K. Matsusue, M. Haluzik, G. Lambert, et al., “LiverSpecific Disruption of PPARγ in Leptin-Deficient mice Improves Fatty Liver but Aggravates Diabetic Phenotypes,” Journal of Clinical Investigation, Vol. 111, No. 5, 2003, pp. 737-747.

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.