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Elevated Plasma Levels of Transforming Growth Factor-β1 in NIDDM

  1. Andreas Pfeiffer, MD,
  2. Kristina Middelberg-Bisping,
  3. Cordula Drewes, MD and
  4. Helmut Schatz, MD
  1. Medizinische Klinik und Poliklinik, Berufsgenossenschaftliche Kliniken Bergmannsheil, Universitätsklinik der Ruhr-Universität Bochum Germany
  1. Address correspondence and reprint requests to Andreas Pfeiffer, MD, Medizinische Klinik und Poliklinik, Berufsgenossenschaftliche Kliniken Bergmannsheil, Ruhr-Universität Bochum, Bürkle de la Camp-Platz 1, D-44789 Bochum, Germany. E-mail: andreas.pfeiffer{at}rz.ruhr-uni-bochum.de

Abstract

OBJECTIVE Transforming growth factor-β (TGF-β) is a potent inducer of extracellular matrix production and of fibrogenesis and has been associated with the occurrence of diabetic micro- and macrovascular complications. Our aim was to determine whether circulating levels of TGF-β1 are altered in NIDDM and, if so, whether they are correlated with blood glucose and show an association with diabetic complications.

RESEARCH DESIGN AND METHODS Plasma levels of TGF-β1 were determined by enzyme-linked immunosorbent assay in 44 NIDDM patients and 28 control subjects of comparable age and weight and were correlated with parameters of metabolic control and the occurrence of micro- and macrovascular complications.

RESULTS TGF-β1 was significantly elevated in NIDDM (7.9 ± 1.0 ng/ml), as compared with control subjects (3.1 ± 0.4 ng/ml, P < 0.001) and correlated with glycosylated hemoglobin (r2 = 0.42; P < 0.001). Thrombocyte levels of TGF-β1 were similar in control subjects (54 ± 7 pg/ml, n = 16) and diabetic patients (61.6 ± 18 pg/ml, n = 13; P = 0.357). Elevated TGF-β1 levels were associated with retinopathy and neuropathy.

CONCLUSIONS We conclude that plasma levels of TGF-β1 are elevated in NIDDM patients and may be related to average blood glucose. Preliminary data suggest that they may contribute to the occurrence of diabetic complications.

  • Received January 17, 1996.
  • Revision received May 30, 1996.
  • Accepted May 30, 1996.
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