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Biomedical subjects

F Lifshitz

Publications and source records attributed to F Lifshitz.

At least 127 records · Page 7Linked to original sources
PubMed1978

Experimental acute hypothermia and intestinal cellular integrity.

Shaven and unshaven rats were exposed to a cold stress at 4 degrees C for 6 hr (SE and UE). Control animals remained at room temperature (SC and UC). Hypothermia was induced in group SE, with mean rectal temperature of 22.0 +/- 2.0 degrees C (+/- S.E.M.). All other groups were normothermic, had similar arterial pO2 and hepatic tryptophan oxygenase levels. Acute hypothermia induced a sloughing of cells from the villi into the lumen of the gut, as indicated by an increased DNA in luminal washings. However, there was an unimpaired 3H-thymidine incorporation into the DNA of the intestinal mucosal cells and those present in lumina washes. Intestinal disaccharidases and alkaline phosphatase were not altered. This suggests that more severe cellular alterations reported earlier in hypothermia may have been caused by associated factors other than a decreased body temperature.

Alkaline Phosphatase↗
PubMed1978

Effects of enteric microbial overgrowth on small intestinal ultrastructure in the rat.

The ultrastructural effects of bacterial proliferation in the upper gastrointestinal tract induced by intraperitoneal injections of mecamylamine HCl were investigated in rats. We found increased populations of nonspecific enteric bacteria in the lumen of the upper small intestine and ultrastructural abnormalities in the absorptive epithelial cells, including increased numbers of lysosomal vacular structures, fused microvilli and dilated endoplasmic reticulum. The bacteria did not penetrate into the damaged mucosal cells and so actual cytoplasmic infiltration is apparently not required in order to cause these ultrastructural changes. The alterations were not merely due to the pharmacologic agent we used, mecamylamine, since rats with subnormal numbers of enteric bacteria in the upper small intestine, whether subjected to the course of the drug or not, did not display the ultrastructural changes noted above. Concomitant with increased numbers of enteric bacteria in the small intestine, there were increased concentrations of deconjugated bile salts and decreased absorption of glucose. These findings are compatible with the following hypothetical sequence of pathogenesis: mecamylamine leads to intestinal stasis leads to bacterial overgrowth leads to deconjugation of the bile salts leads to ultrastructural alterations.

Animals↗
PubMed1977

Interaction between dietary carbohydrates and intestinal disaccharidases in experimental diarrhea.

The effects of carbohydrate intake on jejunal disaccharidases in rats with chronic mannitol-induced, osmotic diarrhea were studied. Weanling rats were force-fed 5 ml/100 g of body weight of water of 20% mannitol (w/v 1300 mOsm) daily for up to 14 days. Diets containing 70% of either starch, sucrose, glucose, or 20% lactose with 50% starch were fed ad libitum. Mannitol-fed rats had increased water intake and diarrhea. They gained weight, but less than controls. The levels of intestinal disaccharidases in mannitol-fed rats were related to dietary carbohydrate intake. Seven days of mannitol treatment led to lactase and sucrase deficiencies in rats fed starch whereas jejunal maltase and alkaline phosphatase were unchanged. Deficiencies in lactase and maltase but not in sucrase were induced when rats were fed a sucrose diet, while a decrease only in sucrase occurred in rats fed a lactose-starch diet. Rats with mannitol-induced diarrhea fed a glucose diet had reduced levels of all disaccharidases. The changes in intestinal disaccharidases were not associated with alterations in the number of epithelial cells or ultrastructural abnormalities. 3H-thymidine incorporation into DNA following 7 days of mannitol treatment was similar to water-fed controls. Absorptive epithelial cells were not damaged and the microvilli were normal in height and appearance. These data suggest that the levels of specific disaccharidases show and enhanced dependence upon the corresponding dietary substrates during diarrhea induced by an osmotic load.

Alkaline Phosphatase↗
PubMed1977

Fasting-induced hypoglycemia in experimentally malnourished rats.

The ability to withstand a fasting stress as related to glucose homeostasis was studied in malnourished rats. Young male Wistar rats were fed a low-protein (D), or a low-protein, low-energy diet (M) containing, respectively, 4% protein with 70% carbohydrate (D) and 4% protein and 45% carbohydrate (M). They were compared with rats fed a control diet with 18% protein and 70% carbohydrate (C). All diets contained 8% fat. After consuming the respective diets for 4 weeks, the rats were either killed or fasted for 24 or 48 hours. Hypoglycemia developed in the malnourished rats upon fasting, but not in those receiving a complete diet. Malnourished rats had a higher blood glycine level after 4 weeks of dietary treatment. There was a marked decrease of circulating alanine and glutamate-glutamine after 48 hours of fasting in all rats. There were no differences in lysine, histidine, glycine and serine-valine. Protein malnutrition produced an increase in brain lysine, gamma-aminobutyric acid, glycine and alanine, and of glycine and alanine in liver. In contrast, D and M rats showed a depletion in muscle lysine, alanine, serine-valine and glutamate-glutamine. The fasting stress produced no changes in brain or muscle glycogen. However, liver glycogen of rats fed the D and M diets was below that of rats fed the C diet for 4 weeks. In addition, after 48 hours of fasting the C rats mobilized more exhaustively their glycogen stores that the M rats. These data suggest that in chronic malnutrition, rats may maintain their glucose homeostasis by mobilization of muscular gluconeogenic amino acids through proteolysis or de novo synthesis. Rats which were fed protein and protein-energy-deficient diets lacked adequate liver glycogen stores and their overall gluconeogenic capacity was exceeded during fasting with resultant hypoglycemia.

Adaptation, Physiological↗
PubMed1977

Isolated thyrotrophin deficiency in diabetes mellitus.

Hypothyroidism in patients with diabetes mellitus is usually primary though rarely secondary hypothyroidism has occurred. An 11 6/12 year old white female developed diabetes mellitus at 8 6/12 years of age. She received treatment up to 40 units NPH daily with adequate control and normal growth. Hypothyroidism was diagnosed after a 3 month history of lethargy, constipation, dryness of skin and decreasing insulin requirement to 10 units NPH per day. Physical examination was entirely normal, except for dry skin. Serum levels of free thyroxine, thyroxine, T3 resin uptake, were low as was 131I uptake. Primary hypothyroidism was ruled out by the absence of goitre, absent antithyroid antibodies, low basal TSH levels and increased 131I uptake after TSH administration. Serum TSH levels rose 4-fold in respone to intravenous TRH administration. The patient was treated with 0.15 mg daily of L-thyroxine with very good response. This report describes a patient with juvenile diabetes mellitus and isolated TSH deficiency with hypothyroidism of probably hypothalamic origin, an association not previously described in children.

17-Hydroxycorticosteroids↗
PubMed1975

Inhibition of sodium intestinal transport and mucosal (Na+-K+)-ATPase in experimental Fanconi syndrome.

The administration of 1.5 or 9.0 mmoles/kg ip of maleate to rats induced, in addition to renal alterations similar to those occurring in the Fanconi syndrome, a decline in the intestinal mucosa (Na+-K+)-ATPase with a simultaneous decrease in sodium intestinal transport and an increase in potassium absorption. Further differences in the behavior of the two electrolytes were observed when the concentration of sodium in the perfusates was altered. No changes occurred in amino acid or glucose transport in experimental animals.

Adenosine Triphosphatases↗