Insulin-like growth factor-I decreases serum lipoprotein(a) during long-term treatment of patients with Laron syndrome

Laron, Z.; Wang, X.L.; Klinger, B.; Silbergeld, A.; Wilcken, D.E.L.

« Previous Next »Metabolism - Clinical and Experimental
Volume 45, Issue 10 , Pages 1263-1266, October 1996

Insulin-like growth factor-I decreases serum lipoprotein(a) during long-term treatment of patients with Laron syndrome

Z. Laron
- Address reprint requests to Z. Laron, MD, Endocrinology and Diabetes Research Unit, Schneider Children's Hospital, 14 Kaplan St, 49202 Petal Tikva, Israel.
- Endocrinology and Diabetes Research Unit, Schneider Children's Hospital, Petal Tikva, Israel
- Department of Cardiovascular Medicine, University of New South Wales at Prince Henry Hospital, Little Bay, Australia
X.L. Wang
- Endocrinology and Diabetes Research Unit, Schneider Children's Hospital, Petal Tikva, Israel
- Department of Cardiovascular Medicine, University of New South Wales at Prince Henry Hospital, Little Bay, Australia
B. Klinger
- Endocrinology and Diabetes Research Unit, Schneider Children's Hospital, Petal Tikva, Israel
- Department of Cardiovascular Medicine, University of New South Wales at Prince Henry Hospital, Little Bay, Australia
A. Silbergeld
- Endocrinology and Diabetes Research Unit, Schneider Children's Hospital, Petal Tikva, Israel
- Department of Cardiovascular Medicine, University of New South Wales at Prince Henry Hospital, Little Bay, Australia
D.E.L. Wilcken
- Endocrinology and Diabetes Research Unit, Schneider Children's Hospital, Petal Tikva, Israel
- Department of Cardiovascular Medicine, University of New South Wales at Prince Henry Hospital, Little Bay, Australia

Received 10 January 1996; accepted 31 March 1996.

Abstract

An increased circulating level of lipoprotein(a) [Lp(a)] is a well-recognized risk factor for coronary artery disease. While much remains to be understood about its regulation and physiological functions, we explored the effect of recombinant insulin-like growth factor-I (IGF-I) administration on circulating Lp(a) levels in 10 Laron syndrome (LS) patients (five children and five adults) with inherited IGF-I deficiency. There was no relationship between pretreatment or posttreatment Lp(a) levels and age and sex of the patients. With IGF-I treatment for 6 to 12 months, there was a significant reduction in Lp(a) (65.7% ± 15.5%, P < .0001) from the pretreatment level of 76 ± 45 mg/L to the posttreatment level of 29 ± 26 mg/L. This decrease was dosage-dependent on the IGF-I administered (r = .685, F = 0.708, P = .029) and correlated more strongly with the dosage ratio of the end to the beginning of treatment (r = .78, F = 12.23, P = .008). The higher the IGF-I dose and the higher the dose ratio, the greater the Lp(a) decrease and the lower the Lp(a) at the end of treatment. In conclusion, we observed a dose-dependent relationship between IGF-I administration and Lp(a) reduction in patients with LS. Further studies are needed to elucidate the mechanism of the effect, but our findings suggest a possible metabolic link between these two and shed more light on the regulation of apolipoprotein (a) [apo(a)] expression. It could also open an avenue for additional therapeutic usage of IGF-I.

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