{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,28]],"date-time":"2026-01-28T20:52:56Z","timestamp":1769633576215,"version":"3.49.0"},"reference-count":28,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2011,3,2]],"date-time":"2011-03-02T00:00:00Z","timestamp":1299024000000},"content-version":"vor","delay-in-days":1,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Diabetes Metabolism Res"],"published-print":{"date-parts":[[2011,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Diabetic nephropathy (DN) is a major complication of diabetes mellitus, and the most common cause of end\u2010stage renal disease. DN is characterized by early hyperfiltration and renal hypertrophy, which are associated with increased renal insulin\u2010like growth factor\u20101 (IGF\u20101) levels. The relationship between IGF\u20101 and nitric oxide (NO) in DN is not established. The aim of this study was to investigate the effects of NO system modulation on the IGF\u20101\u2010mediated hypertrophy and hyperfiltration during the first week after diabetes induction.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Diabetes was induced in rats by streptozotocin (STZ) injection. Diabetic rats were treated with NO synthase inhibitor L\u2010NG\u2010nitroarginine methyl ester (L\u2010NAME). Various serum IGF\u2010binding proteins (IGFBPs) and renal IGFBP1 expression was evaluated. Urine and plasma NO<jats:sub>2<\/jats:sub> + NO<jats:sub>3<\/jats:sub> level analysis was also performed.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>STZ induced hyperglycaemia decreased plasma insulin levels and brought about a decrease in body weight. L\u2010NAME administration to diabetic rats significantly prevented renal hypertrophy and hyperfiltration. Serum IGFBP3, IGFBP4 and 30\u2010kDa IGFBP fraction were all significantly reduced in diabetic rats, compared with those in non\u2010diabetic control rats. However, the renal IGFBP1 mRNA expression in diabetic rats was significantly higher. These changes were accompanied by an increased in NO production. L\u2010NAME administration prevented the serum IGFBP decline, without significantly affecting the renal IGFBP1 mRNA expression.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>We have shown that increased renal IGF\u20101 and increased NO production during the very early stages of STZ\u2010induced DN are associated with renal hypertrophy and hyperfiltration in diabetic rats. Modulating the IGF\u20101 availability to the kidney by nitric oxide synthase inhibition significantly reduced renal hypertrophy and hyperfiltration during the first week of STZ\u2010induced diabetes mellitus. 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