Abstract

Conflicting reports exist on the relationship between systolic BP (SBP) and insulin-like growth factor-1 (IGF-1). Where positive associations are observed in patients with acromegaly, others find a negative association or no relationship. The versatile functions of IGF-1 as a growth factor (vasoprotective versus arterial and cardiac remodelling), the interplay with other hormones as well as IGF-1 resistance phenomena as those shown in chronic renal failure, are mostly regarded as confounding this relationship and thereby resulting in conflicting results. We aimed to review and compare regression coefficients for the association between SBP and total IGF-1 as reported in the literature and two studies from the general population. We searched the literature for studies reporting the mentioned regression coefficients. We also included data from the SAfrEIC and SABPA studies in South Africa (total N=912) including African and Caucasian men and women, aged 20-70 yrs. When plotting the regression coefficients from 13 studies with 20 data points against IGF-1 concentrations, we found a significant association between the regression coefficients and IGF-1 concentration (r=0.80; p<0.001). The slope intercepted the y-axis at IGF-1 concentration of 223.5 ± 14.4 ng/mL. Studies with mean IGF-1 at this range reported weak non-significant regression coefficients (typically young healthy men). Studies including acromegalic patients or adolescents reported significant positive associations, with negative associations for those with compromised cardiovascular function. Our findings suggest that the regression coefficient for the SBP and IGF-1 relationship is dependent on the IGF-1 concentration. Positive associations are observed in situations with overtly high IGF-1 concentrations as those found in acromegaly or conditions of IGF-1 resistance, and beneficial negative relationships seen in those with low-normal IGF-1 and with compromised vascular function such as type 2 diabetes and hypertension. Our results suggest that the complex interplay between IGF-1 and other vasoactive hormones (e.g. growth hormone, insulin, cortisol and adipokines) or the development of a vascular resistance to IGF-1, may hamper the vasoprotective functions of IGF-1.

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