Review
Role and mechanism of endogenous fructose in renal tubular injury in diabetic nephropathy
Xiaoyan Li, Naiqian Zhao, Jinxiang Han, Ziling Feng, Li Wang
Published 2017-08-15
Cite as Chin J Clinicians(Electronic Edition), 2017, 11(16): 2144-2148. DOI: 10.3877/cma.j.issn.1674-0785.2017.16.008
Abstract
In diabetes, hyperglycemia is associated with activation of the polyol pathway, in which fructose is endogenously overproduced. When fructose is metabolized in hepatocytes and tubular epithelial cells, ATP depletion and purine nucleotide turnover occur rapidly and irreversibly, and uric acid is eventually generated. The metabolism of fructose to uric acid is also known as the fructose-uric acid axis. Uric acid derived from endogenous fructose could directly impair renal tubular epithelial cells and peritubular capillary endothelial cells, resulting in diabetic tubulopathy. In the course of diabetic nephropathy, tubular injury may be induced earlier than glomerular injury and may be more closely associated with renal function. For this reason, the fructose-uric acid axis as a novel mechanism for the development of diabetic tubular injury provides new insights into the pathogenesis and treatment of diabetic nephropathy.
Key words:
Diabetic nephropathy; Fructose; Polyol pathway; Tubular injury; Uric acid
Contributor Information
Xiaoyan Li
Department of Infectious Diseases, Jinzhong First People′s Hospital of Shanxi Province, Jinzhong 030600, China
Naiqian Zhao
Department of Geriatrics, Second Hospital of Shanxi Medical University, Taiyuan 030001, China
Jinxiang Han
Department of Geriatrics, Second Hospital of Shanxi Medical University, Taiyuan 030001, China
Ziling Feng
Department of Neurology, Jinzhong First People′s Hospital of Shanxi Province, Jinzhong 030600, China
Li Wang
Department of Geriatrics, Second Hospital of Shanxi Medical University, Taiyuan 030001, China
