Browsing by Subject "Glucose -- Metabolism"
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Item Chromium and vanadium effects on glucose and lipid metabolism of guinea pigs and obese and diabetic mice(Texas Tech University, 1987-12) Li, Yi-chingNot availableItem Development and use of a new perfusion technique to study glucose metabolism of the aortic wall in normal and alloxan-diabetic rabbits(Texas Tech University, 1985-12) Brown, Barbara Jean MauritsonNot availableItem Effect of available glucose on glycogen synthase and phosphorylase of the rat tapeworm, Hymenolepis diminuta and the mouse bile duct tapeworm, Vampirolepis microstoma(Texas Tech University, 1988-08) Wages, Samuel EugeneThe primary purpose of this study was to correlate the available glucose with the activities of glycogen synthase and phosphorylase in two species of tapeworms. One species, Hymenolepls dimlnuta, is located in the small intestine of a rat. The other species, Vampirolepis microstoma, is located in the mouse bile duct. Available glucose was altered by manipulation of the host diet. The tapeworms were recovered from hosts that had been either fed a_d_ lib., starved 24 hr, or starved 24 hr then refed for 1 hr immediately prior to worm recovery. The proportion of glycogen synthase and phosphorylase in the active form was directly correlated with available glucose. In H. dimlnuta glycogen synthase was predominately in the inactive D^ form (> 90y6) in both the fed and fasted worms. When glucose from the diet was again available to fasted worms, D synthase was rapidly converted to the active I form (up to 90$). The tissue concentration of glucose almost tripled when fasted worms were refed 1 hr. Phosphorylase in H. dimlnuta was predominately in the active a form (> 80$) in worms from fed and fasted hosts, but activity of this enzyme was suppressed In worms from refed hosts {%a = 65$). The results obtained with microstoma followed a similar trend, but the changes were not nearly as extreme. The experiments were repeated in_ vitro, by incubating fasted worms in glucose and then measuring glucose uptake and the activity of the enzymes. It was discovered that Krebs-Ringer-Tris buffer was not an adequate incubation medium for incubations lasting for more than a few hours. However, RPMI 1640 tissue culture medium was a satisfactory incubation medium for long-term (overnight) Incubations. If RPMI 1640 was the incubation medium, similar results were obtained with H. dimlnuta and V. microstoma. It is suggested that the differences between the two species, in_ vivo, could be attributed to V. microstoma having access to glucose In the host’s bile.Item Estradiol stimulation of glucose transport in rat uterus(Texas Tech University, 1985-08) Meier, Daniel AlanA study of the mechanism of the estradiol-mediated increase in glucose transport in the uteri of ovariectomized rats was undertaken. An essential first step in this study was the characterization of the glucose transport process using plasma membrane vesicles. Uterine plasma membrane preparations were obtained by centrifugation on discontinuous sucrose gradients. The specific activity of the plasma membrane marker 5'-nucleotidase was increased 10-fold while the specific activity of an endoplasmic reticulum marker glucose-6-phosphatase was increased 3-fold. D-Glucose transport into plasma membrane vesicles was inhibited by sulfhydryl reagents, phloretin, and cytochalasin B. Uptake was prevented by high osmotic pressures. The Km of glucose transport was 12.2 +_ 1.1 mM. Transport was unaffected by sodium and was energy independent. 2-Deoxyglucose transport was determined in uteri of rats grouped by stages of the reproductive cycle, i.e., diestrus 1, diestrus 2, proestrus and estrus. The rate of 2-deoxyglucose transport was highest in proestrus and lowest in diestrus 1. The increase in glucose transport in ovariectomized rats was half-maximal at approximately 5 ng estradiol/rat and reached the maximal 2 to 3-fold response after 2 hours whether measured in whole tissue or in uterine plasma membrane vesicles. Estrone and estriol treatment resulted in a similiar 2-fold increase in glucose transport while progesterone and dihydrotestosterone had no effect. Injection of protein synthesis inhibitors cycloheximide and emetine resulted in an increase in the basal glucose transport rate while having no effect on the estradiolstimulated increase in glucose transport. Treatment with the transcriptional inhibitor actinomycin D resulted in a slight increase in glucose transport with no effect on the estradiol-stimulated increase in glucose transport. Antiestrogen treatment (nafoxidine and tamoxifen) resulted in a 85-90 % decrease in the total estradiol binding sites in the cytosol but did not effect the estradiol stimulated increase in 2-deoxyglucose transport in uterine tissue. Insulin injection (0.2 mg/rat) resulted in a 40 % increase in 2-deoxyglucose transport in 24 h-starved rats in contrast to the 200 % increase seen with estradiol treatment. Insulin and estradiol treatment together were not additive in regard to the increase in 2-deoxyglucose transport in tissue. Estradiol treatment did not change binding of [1251 ] insulin to uterine plasma membranes. Estradiol treatment resulted in a 3-fold increase in the Vmax with no apparent change in the Km for 2-deoxyglucose transport. Also, estradiol treatment did not result in an increase in the amount of glucose transporters in uterine plasma membranes as measured by antibodies raised against the glucose transporter protein from human erythrocytes. In summary, estradiol stimulates the rate of glucose transport in rat uterus by increasing the rate by which the transporter protein moves glucose across the plasma membrane .Item Regulation of glucose metabolism in Aspergillus niger by fatty acids(Texas Tech University, 1968-05) Ehrlich, Robert TracyNot available