Exp Clin Endocrinol Diabetes 2006; 114(7): 371-376
DOI: 10.1055/s-2006-924320

J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Insulin-like Growth Factor Binding Protein-2 (IGFBP-2) is a Marker for the Metabolic Syndrome

A. H. Heald1 , 2 , K. Kaushal1 , K. W. Siddals1 , A. S. Rudenski1 , S. G. Anderson1 , J. M. Gibson1
  • 1Diabetes & Endocrinology, University of Manchester, Hope Hospital, Salford, United Kingdom
  • 2Department of Medicine, Bishop Auckland Hospital, Co Durham, United Kingdom
Weitere Informationen


Received: August 8, 2005 First decision: February 24, 2006

Accepted: March 30, 2006

16. August 2006 (online)


Aims/hypothesis: IGFs and their binding proteins are increasingly recognised as important in understanding the pathogenesis of cardiovascular disease. Low IGFBP-1, particularly coupled with low IGF‐I, is associated with increased cardiovascular risk. In relation to structural and regulatory parallels between IGFBP-1 and ‐ 2 we have now examined the hypothesis that IGFBP-2 may be a marker for cardiovascular risk. Methods: Fasting IGFBP-2, IGFBP-1, IGFBP-3, IGF‐I, IGF‐II, insulin, C-peptide, glucose, lipids, NEFAs, and HbA1c were measured in a cohort of 163 patients with type 2 diabetes. Individuals were categorised according to the presence or absence of the metabolic syndrome. Results: Patients with the metabolic syndrome had a lower IGFBP-2 concentration. Low circulating IGFBP-2 was associated with elevated fasting glucose (ρ = - 0.23, p = 0.003). IGFBP-2 correlated negatively with triglycerides (ρ = - 0.19, p = 0.01) and LDL-cholesterol (ρ = - 0.20, p = 0.01), and positively with insulin sensitivity (HOMA‐S) (ρ = 0.26, p = 0.02). Multivariate logistic regression demonstrated that low IGFBP-2 was independently associated with an increased risk of the metabolic syndrome (OR 0.31 [95 % CI 0.11 - 0.90]; p = 0.03). IGFBP-3 did not differ according to the presence or absence of metabolic syndrome. Conclusion/interpretation: Low IGFBP-2 is associated with multiple cardiovascular risk factors similarly to IGFBP-1. Such associations were not apparent for IGFBP-3. Lack of marked prandial regulation of IGFBP-2, in contradistinction to IGFBP-1, may make IGFBP-2 a more robust biomarker for identification of insulin-resistant individuals at high cardiovascular risk in epidemiological studies.


Dr A. H. Heald

Department of Diabetes and Endocrinology
Salford Royal Hospitals University Trust
Hope Hospital

Stott Lane

Salford M6 8HD

United Kingdom

Telefon: 01612065157

Fax: 0 16 12 06 59 89

eMail: aheald@fs1.ho.man.ac.uk