Thesis (Ph. D.)--University of Chicago. / "Reprinted from the American Journal of Physiology. Vol. XIX--July 1, 1907--No. II." "A Study of the Oxidizing Power of Cupric Acetate Solutions / by A.P. Mathews and Hugh McGuigan"--P. 199-222. Includes bibliographical references.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1959. / Typescript. Abstracted in Dissertation abstracts, v. 19 (1959) no. 8, p. 2107-2108. Includes Metabolic differences between hepatic parenchymal cells and a cultured cell line from liver, by W.F. Perske, R.E. Parks, Jr., and D.L. Walker, reprinted from Science, vol. 125 (1957) no. 3261, p. 1290-1291. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

In an attempt to find out whether decreased blood sugar level is associated with impaired cognitive function, adverse emotional changes, or somatic symptoms, 36 subjects who believed or suspected that they had hypoglycemia were given 5-hour glucose tolerance tests (GTTs). After each of the nine blood samples taken during the GTT, the subject's mood, performance on the Serial Sevens Test (SST), and somatic symptom reports were recorded. The subjects reported significantly more negative affect after glucose nadir (the lowest level of blood sugar reached) than before nadir, and endorsed more somatic symptoms after nadir than before nadir. SST performance deteriorated at glucose nadir. All of these effects were more pronounced for subjects with high hypoglycemic index scores than for subjects with low index scores. The index is calculated from the speed and magnitude of the decrease in blood sugar, and the absolute value of the nadir. The impairment in SST performance was greater for subjects who showed rapid decreases in blood sugar than for subjects who showed slow decreases. Dividing subjects by high and low nadirs, large and small magnitudes of decrease, and by large and small decreases below fasting level, did not reveal any differences in symptomatology. It is concluded that changes in mood, reports of somatic symptoms, and inferior performance on a mental arithmetic task are associated with lowered blood sugar levels, especially in subjects with high hypoglycemic index scores. / Arts, Faculty of / Psychology, Department of / Graduate

No description available.

In an effort to assess whether the craving for sweets experienced by some abstaining alcoholics is physiologically based, 48 Wistar rats were divided into 4 groups. Groups 1 and 3 were fed a liquid diet containing 35.5 percent energy as alcohol; groups 2 and 4 were fed a control diet with dextrins substituted for alcohol, all for 24 days. Group 4 was pair-fed to group 3. For the next 10 days, all rats were provided with sucrose and water ad libitum and all groups were continued on their liquid diet except that alcoholic group 3 was placed on the control diet and pair-fed group 4 was no longer pair-fed. Urine was collected at the end of the baseline, alcohol-induction, and recovery periods and analyzed for L-ascorbic acid. The mean consumption of sucrose was highest for rats still receiving alcohol and declined in all groups during the 10 days. The mean consumption of sucrose (% kcal as sucrose) for the first 4 days was 33.2, 19.5, 19.0, and 13.8% for groups 1, 2, 3, and 4 declining to 24.6, 11.2, 9.0, and 8.5 percent, respectively by the last 4 days. The sugar intake of alcoholic group 3 animals was significantly higher than pair-fed control group 4 during the first 4 days. L-ascorbic acid excretion was significantly increased in the groups receiving alcohol and declined during the recovery period. This study has raised the possibility that increased urinary excretion of ascorbic acid may suppress glycogen synthesis, leading to hypoglycemia. / Master of Science

No description available.

No description available.

Indiana University-Purdue University Indianapolis (IUPUI) / The expression of pyruvate dehydrogenase kinase (PDK) 2 and 4 are increased in the fasted state to inactivate the pyruvate dehydrogenase complex (PDC) by phosphorylation to conserve substrates for glucose production. To assess the importance of PDK2 and PDK4 in regulation of the PDC to maintain glucose homeostasis, PDK2 knockout (KO), PDK4 KO, and PDK2/PDK4 double knockout (DKO) mice were generated. PDK2 deficiency caused higher PDC activity and lower blood glucose levels in the fed state while PDK4 deficiency caused similar effects in the fasting state. DKO intensified these effects in both states. PDK2 deficiency had no effect on glucose tolerance, PDK4 deficiency produced a modest effect, but DKO caused a marked improvement, lowered insulin levels, and increased insulin sensitivity. However, the DKO mice were more sensitive than wild-type mice to long term fasting, succumbing to hypoglycemia, ketoacidosis, and hypothermia. Stable isotope flux analysis indicated that hypoglycemia was due to a reduced rate of gluconeogenesis. We hypothesized that hyperglycemia would be prevented in DKO mice fed a high saturated fat diet for 30 weeks. As expected, DKO mice fed a high fat diet had improved glucose tolerance, decreased adiposity, and were euglycemic due to reduction in the rate of gluconeogenesis. Like chow fed DKO mice, high fat fed DKO mice were unusually sensitive to fasting because of ketoacidosis and hypothermia. PDK deficiency resulted in greater PDC activity which limited the availability of pyruvate for oxaloacetate synthesis. Low oxaloacetate resulted in overproduction of ketone bodies by the liver and inhibition of ketone body and fatty acid oxidation by peripheral tissues, culminating in ketoacidosis and hypothermia. Furthermore, when fed a ketogenic diet consisting of low carbohydrate and high fat, DKO mice also exhibited hypothermia, ketoacidosis, and hypoglycemia. The findings establish that PDK2 is more important in the fed state, PDK4 is more important in the fasted state, survival during long term fasting depends upon regulation of the PDC by both PDK2 and PDK4, and that the PDKs are important for the regulation of glucose and ketone body metabolism.