:1 were optimal for amino acids and dipeptides such as L-glutamate, glycine, L-histidine, L-tryptophan and glycylglycine. An excess of ligand reduced zinc absorption. At a 130:1 L-histidine:zinc ratio the absorption of zinc was less than one-fourth that obtained at a 3:1 ratio. Picolinate was a less effective ligand. The kinetics of the complex L-histidine:zinc at a 2:1 ratio and at pH 7.5 were determined in the absence and presence of a 20 mM excess of amino acid in a zinc concentration range between 0.038 mM and 6.00 mM. In both cases the Vmax was 2200 pmol/(minute . cm), but the Kt increased from 0.54 mM to 1.46 mM in the presence of the L-histidine excess. These data suggest a competitive inhibition of the L-histidine:zinc complex by the amino acid. Such an effect was dependent on the stereoisomerism of histidine, since the unnatural D-isomer was far less effective than the natural L-isomer in facilitating zinc absorption. The presence of an intact protein (bovine serum albumin) sharply decreased the ileal absorption of the L-histidine:zinc complex.

Amino Acids↗
PubMed1983

Disaccharide feedings enhance rat jejunal macromolecular absorption.

Disaccharide feedings to post-weaning rats alters their jejunal barrier to macromolecular absorption. Penetration of horseradish peroxidase (HRP) across the jejunum was enhanced after short-term high concentration gavage (30 g . kg-1 . day-1) of lactose that produces weight loss, osmotic diarrhea, and jejunal mucosal damage. HRP absorption was also increased by longer term feedings of lower levels of disaccharide that did not produce body weight alterations, diarrhea, or cell damage. Rats without diarrhea and gavaged with 7.5 g . kg-1 . day-1 of either lactose or maltose showed an increase in lumen to blood HRP absorption after 21 days of feedings. Also, lactose or maltose in the solid food diet at 30 g . kg-1 . day-1 for 21 days did not lead to diarrhea but produced an increase in jejunal lumen to blood HRP absorption. Rats having no diarrhea and receiving 15 g . kg-1 . day-1 of lactose or maltose in the drinking water for 21 days, showed an increase in jejunal HRP absorption. When rats were fed either lactose or maltose for 21 days glucose absorption became totally dependent upon the sugar concentration in the perfusion medium. The kinetics of this glucose absorption are compatible with a decrease in the "unstirred" layer. Disaccharide-induced HRP absorption may be mediated by transport from endocytotic vesicles across the jejunal epithelium.

Animals↗
PubMed1983

Jejunal transport in experimental nephrotic syndrome.

In vivo jejunal transport of amino acids, monosaccharides, sodium, and electrolytes were studied in rats made nephrotic with puromycin aminonucleoside (PAN) and in pair-fed controls. Studies were performed 14 days after a single intravenous dose of PAN when rats were no longer edematous, but were still hypoproteinemic. There was decreased absorption of glucose, 3-0-methyl glucose, glycine, phenylalanine, histidine, water, and sodium in the nephrotic animals but transport of fructose, lysine and potassium was similar in the nephrotic and control animals. Enzyme kinetic studies for glucose transport showed a mixed type of inhibition affecting both Vm and Km. The jejunal mucosa of nephrotic and control rats had similar ATP content and enzyme activity for lactase, sucrase, maltase and (Na-K)-ATPase and the ratios of RNA to DNA were similar in the nephrotic and control rats. No abnormality of the jejunum was detected by light or electron microscopy. The data suggest that the impairment of absorption is a result of decreased activity of jejunal membrane carrier mechanisms. The altered transport may be secondary to effects related to the metabolic consequences of nephrotic syndrome and does not appear to be related to acute purine aminonucleoside toxicity, edema or malnutrition.

3-O-Methylglucose↗
PubMed1982

Placental permeability and energy metabolism enzymes in fetuses of lipemic rats.

A model of maternal lipemia without hyperglycemia, in the rat, produced by high-fat feedings, was developed to study the effects of and abnormal maternal lipid homeostasis on placental transport of nutrients and possible alterations of key enzymes of energy metabolism in the liver and brain of the fetuses. Pregnant rats fed lower concentrations of fat served as controls. All studies were carried out in dams and fetuses one day prior to delivery. The dietary treatment of the dams and fetuses produced in the fetuses ketonemia as well as lipemia. Following a bolus of 14C-3-0-methyl-D-glucose to the dams, the levels of the tracer remained higher in the blood and brain of lipemic than in control fetuses. By contrast, there was a decrease in the fluxes of 14C-alpha-amino-isobutyric acid in the fetuses of lipemic dams as compared to controls. Among enzymes of energy metabolism, fetal liver glucose-6-phosphatase and succinic dehydrogenase were enhanced by lipemia. Fetal brain glucose-6-phosphatase was depressed. Thus, lipemia, as occurring in poorly controlled maternal diabetes, may be a factor in determining the access to the fetus of essential, neutral amino acids and alter the normal activity of energy metabolism enzymes in the fetus.

Aminoisobutyric Acids↗
PubMed1982

Comparative ontogenesis of gamma-glutamyl transpeptidase in rat tissues.

In rats, placental gamma glutamyl transpeptidase (GGTP) specific activity declined linearly during the last third of gestation. In contrast, the kidney enzyme activity progressively increased 15-fold. In the gut, peak activity was reached at mid-lactation (age 12 days). Hepatic GGTP levels were maximal during the foetal stage. Brain GGTP was negligible at birth and attained its highest specific activity at weaning.

