Abstract
Diabetic nephropathy is the leading cause of end stage renal disease in the world. Although tremendous efforts have been made, scientists have yet to identify an ideal animal model that can reproduce the characteristics of human diabetic nephropathy. In this study, we hypothesize that taurine insufficiency is a critical risk factor for development of diabetic nephropathy associated with diabetes mellitus. This hypothesis was tested in vivo in TauT heterozygous (TauT +/-) and homozygous (TauT-/-) knockout in C57BL/6 background mice. We have shown that alteration of the TauT gene (also known as SLC6A6) has a substantial effect on the susceptibility to development of extensive diabetic kidney disease in both TauT +/- and TauT-/-mouse models of diabetes. These animals developed histological changes characteristic of human diabetic nephropathy that included glomerulosclerosis, nodular lesions, arteriosclerosis, arteriolar dilation, and tubulointerstitial fibrosis. Immunohistochemical staining of molecular markers of smooth muscle actin, CD34, Ki67 and collagen IV further confirmed these observations. Our results demonstrated that both homozygous and heterozygous TauT gene deletion predispose C57BL/6 mice to develop end-stage diabetic kidney disease, which closely replicates the pathological features of diabetic nephropathy in human diabetic patients.
Highlights
The impact of diabetic kidney disease on the health of the United States population is staggering
Recent studies show that both BRKO-Akita and BTBR ob/ob mice develop more advanced diabetic nephropathy than other murine models [10,11]
The BTBR ob/ob mouse model is dependent on leptin deficiency, which is not a characteristic of human diabetes [10].The lack of reliable animal models that closely mimic human disease has delayed the identification of specific factors that cause diabetic nephropathy
Summary
The impact of diabetic kidney disease on the health of the United States population is staggering. Highly prevalent in older patients, are major risk factors for chronic kidney disease and end stage renal disease [1]. This form of chronic kidney disease poses a considerable medical and public health challenge, in the elderly. The marked variability in the development of chronic kidney disease in individuals with. While clear progress has been made in understanding the disease process, there has been limited success in identifying specific factors that cause or even predict human nephropathy and its progression. One of the reasons for the slow evolution in the understanding of diabetic nephropathy is the lack of reliable animal models that mimic human disease
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