کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6000633 | 1182931 | 2015 | 6 صفحه PDF | دانلود رایگان |

- Blacks presented higher blood pressure and von Willebrand factor antigen (WFag) and lower IGF-1 levels compared to whites.
- vWFag was inversely associated with IGF-1 and IGF-1/IGFBP-3 in blacks, with no associations found in whites.
- When patients with diabetes were included, the aforementioned associations found in blacks remained robust.
IntroductionInsulin-like growth factor-1 (IGF-1) has vasculoprotective effects and can directly oppose endothelial dysfunction in several ways. To improve our understanding on the potential contribution of reduced IGF-1 to the development of vascular endothelial damage, we investigated the link between bioavailable IGF-1 and von Willebrand factor (vWF) as a marker of endothelial damage. We performed this study in black South African school teachers, known to be prone to hypertension.Materials and methodsFrom the larger Sympathetic activity and Ambulatory Blood Pressure in Africans (SABPA) study we included 179 black and 207 white non-diabetic men and women (aged 44.5 ± 9.96 years). We measured ambulatory blood pressure and determined IGF-1, insulin-like growth factor binding protein 3 (IGFBP-3) and vWF antigen from blood samples. We used the molar IGF-1/IGFBP-3 ratio as an estimate of bioavailable IGF-1.ResultsBlack individuals presented higher blood pressure and vWFag and lower IGF-1 than the white group (all p < 0.001). In multivariate-adjusted analyses, vWFag was inversely associated with IGF-1 (R2 = 0.18; β = â 0.17; p = 0.044) and IGF-1/IGFBP-3 (R2 = 0.18; β = â 0.17; p = 0.030) in blacks, with no associations in whites. Since IGF-1 is attenuated and vWFag elevated in diabetes, we included patients with diabetes (n = 38) and the aforementioned associations found in blacks remained robust.ConclusionThe inverse association between bioavailable IGF-1 and vWF in black South Africans suggests that suppressed IGF-1 may result in endothelial damage independent of traditional risk factors.
Journal: Thrombosis Research - Volume 136, Issue 5, November 2015, Pages 1007-1012