Degree
Doctor of Philosophy (PhD)
Department
Kinesiology
Document Type
Dissertation
Abstract
Hyperosmolar hyperglycemic syndrome (HHS) is a life-threating endocrine emergency commonly seen with type 2 diabetes. HHS has been identified to begin when hyperglycemia leads to glucosuria diuresis, which eventually leads to hyperosmotic conditions. However, hyperosmolality has not been considered as an initiator of HHS, although past research would suggest that it can initiate HHS, specifically through systemic inflammation and glucose insensitivity.
The first study examined the impact of exercise induced hypohydration effect on T-cell populations. After healthy participants reached hypohydration they were then rehydrated with water and monitored for 3-hours. Results indicated that rehydration attenuated the efflux of T-cells from the blood compartment, although at 3-hours post rehydration this attenuation was reversed as fluid was lost. This data indicates that fluid shifts influence T-cell mobility.
The second study examined hyperosmotic and HHS conditions effect on T-cells compared to normal osmotic conditions. Peripheral blood mononuclear cells (PBMCs) were cultured either simulated or non-stimulated in different osmotic and glycemic conditions. The results indicate that hyperosmotic conditions increase proinflammatory cytokine production, increases mitochondrial depolarization, and an increase in CD36/Glut-1 ratio indicating hyperosmotic conditions can potentially initiate HHS.
Date
11-2-2023
Recommended Citation
Granger, Joshua, "THE EFFECTS OF ACUTE HYPEROSMOLALITY ON IMMUNE CELL FUNCTIONS AND NUTRIENT SENSING" (2023). LSU Doctoral Dissertations. 6322.
https://repository.lsu.edu/gradschool_dissertations/6322
Committee Chair
Spielmann, Guillaume