xvii, 214 leaves : ill., graphs, tables ; 29 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Plant Physiology, 1980

Thesis (Ph. D.)--University of Washington, 2007. / Vita. Includes bibliographical references (leaves 52-61).

The effect of intramuscular corticosterone injection on post mortem muscle metabolism and shear resistance of Pectoralis Major muscle was studied. Short term studies, conducted over an 8 hour post-injection period, showed no significant effect of injection until 6 hours post injection at which time shear values increased from those of the controls. Blood glucose levels rose significantly from 2 to 8 hours post injection. A comparison of shear values of P. Major muscle from 6 week-old broilers and 8 week-old broilers after both had received corticosterone injections showed that the only difference was due to the difference of age not to any alteration in the physiological handling of the injected corticosterone. The greatest difference in treatment effect was found between birds of different stress level. Stress level was subjectively evaluated with respect to the birds reaction to a person entering the range house and to the birds response to handling. Long term studies conducted over 5 and 15 days illustrated homeostatic adjustments to daily corticosterone injections and recovery after cessation of injections. Shear testing was performed on P. Major muscle which was chilled on the carcass and on muscle excised at death. Excised muscle displayed a greater reaction to injection and cessation of injection than did intact muscle due to a lack of skeletal restriction. Shear values decreased on initial injection and increased upon cessation of injection. Homeostatic adjustments returned values to near-normal between these times. Chemical tests were found to display a much more definite reaction to corticosterone injection than did shear testing. Blood glucose and tissue glycogen increased steadily on injection of corticosterone and decreased rapidly at cessation. As expected ultimate muscle pH decreased with muscle glycogen increase. Blood cholesterol increased during injection period as endogenous corticosterone production, for which it is a precursor, was not required. / Land and Food Systems, Faculty of / Graduate

This document only includes an excerpt of the corresponding thesis or dissertation. To request a digital scan of the full text, please contact the Ruth Lilly Medical Library's Interlibrary Loan Department (rlmlill@iu.edu).

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Mammals and fish rely on hormones to regulate blood glucose levels. The two major glucose regulating hormones are insulin and glucagon. Literature on mammalian insulin and glucagon is quite extensive, however, there is limited information on how these hormones regulate blood glucose levels in fish. The material available for fish mostly pertains to changes in glucose concentration and gene expression of enzymes, but there is no information on the direct influence they have on glucose kinetics. Therefore, the main goal of my thesis is to measure the change in hepatic glucose production and glucose disposal when rainbow trout are administered insulin or glucagon. The beginning of my research focused on insulin. I hypothesized that rainbow trout respond to insulin by decreasing hepatic glucose production and increase glucose disposal, just like mammals. To test this, I infused insulin for 4 hours at 1.5 g insulin kg 1 min-1. I measured glucose disposal (Rd glucose), hepatic glucose production (Ra glucose), and blood glucose concentration. Following insulin administration the glucose fluxes decreased steadily (Rd glucose -37% and Ra glucose -43%). The decline in blood glucose levels follows the difference between Rd and Ra. These results explain why rainbow trout are unable to clear a glucose load to the same degree as mammals. The second major glucose hormone (glucagon) is what interested me for the second part of the research. The limited information on fish glucagon is even less than that of fish insulin. I speculated that trout respond to glucagon the same way mammals do (increase hepatic glucose production and show no affect on glucose disposal). To study the effects of glucagon on glucose fluxes, I tracked the changes in Ra and Rd glucose. The results showed glucose fluxes showed no siginificant difference from baseline in the first few hours, then steadily decreasing until the final time point reached values below baseline. Therefore, these experiments revealed that glucagon follows a similar pattern of effects in trout as mammals. However, the strength of the response to glucagon is different between trout and mammals. This thesis is the first to investigate the effects of insulin and glucagon on glucose kinetics in rainbow trout. I have concluded that rainbow trout have different responses to insulin and glucagon when compared to mammals. Furthermore, fish showing limited glucoregulatory capacity can be partially explained by their responses to insulin and glucagon.

The Mitochondrial Pyruvate Carrier (MPC) occupies a central metabolic node by transporting cytosolic pyruvate into the mitochondrial matrix, thereby linking glycolysis with mitochondrial metabolism. Two reported human MPC1 mutations cause developmental abnormalities, neurological problems, metabolic deficits, and for one patient, early death. We aimed to understand biochemical mechanisms by which the human patient c.C289T and c.T236A MPC1 alleles disrupt MPC function. MPC1 c.C289T encodes two protein variants, a mis-spliced, truncation mutant (A58G) and full-length point mutant (R97W). MPC1 c.T236A encodes a full-length point mutant (L79H). Using human patient fibroblasts and complementation of CRISPR-deleted, MPC1 null mouse C2C12 cells, we investigated how MPC1 mutations cause MPC deficiency. Truncated MPC1 A58G protein was intrinsically unstable and failed to form MPC complexes. The MPC1 R97W protein was less stable but when overexpressed formed complexes with MPC2 that retained pyruvate transport activity. Conversely, MPC1 L79H protein formed stable complexes with MPC2, but these complexes failed to transport pyruvate. These findings inform MPC structure-function relationships and delineate three distinct biochemical pathologies resulting from human patient MPC1 mutations and inform fundamental MPC structure-function relationships. These results also demonstrate an efficient molecular genetic system using the mouse C2C12 cell line to mechanistically investigate human inborn errors in pyruvate metabolism.

Thesis (doctoral)--University of Lund.

Goldfish subjected to an intermittent short-term aerobic exercise training regime prior to acute hypoxic exposure demonstrated a shift in hypoxia response. Intermittent aerobic training enhanced the aerobic potential of goldfish in the red muscle by increasing maximal activity of citrate synthase by 72% and reduced pyruvate kinase activity by 21% in white muscle. Across red and white muscle tissue, aerobic training caused a decrease in glycogen storage by 19% and 32%, respectively. Liver glycogen stores remained unchanged by training during normoxia. Subsequent hypoxic exposure demonstrated a significant training effect with a77% glycogen depletion in the liver of trained fish compared to a 53% depletion in untrained fish. Hypoxia caused glycogen depletion, glucose mobilization, and ATP depletion in trained and untrained fish muscle tissue. Meanwhile, the liver of trained recovered ATP slower than untrained fish and both liver and plasma had greater lactate accumulation by 1 h hypoxic recovery in trained fish. Alcohol dehydrogenase maximal activity of trained fish responded to hypoxia with a 50% reduction and trained white muscle significantly reduced alcohol dehydrogenase activity during hypoxic recovery. Ethanol was produced with and without training preconditioning in response to hypoxia in red muscle; however, trained fish white muscle showed an ethanol accumulation trend following training and 12 h hypoxia that was significantly cleared during recovery. Ethanol accumulation in white muscle of trained fish may reveal greater perturbation caused by training and hypoxia and/or some developed mechanism for ethanol retention. In effect, this training regime created a very different metabolic profile in goldfish such that during environmental oxygen limitation, trained fish may experience an enhanced metabolic perturbation and greater glycogen depletion which may compromise hypoxic tolerance. / Thesis (Master, Biology) -- Queen's University, 2011-09-30 13:25:36.148

Diss. (sammanfattning) Umeå : Umeå universitet, 2008. / Härtill 4 uppsatser.