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Determination Of The Molecular Mechanisms Of Hyperglycemia-Induced Changes In Cav3.2 Calcium Channel Properties, Ginny Marie Keeling
Determination Of The Molecular Mechanisms Of Hyperglycemia-Induced Changes In Cav3.2 Calcium Channel Properties, Ginny Marie Keeling
Master's Theses
Hyperglycemia can cause altered excitability due to increased CaV3.2 T-type calcium channel function, bestowing diabetics an increased neuropathy risk. The objective of this study was to understand the molecular mechanisms of increased CaV3.2 function during hyperglycemia in vitro, which leads to a 58% increase in current density and increased channel open probability (PO), among other changes. Two major findings are reported in this study:
1) The enzymatic elimination of extracellular N-acetylneuraminic acid (NANA) moieties reversed the increase in current density and the shift in PO, showing that hyper-glycosylation alters channel function in disease.
2) Treatment with GM1 (a ganglioside highly …
Sugar Consumption And Cognitive Aging In The Swedish Adoption/Twin Study Of Aging, Shyam Seetharaman
Sugar Consumption And Cognitive Aging In The Swedish Adoption/Twin Study Of Aging, Shyam Seetharaman
USF Tampa Graduate Theses and Dissertations
Abstract
Consumption of foods high in sugar content has been linked with the development of metabolic abnormalities such as cardiovascular disease and type II diabetes, major sources of global health concerns. Although the detrimental consequences of high intake of sugar on abnormal metabolic processes are established, it is not known how this association affects (or accelerates) cognitive aging.
The current project was based on data from the Swedish Adoption/Twin Study of Aging (SATSA) to test the hypothesis that high refined sugar intake contributes to accelerated trajectories of cognitive decline assessed longitudinally. Trajectories of cognitive change were assessed as a function …