Cytokine-induced beta-cell death is independent of endoplasmic reticulum stress signaling.

Objective: Cytokines contribute to beta-cell destruction in type 1 diabetes. Endoplasmic reticulum (ER) stress-mediated apoptosis has been proposed as a mechanism for beta-cell death. We tested whether ER stress was necessary for cytokine-induced beta-cell death and also whether ER stress gene activation was present in beta-cells of the NOD mouse model of type 1 diabetes.

The role of SGK-1 in angiotensin II-mediated sodium reabsorption in human proximal tubular cells.

Background: The role of angiotensin II (Ang II) in mediating excessive sodium reabsorption in diabetic nephropathy is recognized. Serine-glucocorticoid kinase-1 (SGK-1) increases sodium-hydrogen exchanger-3 (NHE3) expression and is known to be upregulated in in vitro and in vivo models of diabetic nephropathy. However, a link between Ang II and SGK-1 in diabetic nephropathy has not been established.

The interdependence of EGF-R and SGK-1 in fibronectin expression in primary kidney cortical fibroblast cells.

Background: Epidermal growth factor (EGF) has been shown to play a role in the nephromegaly and enhanced sodium reabsorption observed in diabetic nephropathy. This is recognized to be dependent on activation of serine threonine glucocorticoid kinase-1 (SGK-1). However, the roles of EGF and SGK-1 in renal fibrogenesis observed under high glucose conditions have not been established.

High glucose transactivates the EGF receptor and up-regulates serum glucocorticoid kinase in the proximal tubule.

Background: Serum glucocorticoid regulated kinase (SGK-1) is induced in the kidney in diabetes mellitus. However, its role in the proximal tubule is unclear. This study determined the expression and functional role of SGK-1 in PTCs in high glucose conditions.