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ORIGINAL ARTICLE

Insulin‐like growth factor (IGF)‐I, IGF‐II and IGF‐binding protein (IGFBP)‐3 levels in Arab subjects with coronary heart disease

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Pages 553-559 | Received 28 Aug 2006, Accepted 14 Dec 2006, Published online: 08 Jul 2009
 

Abstract

Objective. Insulin‐like growth factors (IGF‐I, IGF‐II) and their binding protein (IGFBP‐3) may be risk markers for coronary heart disease (CHD). This study aimed to assess the levels and determinants of the serum levels of IGF‐I, IGF‐II and IGFBP‐3 in Arab patients with established CHD. Material and methods. Two groups of subjects were matched for age, gender, BMI and waist–hip ratio (WHR): (i) CHD (n = 105), median age 51.0 (range 40.0–60.0) years; (ii) controls (n = 97) aged 49.0 (range 37.0–60.0) years. We measured fasting serum levels of glucose and lipoproteins (total cholesterol, triglycerides, LDL, HDL, apo B), insulin, HOMA‐IR, IGF‐I, IGF‐II and IGFBP‐3 and compared the results between groups. The effects of body mass and the metabolic syndrome (MS) on IGF levels were also examined, and linear correlations were sought between the various parameters. Results. The levels of IGF‐I, IGF‐II and IGFBP‐3 were significantly lower (all p<0.01) for the CHD group than for the control group. These differences were not influenced by BMI or with the presence of MS. In CHD, there were no significant correlations between levels of IGF‐I and IGF‐II and age, BMI, WHR, lipoprotein concentrations and insulin sensitivity, although IGFBP‐3 had weakly significant relationships with some of the lipoproteins. Conclusions. Levels of IGF‐I, IGF‐II and IGFBP3 are reduced in male Arab patients with CHD, and did not appear influenced by traditional CHD risk factors such as age, BMI, insulin sensitivity and presence of MS. Perturbations in the IGF/IGFBP‐3 axis may be potential additional targets for pharmacological manipulation in CHD.

Acknowledgements

We acknowledge the technical help of Dr S. George and Mr. P. K. Shihab. The study was supported by a Kuwait University Research Administration Grant no. MG 01/03.

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