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Y. Endo, M. Suzuki, H. Yamada, et al., “Thiazolidinediones Enhance Sodium-Coupled Bicarbonate Absorption from Renal Proximal Tubules via PPARγ-Dependent Nongenomic Signaling,” Cell Metabolism, Vol. 13, No. 5, 2011, pp. 550-561. doi:10.1016/j.cmet.2011.02.015

has been cited by the following article:

• TITLE: The Effects of Insulin Resistance and Inflammation on Renal Proximal Tubule Sodium Transport and Hypertension

  AUTHORS: Shoko Horita, Motonobu Nakamura, Masashi Suzuki, Hideomi Yamada, George Seki

  KEYWORDS: Insulin; Inflammation; TNF-α; Proximal Tubule; Insulin Resistance; PPARγ; Thiazolidinediones

  JOURNAL NAME: Open Journal of Endocrine and Metabolic Diseases, Vol.3 No.5A, August 19, 2013

  ABSTRACT: Insulin resistance, closely linked to inflammation, is recognized as a key factor in the onset and aggravation of diabetes, cardio-renal syndrome, hypertension, and obesity. In the renal proximal tubule, insulin resistance may increase renal sodium reabsorption, leading to hypertension, edema and sometimes heart failure. Recently some anti-diabetic agents have been shown to have effects on the transporters in renal proximal tubule. Because renal proximal tubule mediates about 70% of sodium reabsorption, it is quite important to clarify the function of renal proximal tubule under insulin resistance and inflammation.