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VEGF is indirectly associated with NO production and acutely increases in response to hyperglycaemia 1
Author(s) -
Siervo Mario,
Tomatis Virginia,
Stephan Blossom C. M.,
Feelisch Martin,
Bluck Les J. C.
Publication year - 2012
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.2012.02684.x
Subject(s) - medicine , endocrinology , vascular endothelial growth factor , metabolic syndrome , blood pressure , nitric oxide , insulin , obesity , vascular endothelial growth factor a , body mass index , vegf receptors
Eur J Clin Invest 2012; 42 (9): 967–973 Abstract Background  Increased levels of vascular endothelial growth factor (VEGF) have been observed in patients with metabolic syndrome (MetS). Nitric oxide (NO) formation is reduced in MetS, but its relationship to VEGF production remains poorly defined. We evaluated the association between VEGF/NO synthesis and insulin sensitivity in obese subjects and investigated the secretory response of VEGF to an acute elevation of glucose. Materials and methods  Seven healthy normal‐weight subjects, seven obese subjects without MetS and seven obese subjects with MetS were recruited. Anthropometry, body composition and cardiometabolic functions (blood pressure, glucose, insulin, triglycerides, total cholesterol, HDL‐C and VEGF) were measured, and a novel stable isotope method was used to assess in vivo rates of NO production. A frequent sampling intravenous glucose tolerance test was performed to study the dynamics of VEGF release. Results  Fasting VEGF levels were significantly higher in the two obese groups compared to the control group ( P for trend = 0·02), but the difference was not significant after adjustment for age. Vascular endothelial growth factor levels were associated with systolic blood pressure (ρ = 0·54; P  = 0·01) and NO production (ρ = −0·44; P  = 0·04). Vascular endothelial growth factor levels increased in response to acute hyperglycaemia in normal‐weight and obese subjects ( P  < 0·001). Conclusions  Vascular endothelial growth factor levels rapidly increase during hyperglycaemia and are inversely related to NO production at steady state. The potential link between the acute secretion of VEGF and atherosclerotic risk in subjects with poorly controlled glycaemia as well as the potential of lowering elevated VEGF levels by increasing NO production and/or availability warrants further investigation.

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