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dc.contributor.authorMannon, Elinor
dc.date.accessioned2021-11-05T19:03:00Z
dc.date.available2021-11-05T19:03:00Z
dc.date.issued2021-10
dc.identifier.urihttp://hdl.handle.net/10675.2/624142
dc.description.abstractSodium bicarbonate (NaHCO3) is a therapeutic used in chronic kidney disease (CKD). NaHCO3 is typically used to treat metabolic acidosis, but clinical studies have indicated that NaHCO3 supplementation may slow CKD progression. As such, NaHCO3 is now given to patients with CKD to slow the decline of glomerular filtration rate. However, the consequences of chronic NaHCO3 supplementation in CKD remain unclear. Acidosis has been associated with insulin resistance, and correction of acidosis with NaHCO3 was reported to improve insulin sensitivity. Our goal in Aim 1 was to determine whether acid and alkali loading would promote loss of acid-base homeostasis and consequently decrease insulin sensitivity. We determined that the blood glucose response to insulin is enhanced following renal mass reduction, and that this response is not reversed by an acidosis. Additionally, the development of an alkalosis did not impair the blood glucose response to insulin. Alkali can promote potassium (K+) wasting, and an association between K+ wasting and insulin resistance has been identified in clinical and basic science research. Our goal in Aim 2 was to identify whether chronic NaHCO3 treatment may promote loss of insulin sensitivity through effects on K+ status. We determined that chronic NaHCO3 treatment impairs insulin sensitivity when combined with other K+ wasting stimuli. K+ deprivation alone also impaired the blood glucose response to insulin, however these impairments in insulin sensitivity were not directly related to decreases in intracellular [K+]. Salt-sensitivity increases as functional renal mass declines, and chronic sodium (Na+) loading with NaHCO3 may contribute to hypertension in patients with CKD. Our goal in Aim 3 was to investigate whether NaHCO3 loading promotes similar levels of Na+ and volume retention, and hypertension as sodium chloride (NaCl) loading does in a rat model of CKD. We found that NaHCO3 was pro-hypertensive, but to a lesser degree than NaCl, despite similar amounts of Na+ and volume retention. From these studies we concluded that NaHCO3 does not improve insulin sensitivity through its effects on acid-base status. Further, access to dietary K+ may improve insulin sensitivity with chronic NaHCO3 treatment. Finally, NaHCO3 can promote hypertension in CKD.
dc.publisherAugusta University
dc.subjectPhysiology
dc.subjectAlkali, Hypertension, Insulin sensitivity, Remnant kidney rats
dc.titleEFFECTS OF SODIUM BICARBONATE ON GLUCOSE HOMEOSTASIS AND BLOOD PRESSURE IN CHRONIC KIDNEY DISEASE
dc.typedissertationen_US
dc.contributor.departmentDepartment of Philosophy
dc.language.rfc3066en
dc.date.updated2021-11-05T19:03:01Z
dc.description.advisorO'Connor, Paul M
dc.description.committeeSullivan, Jennifer C
dc.description.committeeMattson, David L
dc.description.committeeStepp, David W
dc.description.committeeWhite, John J
dc.description.degreePh.D.


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