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Biomedical subjects

F Lifshitz

Publications and source records attributed to F Lifshitz.

At least 109 records · Page 6Linked to original sources
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

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↗
PubMed1981

Jejunal macromolecular absorption and bile salt deconjugation in protein-energy malnourished rats.

The combined stress of protein-energy malnutrition (PEM) and exposure of the jejunum to pathophysiological (0.5 mM) levels of a bacterial metabolite, deconjugated bile salts, led to alterations not apparent with either stress alone. Perfusion of the jejunum of PEM rats with 0.5 mM deoxycholate (DCh) and a 40,000 dalton macromolecular tracer, horseradish peroxidase, led to higher serum horseradish peroxidase levels than were seen in PEM rats not exposed to DCh or in well-nourished controls treated with DCh. Semiquantitative cytochemical analysis indicated an increased number of villi with horseradish peroxidase penetration in PEM rats treated with 0.5 mM DCh. DCh perfusion of PEM rats also produced fine structural damage to epithelial cells not apparent in other preparations. And, perfusion with 0.5 mM cholate only produced sodium secretion in PEM rats. These observations in an animal model of PEM suggest that malnourished children with a colonic type of bacterial overgrowth of the small bowel may attain increased levels of foreign antigens or toxins from the intestinal lumen.

Animals↗
PubMed1981

Bile salt-enhanced rat jejunal absorption of a macromolecular tracer.

Bile salt deconjugation may occur in the jejunum under conditions of fecal colonic overgrowth of the small intestine. We studied the effects of conjugated and deconjugated bile salts on rat jejunal absorption of a macromolecular tracer, horseradish peroxidase, in an in vivo perfusion system. At a 0.5 mM perfusion concentration, only the deconjugated bile salts, cholate and deoxycholate, produced a significant increase in horseradish peroxidase absorption into serum. At a 0.5 mM concentration of the conjugated salt, taurocholate, horseradish peroxidase-absorption was indistinguishable from that seen in bile salt-free preparations. At a higher 5 mM concentration, both the conjugated and deconjugated salts increased jejunal HRP absorption into serum over that seen in bile salt-free preparations; this absorption wa most marked with the deconjugated salts. At a 0.5 mM level, the bile salts induced minimal sodium and glucose transport alterations but did not produce evidence of morphologic damage to villi or absorptive epithelial cell organelles. At a 5 mM level, the deconjugated salts induced glucose and sodium transport abnormalities and appeared to damage cellular organelles. Our observations suggest that an alteration in the tight junctional barrier to macromolecular absorption may play a role in some of the enhanced horseradish peroxidase absorption seen with deoxycholic acid in these experiments. The process of an increased absorption of intact macromolecules induced by products of bacterial metabolism may be of pathologic significance in the etiology of immunologically related intestinal disease or in toxigenic processes.

Animals↗
PubMed1980

Low-dose insulin infusion in the treatment of diabetic ketoacidosis: bolus versus no bolus.

The effects of an initial iv bolus of insulin upon plasma glucose, blood gases, and electrolytes were assessed in 19 children with 20 episodes of diabetic ketoacidosis treated by a continuous low-dose insulin infusion of 0.1 unit/kg/hour. An iv bolus of insulin administered prior to low-dose insulin infusion accelerated the decline of plasma glucose concentration during the first hour of treatment, but differences in decline of mean plasma glucose concentration were not apparent thereafter. The mean time required for attaining "normoglycemia" (250 mg/dl) was similar, whether or not the initial bolus of insulin was given, with a smooth and predictable correction of initial hyperglycemia in the majority of children. However, an accelerated response was more frequent in those patients with compensated metabolic acidosis, who received an initial iv bolus of insulin; those with more severe metabolic acidosis took longer to recover. The data suggest that an initial iv bolus of insulin may not be required nor desirable in the majority of children with diabetic ketoacidosis treated by a standard low-dose insulin infusion regimen.

Adolescent↗
PubMed1980

Zinc status and its relation to growth retardation in children with chronic inflammatory bowel disease.

Zinc status was studied in 30 patients with chronic inflammatory bowel disease (CIBD) as well as in 17 normal children, 13 primordial short stature, and 17 anorexia nervosa patients. Basal serum and urinary excretion levels of zinc were measured in all patients. In addition, a zinc loading test was performed in 16 CIBD patients, 21 normal and/or short stature children, and nine patients with anorexia nervosa. Eleven of 30 patients with CIBD had serum zinc values less than 0.7 microgram/ml, whereas none of the other patients had hypozincemia. In addition, the mean urinary zinc excretion of CIBD patients was significantly lower than that of patients with primordial short stature and with anorexia nervosa. An altered response to oral zinc load was the most frequent abnormality in CIBD patients. Those with moderate and severe clinical disease activity had a decreased serum rise of zinc after the oral load of this ion. Urinary excretion of zinc after oral load was also marked by deficiency in all CIBD patients. The abnormalities of zinc metabolism were more frequent among the CIBD patients with growth abnormalities, although they were also found in patients who had normal growth. Among the 14 patients with CIBD and growth abnormalities, seven were hypozincemic and four hypozincuric. Hypozincemia was only found in four patients who had normal height; however, the growth velocity was not known. The zinc tolerance test revealed abnormalities in four of five CIBD patients with short stature and in two of three patients with slow growth. On the other hand, similar alterations in zinc tolerance tests were seen in three of seven CIBD patients with normal height and growth.

