{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,5,17]],"date-time":"2024-05-17T15:01:20Z","timestamp":1715958080912},"reference-count":39,"publisher":"Oxford University Press (OUP)","issue":"1","content-domain":{"domain":["eje.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":["eur j endocrinol"],"published-print":{"date-parts":[[2007,1]]},"abstract":"<jats:p><jats:italic>Objective<\/jats:italic>: Derangements of the GH\u2013IGF-I axis have been associated with microalbuminuria (MA) in type 1 diabetes. The aim of this study was to investigate whether an<jats:italic>IGF-I<\/jats:italic>gene promoter polymorphism influenced the development of persistent MA in type 1 diabetes.<\/jats:p><jats:p><jats:italic>Design<\/jats:italic>: A prospective follow-up study of a cohort of 277 patients with newly diagnosed type 1 diabetes consecutively enrolled between September 1979 and August 1984.<\/jats:p><jats:p><jats:italic>Methods<\/jats:italic>: Urinary albumin excretion rate over 24 h was measured in each patient at least once a year. Persistent MA was defined as a urinary albumin excretion rate between 30 and 300 mg\/24 h.<\/jats:p><jats:p><jats:italic>Results<\/jats:italic>: During a median follow-up of 18.0 years (range 1.0\u201321.5), 79 of 277 patients developed persistent MA.<jats:italic>IGF-I<\/jats:italic>gene genotype was available for 216 subjects; in 73% of the subjects, the wild-type genotype of this IGF-I gene polymorphism was present, while 27% had the variant type. At baseline, there were no differences in IGF-I levels and HbA<jats:sub>1c<\/jats:sub>values between subjects with the wild type and subjects with variant type. By Kaplan\u2013Meier analysis, subjects with the variant type of this polymorphism had during follow-up a higher risk of development of MA compared subjects with the wild type (<jats:italic>P<\/jats:italic>= 0.03).<\/jats:p><jats:p><jats:italic>Conclusions<\/jats:italic>: Subjects with the variant type of an<jats:italic>IGF-I<\/jats:italic>gene polymorphism had a significantly increased risk of developing MA. This risk was not mediated through changes in circulating IGF-I levels. Our study suggests that in type 1 diabetes, this<jats:italic>IGF-I<\/jats:italic>gene polymorphism is a risk factor of MA.<\/jats:p>","DOI":"10.1530\/eje.1.02308","type":"journal-article","created":{"date-parts":[[2007,1,12]],"date-time":"2007-01-12T00:27:47Z","timestamp":1168561667000},"page":"83-90","update-policy":"http:\/\/dx.doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":5,"title":["An IGF-I gene polymorphism modifies the risk of developing persistent microalbuminuria in type 1 diabetes"],"prefix":"10.1093","volume":"156","author":[{"given":"Peter","family":"Hovind","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Steven","family":"Lamberts","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wim","family":"Hop","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jaap","family":"Deinum","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lise","family":"Tarnow","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hans-Henrik","family":"Parving","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joop A M J L","family":"Janssen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","reference":[{"key":"1_28288650","first-page":"12S","volume":"60","year":"1997","journal-title":"KIDNEY INTERNATIONAL SUPPLEMENT"},{"issue":"3","key":"2_10768009","doi-asserted-by":"crossref","first-page":"495","DOI":"10.2337\/diacare.22.3.495","volume":"22","author":"Schultz","year":"1999","journal-title":"Diabetes Care","ISSN":"http:\/\/id.crossref.org\/issn\/0149-5992","issn-type":"print"},{"issue":"4","key":"3_15655224","doi-asserted-by":"crossref","first-page":"517","DOI":"10.1111\/j.1365-2265.1994.tb02584.x","volume":"41","author":"Clayton","year":"1994","journal-title":"Clinical endocrinology","ISSN":"http:\/\/id.crossref.org\/issn\/0300-0664","issn-type":"print"},{"issue":"9","key":"4_5723917","doi-asserted-by":"publisher","first-page":"2809","DOI":"10.1210\/jc.82.9.2809","volume":"82","author":"Janssen","year":"1997","journal-title":"Journal of Clinical Endocrinology &amp; 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