Aging↗
PubMed1982

Glycerol-induced hypoglycemia: a syndrome associated with multiple liver enzyme deficiencies. Clinical and in vitro studies.

A 4 10/12 yr-old white male presented with a history of occasional grand mal seizures and hypoglycemic episodes after overnight fasting. Upon evaluation, he became hypoglycemic after 1 g/kg oral glycerol challenge (plasma glucose: 31 mg/dl in 45 min), but had normal glucose, alanine and fructose tolerance tests. He responded well to a glucagon challenge after 11 hr fast but he became hypoglycemic and could not normalize his blood glucose after a 2nd glucagon stimulation test after 17 hr of fasting. Studies conducted on a percutaneous liver biopsy, and compared with 3 non-hypoglycemic controls, showed reduced activities (20%-30% of normal) of alpha-glycerophosphate dehydrogenase, alpha-glycerophosphate oxidase and fructose-1,6-diphosphatase. Alpha glycerophosphate in the patient's liver was elevated. Two types of electrophoresis showed absence of one enzymatically active zone and overall decrease of staining intensity for alpha-glycerophosphate dehydrogenase. Other liver enzymes tested were normal. The 50% inhibition of the patient's liver fructose-1,6-diphosphatase by alpha-glycerophosphate occurred, in vitro, or lower concentration than in controls (11 versus 22-40 mM). Electron microscopy revealed hepatocytes with moderately swollen mitochondria that very occasionally contained dense inclusions in the inner mitochondrial matrix. After discharge from the hospital, the patient followed a normal course, with a regimen of multiple snacks and avoidance of high-fat food in the morning.

Child, Preschool↗
PubMed1979

beta-2-Thienyl-DL-alanine as an inhibitor of phenylalanine hydroxylase and phenylalanine intestinal transport.

The inhibitory properties of beta-2-thienyl-dl-alanine on rat phenylalanine hydroxylase from crude liver and kidney homogenates were assessed in vitro and in vivo, as well as its effects on the intestinal transport of phenylalanine, by using a perfusion procedure in vivo. The apparent K(m) for liver phenylalanine hydroxylase changed from 0.61mm in the absence of the inhibitor to 2.70mm in the presence of 24mm-beta-2-thienyl-dl-alanine, with no significant change in the V(max.). For kidney the corresponding values were 0.50 and 1.60mm respectively. A single dose of beta-2-thienyl-dl-alanine (2mmol/kg) failed to inhibit phenylalanine hydroxylase in either organ. Repeated injections during a 4-day period caused a decline of the enzymic activity to about 40% of controls. Intestinal absorption of phenylalanine when perfused at 0.2-2.0mm concentration was also competitively inhibited by beta-2-thienyl-dl-alanine. Its K(i) value was estimated at 81mm. The limited inhibitory effects of beta-2-thienyl-dl-alanine towards hepatic phenylalanine hydroxylase and phenylalanine intestinal transport, and its rapid metabolism, as suggested by the small elimination of this compound in the urine and its virtual absence from animal tissues, are factors that restrict its potential usefulness as an inducer of phenylketonuria in rats or as an effective blocker of phenylalanine absorption by the gut.

Alanine↗
PubMed1979

Alterations of intestinal and renal functions in rats after intraperitoneal injections of lead acetate.

When lead acetate was administered intraperitoneally to young rats at a dose of 20 mg/kg (five times a week for 6 weeks), their growth rate was retarded when compared with controls injected with sodium acetate. Only a small amount of the heavy metal reached the circulation and exerted limited effects on typical target organs. However, large, electron-dense inclusion bodies were found in the abdominal cavity. The in vivo intestinal absorption of glucose was reduced. When perfused at 40 mM concentration, the experimental animals had a mean absorption rate of 152.1 nmol/min . cm vs. 230.6 in the controls (p less than 0.01). Also, sodium and potassium transport was reduced. No effects were observed on amino acid transport and (Na+-K+)-ATPase. Mg++-ATPase, glucose-6-phosphatase, fructose-1, 6-diphosphatase, pyruvate kinase, succinic dehydrogenase, and tryptophan hydroxylase in the small intestinal mucosa and the kidney were unaltered. Renal alkaline phosphatase was decreased. These studies confirm the greater susceptibility of some active transport mechanisms of the small intestinal mucosa to lead toxicity, compared to those of the kidney.

Amino Acids↗
PubMed1978

A pyridoxine-dependent behavioral disorder unmasked by isoniazid.

A 3-year-old girl had behavioral deterioration, with hyperkinesis, irritability, and sleeping difficulties after the therapeutic administration of isoniazid. The administration of pharmacologic doses of pyridoxine hydrochloride led to a disappearance of symptoms. After discontinuing isoniazid therapy a similar pattern of behavior was noted that was controlled by pyridoxine. A placebo had no effect, but niacinamide was as effective as pyridoxine. Periodic withdrawal of pyridoxine was associated with return of the hyperkinesis. The level of pyridoxal in the blood was normal during the periods of relapse. Metabolic studies suggested a block in the kynurenine pathway of tryptophan metabolism. The patient has been followed for six years and has required pharmacologic doses of pyridoxine to control her behavior.

Child Behavior Disorders↗