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Nathan Goodyear

Original Articles: Comparison of Insulin Action on Glucose versus Potassium Uptake in H... - 0 views

  • When treating hyperkalemia, insulin remains efficacious in diabetics and nondiabetics and one does not need to resort to b-agonists, and diabetics do not require different doses of insulin to shift potassium
  • the commonly encountered “insulin-resistant” patients actually have preserved insulin-induced potassium disposal, one wonders why their high insulin levels are not causing hypokalemia
  • insulin independently regulates glucose and potassium uptake into cells and this independence explains why in noninsulin-dependent diabetic insulin resistance leads to impaired insulin uptake into cells but has no effect on the cell's potassium disposal
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  • insulin suppresses glycogenolysis, gluconeogenesis, lipolysis and fatty acid release, and protein catabolism and is the principal hormone that stimulates glucose uptake into mainly skeletal muscle and to a certain extent adipocytes
  • Plasma [K+] is a major determinant of the resting potential of all cells
  • Hyperkalemia and hypokalemia are silent yet fatal disturbances because of their arrhythmogenic potentials
  • Basal insulin maintains fasting plasma [K+] within the normal range
  • When insulin levels are suppressed, plasma [K+] rises and pronounced hyperkalemia develops after a potassium load
  • Potassium is a well proven insulin secretagogue
  • Insulin is a key defender against exogenous potassium load by using intracellular buffering to minimize hyperkalemia before renal excretion
  • Hyperkalemia is often encountered in patients with diabetes
  • The insulin-deficient state in type 1 diabetes predisposes to hyperkalemia because of an impaired ability of potassium to enter cells. During hyperglycemic hypertonic states in type 1 and type 2 diabetics, potassium is carried out of cells by convective flux as the most abundant intracellular cation
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    good review of the potassium, glucose, insulin relationship mostly in diabetes.  In diabetes, hyperkalemia is present due to the hyperglycemia and the associated exchange.  Inuslin independantly regulates potassium and glucose intake into the cell.  INterestingly, in IR found in diabetes, the hyperkalemia is the norm, which should cause hypokalemia--the authors were perplexed by this finding.
Nathan Goodyear

Association of Hypertension and Hypokalemia with Cushing's Syndrome Caused by Ectopic A... - 0 views

  • cortisol may act as a mineralocorticoid when in excess, perhaps by saturating the 11β-hydroxysteroid-dehydrogenase (11β-HSD2 enzyme) that inactivates cortisol at the renal tubule
  • high cortisol levels may be the principal cause of hypokalemic alkalosis
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    high cortisol, whether exogenous or endogenous, can have a mineral corticoid effect and resultant low potassium.
Nathan Goodyear

Syndrome of apparent mineralocorticoid excess. A defect in the cortisol-cortisone shuttle. - 0 views

  • These results suggest that cortisol acts as a potent mineralocorticoid in 11 beta-OHSD deficiency
  • major site for the oxidation of cortisol to cortisone is the kidney
  • congenital deficiency of 11 beta-OHSD results in high intrarenal cortisol levels which then act on renal type I mineralocorticoid receptors
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  • deficiency of 11 beta-OHSD results in high intrarenal cortisol concentrations that then bind to the type I receptor.
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    mechanism of how cortisol acts as a mineralcorticoid in those with dysfunctional 11-beta HSD activity.
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