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作 者:Shoko Horita Motonobu Nakamura Masashi Suzuki Hideomi Yamada George Seki
机构地区:[1]Department of Internal Medicine, The University of Tokyo Hospital, Tokyo, Japan
出 处:《Open Journal of Endocrine and Metabolic Diseases》2013年第5期34-41,共8页内分泌与新陈代谢疾病期刊(英文)
摘 要: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.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.
关 键 词:INSULIN INFLAMMATION TNF-α PROXIMAL TUBULE INSULIN Resistance PPARγ THIAZOLIDINEDIONES
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