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Biomedical subjects

S W Thenen

Publications and source records attributed to S W Thenen.

30 records · Page 2Linked to original sources
PubMed1978

Blood and liver folacin activity, formiminoglutamic acid excretion, growth and hematology in guinea pigs fed a folacin deficient diet with and without sulfonamides.

Dietary folacin deficiency in the presence and absence of dietary sulfonamides was studied in the guinea pig for the purpose of relating the growth and hematologic effects of folacin deficiency to tissue and biochemical changes. Six-week old female guinea pigs fed control and folacin deficient diets with and without 0.1% sulfonamides for 6 to 7 weeks. Growth was significantly reduced in both groups fed the folacin deficient diets, and 25% of all deficient animals died. Macrocytic anemia was not present, but reduced leukocyte numbers were observed in folacin deficiency. Plasma and red blood cell folacin activities were reduced by about 50% in deficient guinea pigs in the presence and absence of dietary sulfonamides. Both liver total folacin activity and urinary formiminoglutamic acid excretion were not significantly altered by the degree of folacin deficiency obtained in this study.

Animals↗
PubMed1978

Megaloblastic erythropoiesis and tissue depletion of folic acid in the cat.

Dietary requirement for folic acid was shown in the cat. Folic acid deficiency was produced by feeding young cats a deficient diet (0.125 mg of total folate/kg of dry weight by analysis) for 22 weeks. The folic acid-deficient cats grew normally, but had reduced plasma, red blood cell, and liver folate concentrations in comparison with those concentrations in cats fed a control diet (1.36 mg of total folate/kg).. Urinary excretion of formiminoglutamic acid was increased in all deficient diet cats 24 hours after L-histidine injection. Erythroblasts in bone marrow smears from folic acid-deficient cats were megaloblastic; they showed abnormal nuclear chromatin patterns and had nuclear-cytoplasmic asynchronism.

Animals↗
PubMed1977

Energy utilization of a low carbohydrate diet fed genetically obese rats and mice.

Genetically obese Zucker rats, ob/ob mice and non-obese littermates were fed low carbohydrate (2%, 48%, and 50% of energy as carbohydrate, protein, and fat, respectively) and control (60%, 19%, and 21%, as carobhydrate, protein, and fat) diets. The oxidation of the energy components of these diets was measured by adding D-[U-14C]glucose, L-[U-14C]glutamic acid, and glyceryl tri-[1-14C]oleate to test meals given intragastrically and collecting respiratory CO2 for 4 hours. The animals responded to the low carbohydrate diet by oxidizing less glucose and more glutamic acid, but these amounts were proportional to dietary carbohydrate and protein composition, In contrast, the animals oxidized both higher amounts and percentages of glyceryl trioleate when fed the low carbohydrate diet. Obese Zucker rats oxidized less fat than non-obese rats when fed both diets, while obese mice oxidized fat to the same extent as non-obese mice. Feeding the low carbohydrate diet significantly increased body weight in the obese mice, but not in obese rats and non-obese mice and rats. The effect of obesity and the low carbohydrate diet on food intake, serum glucose and lipid values and CO2 production are also reported.

Animals↗
PubMed1975

Adipose tissue glycerokinase activity in genetic and acquired obesity in rats and mice.

Glycerokinase activity in isolated fat cells was elevated in both Ob/Ob and Db/Db mice in comparison to their lean controls and this elevation was associated with obesity, hyperinsulinemia and hyperglycemia. In the other forms of acquired and genetic obesity in the rats and mice studied (also associated with hyperinsulinemia), adipose tissue glycerokinase activity was not elevated in comparison to lean control groups when expressed on a mg protein basis. It is concluded that the elevated glycerokinase activity is not due to the specific Db or Ob mutation, but is secondary to the obesity and hyperinsulinemia interacting with the similar genetic background in the C57BL/KsJ and the C57BL/6J mouse strains.

Adipose Tissue↗