Role fo AMP-activated protein kinase (AMPK) in diabetic nephropathy: change of tubuloglomerular feeedback and salt transport
Final Report Abstract
1) Immunofluorescence study revealed that AMPKα1 subunit was expressed in renal proximal and distal tubules in STZ-induced diabetic rats. The activated AMPKα protein abundance is reduced in experimental diabetes despite of increased AMPKα subunit expression, suggesting different AMPK subunits play distinct roles in STZ-induced diabetic kidneys. 2) Neither intratubular nor systemic application of AMPK activator AICAR could change TGF response and proximal tubular absorption in diabetic rats, implying acute AMPK activation may not alter TGF and tubular transport in diabetes. However, chronic effects of AMPK activation on TGF and tubular absorption could not be excluded. 3) AMPKα1 knockout mice exhibit enhanced renal K+ excretion after an acute intravenous K+ loading, indicating that loss function of AMPKα1 promotes urinary K loss possibly by up-regulation of ROMK during high K+ intake.
Publications
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(2010) In vivo stimulation of AMP-activated protein kinase enhanced tubuloglomerular feedback but reduced tubular sodium transport during high dietary NaCl intake. Pflugers Arch. 460:187-196
Huang DY, Gao H, Boini KM, Osswald H, Nürnberg B, Lang F
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(2013). Downregulation of the renal outer medullary K(+) channel ROMK by the AMP-activated protein kinase. Pflugers Arch. 465:233-245
Siraskar B, Huang DY, Pakladok T, Siraskar G, Sopjani M, Alesutan I, Kucherenko Y, Almilaji A, Devanathan V, Shumilina E, Föller M, Munoz C, Lang F
