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Lang, K.S., Mueller, M.M., Tanneur, V., Wallisch, S., Fedorenko, O., Palmada, M., Lang, F., Broer, S., Heilig, C.W., Schleicher, E. and Weigert, C. (2003) Regulation of cytosolic pH and lactic acid release in mesangial cells overexpressing GLUT1. Kidney International, 64, 1338-1347.
http://dx.doi.org/10.1046/j.1523-1755.2003.00213.x

has been cited by the following article:

• TITLE: Treatment of peripheral diabetic neuropathy in Zucker diabetic fatty (ZDF) rats with cariporide

  AUTHORS: Sergey Lupachyk, Hanna Shevalye, Pierre Watcho, Alexander Obrosov, Irina G. Obrosova, Mark A. Yorek

  KEYWORDS: Diabetic Neuropathy; Sodium/Hydrogen Exchanges; Oxidative Stress

  JOURNAL NAME: Journal of Diabetes Mellitus, Vol.4 No.1, February 24, 2014

  ABSTRACT: To determine the effect of Na+/H+-exchanger-1 on diabetic neuropathy in Type 2 diabetes Zucker diabetic fatty (ZDF) rats and lean controls were treated with cariporide (10 or 20 mg/kg/d), a Na+/H+-exchanger-1 inhibitor, for 4 weeks at 15 weeks of age. Neuropathy endpoints included motor (MNCV) and sensory (SNCV) nerve conduction velocities, thermal nociception, tactile allodynia and intraepidermal nerve fiber density. Advanced glycation endproduct and markers of oxidative stress including nitrated protein levels in sciatic nerve and dorsal root ganglion were also evaluated. Expression of Na+/H+-exchanger-1 in dorsal root ganglion neurons was increased in ZDF rats. At 15 weeks of age ZDF rats displayed hyperglycemia, MNCV and SNCV deficits, thermal hypoalgesia and tactile allodynia. At 20 but not 10 mg/kg/d, cariporide significantly improved MNCV and SNCV deficits, thermal hypoalgesia and tactile allodynia. Cariporide treatment was also associated with reduction of diabetes-induced accumulation of advanced glycation end-product (AGE), oxidative stress and nitrated proteins in sciatic nerve and dorsal root ganglion neurons. In conclusion, these findings support an important role for Na+/H+-exchanger-1 in peripheral diabetic neuropathy, and provide rationale for development of Na+/H+-exchanger-1 inhibitors for treatment of diabetic neural complications.