Adolescent↗
PubMed1979

The response to an oral glucose load during convalescence from hypoxia in newborn infants.

The ability to tolerate an oral glucose load during convalescence from hypoxia was studied in four term and 11 premature appropriate-for-gestational-age infants by sequential measurements of the changes occurring in blood pH, bicarbonate, plasma lactic acid, and plasma glucose following an oral glucose load. All infants developed metabolic acidosis and lactic acidemia after the oral glucose load. The maximum fall in blood bicarbonate occurred at 30 minutes, and the maximum rise in plasma lactic acid concentration was attained at 60 minutes. The metabolic changes were found to be more severe in infants given the oral glucose load early in their convalescence and in those infants less than 10 days of age. The absorption of glucose was also decreased in these infants, as shown by a reduced rise in blood sugar. These observations indicate that newborn infants, term or premature, tolerate glucose loads poorly during convalescence from hypoxia.

Acidosis↗
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

The effects of small intestinal colonization by fecal and colonic bacteria on intestinal function in rats.

The effects of colonic and fecal bacterial proliferation on jejunal function were studied in normal rats and in low-germ rats after intraperitoneal injections of mecamylamine HCl. Jejunal bacteriology, bile salts, ultrastructure, and transport capacity were assessed. Normal rats given mecamylamine for 3 days had increased anaerobic bacteria in the intestinal fluid, and had high concentrations of deconjugated bile salts in the intraluminal contents. Jejunal bacteria were lodged between microvilli without penetrating the cell cytoplasm. However, there was focal cellular damage, including fused microvilli, dilated endoplasmic reticulum, and secondary lysosomes. In the mecamylamine treated normal rats intestinal glucose transport was reduced with an alteration compatible with noncompetitive inhibition. The absorption rates of galactose, fructose, 3-0-methyl-D-glucose, tyrosine, Na, and K were also decreased. In contrast, low-germ mecamylamine-treated rats showed no evidence of either increased anaerobic bacterial proliferation or deconjugation of bile salts, and had none of the fine structural alterations seen in regularly raised rats. Also, the transport of carbohydrates was unaltered. The findings suggest that non-invasive enteric proliferation of colonic and fecal bacterial anaerobes in rats may be associated with deconjugation of bile salts, ultrastructural alterations of the intestinal epithelial cells, and a diminished jejunal transport capacity of carbohydrates and other solutes.

Anaerobiosis↗
PubMed1978

Response of rat intestine to a hyperosmotic feeding.

After a single force-feeding of hypertonic (1300 mOsm) mannitol to rats there is rapid osmotic equilibration of the jejunal fluid, a sharp drop in luminal mannitol concentration and large influxes of water and sodium. During osmotic equilibration there was a significant loss of cells from the jejunal mucosa. In hypertonically fed rats there was an accumulation of protein, DNA, [3H]thymidine-labeled DNA, and disaccharidases in intestinal washings. Brush border disaccharidase specific activities on the jejunal mucosa were unaltered. Under the light microscope jejunal villi from hypertonic mannitol rats were comparable to controls. Some epithelial cells from rats force-fed hypertonic mannitol showed transient ultrastructural damage. Microvilli of some cells were shortened and fused at their bases 20 and 40 min after the force-feeding. By 120 min epithelial cell microvilli were all normal in appearance. In hypertonically fed rats the lateral interdigitating plasma membranes became disorganized. Large fragments budded off into one cell and fused to form larger stuctures. By 120 min many lysosomal autophagic vacuoles and residual bodies were seen. A single hypertonic force feeding produced jejunal cell loss associated with loss of brush border disaccharidases and focal ultrastructural damage.

Animals↗
PubMed1978

Alterations in rat jejunal permeability to a macromolecular tracer during a hyperosmotic load.

The effects of intraluminal hyperosmolality on the intestinal permeability of a macromolecular tracer, horseradish peroxidase, was assessed in rats by light and electron microscopic cytochemistry. After 60 minutes of an intraluminal hypertonic perfusion of 600 mOsM mannitol, horseradish peroxidase was demonstrable in the intercellular spaces between adjacent absorptive epithelial cells of jejunal villi, along the microvillar brush border, in numerous pinocytotic vesicles, in multivesicular bodies, as well as in large lysosomes. Horseradish peroxidase was frequently found extending from the luminal surface of the cell through the tight junctional region and into more basal portions of the intercellular space. In occasional cells, fragments of the interdigitating plasma membranes of two adjacent absorptive cells appeared to bud off into the cytoplasm of one cell. In contrast, after 60 minutes of isotonic perfusion, horseradish peroxidase was confined to the microvillar brush border, a few pinocytotic vesicles, and occasional multivesicular bodies. These experiments suggest that the passage of macromolecules across the jejunal epithelium of adult rats is enhanced under conditions of luminal hyperosmotic stress. This may be due to an alteration in the functional integrity of the tight junctional macromolecular barrier or to an enhanced rate of pinocytosis.

Animals↗