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High Glucose Up-Regulates ENaC and SGK1 Expression in HCD-Cells
Author(s) -
Claire E. Hills,
Rosemary Bland,
Jeanette Bennett,
Pierre Ronco,
Paul E. Squires
Publication year - 2006
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000097611
Subject(s) - epithelial sodium channel , sgk1 , endocrinology , medicine , diabetic nephropathy , ionomycin , renal sodium reabsorption , western blot , chemistry , diabetes mellitus , sodium , kidney , reabsorption , glucocorticoid , biochemistry , calcium , organic chemistry , gene
Diabetic nephropathy is associated with progressive renal damage, leading to impaired function and end-stage renal failure. Secondary hypertension stems from a deranged ability of cells within the kidney to resolve and appropriately regulate sodium resorption in response to hyperglycaemia. However, the mechanisms by which glucose alters sodium re-uptake have not been fully characterised.

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