Transforming growth factor β (TGF-β) levels in otherwise healthy subjects with impaired glucose tolerance

Serum transforming growth factor beta (TGF-β) level is increased in type-2 diabetes mellitus (T2DM) and certain diabetic complications are mediated by this cytokine. Impaired glucose tolerance (IGT) is a prediabetic condition, and confers a risk for the development of certain diabetes-specific compl...

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Published inEndokrynologia polska Vol. 61; no. 6; pp. 691 - 694
Main Authors Genc, Halil, Karadurmus, Nuri, Kisa, Ucler, Tapan, Serkan, Naharci, Ilkin, Sonmez, Alper, Dogru, Teoman
Format Journal Article
LanguageEnglish
Published Poland Wydawnictwo Via Medica 01.11.2010
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Summary:Serum transforming growth factor beta (TGF-β) level is increased in type-2 diabetes mellitus (T2DM) and certain diabetic complications are mediated by this cytokine. Impaired glucose tolerance (IGT) is a prediabetic condition, and confers a risk for the development of certain diabetes-specific complications. However, no data is available regarding the alteration of TGF-β in IGT subjects. Therefore, we aimed to investigate TGF-β levels in otherwise healthy subjects with IGT. Thirty IGT subjects and 30 subjects relatively matched for age, sex and body mass index with normal glucose tolerance were enrolled. Subjects with overt diabetes, cardiovascular, renal or inflammatory disease, or on any medication were excluded. Relevant laboratory examinations were performed by routine methods. Assessment of TGF-β was made by a commercially available enzyme-linked immunosorbent assay kit. IGT and control subjects were compared for their clinical and laboratory parameters. Serum TGF-β levels were found to be similar in IGT and normal glucose tolerance subjects (p 〈 0.05). No statistically significant correlation was found between TGF-β and other laboratory parameters, either in IGT subjects or in the whole study population. Serum TGF-β is not elevated in otherwise healthy subjects with IGT. The results of our study imply that the presence of IGT alone is not sufficient to induce TGF-β elevation; and for the alteration of TGF-β, worsening of metabolic risk factors may be required.
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ISSN:0423-104X