title: Vitamin C status is related to proinflammatory responses and impaired vascular endothelial function in healthy, college-aged lean and obese men.
abstract: Vitamin C supplementation has been suggested to reduce cardiovascular disease risk. However, no studies have examined the relationship between vitamin C status and vascular dysfunction in lean and obese individuals in the absence of supplementation. We examined whether vascular function is interrelated with vitamin C status and inflammation in healthy, college-aged lean and obese men with no history of dietary supplementation. A cross-sectional study was conducted during winter 2008 in lean and obese men aged 21±3 years (n=8/group). Brachial artery flow-mediated dilation (FMD) was measured to determine vascular endothelial function. Plasma antioxidants (vitamin C, vitamin E, and thiols), inflammatory proteins (C-reactive protein [CRP], myeloperoxidase [MPO], and cytokines), and cellular adhesion molecules were measured. Participants also completed 3-day food records on the days preceding their vascular testing. Group differences were evaluated by t tests, and correlation coefficients were determined by linear regression. FMD was 21% lower (P<0.05) in obese men. They also had 51% lower vitamin C intakes and 38% lower plasma vitamin C concentrations. Obese men had greater plasma concentrations of CRP, MPO, inflammatory cytokines, and cellular adhesion molecules. Participants' CRP and MPO were each inversely related (P<0.05) to FMD (r=-0.528 and -0.625) and plasma vitamin C (r=-0.646 and -0.701). These data suggest that low vitamin C status is associated with proinflammatory responses and impaired vascular function in lean and obese men. Additional study is warranted to determine whether improving dietary vitamin C intakes from food attenuate vascular dysfunction.
authors.affiliation: Department of Nutritional Sciences, University of Connecticut, Storrs, CT 06269, USA.
authors.forename: Eunice
authors.initials: E
authors.lastname: Mah
authors.forename: Manuel D
authors.initials: MD
authors.lastname: Matos
authors.forename: Diana
authors.initials: D
authors.lastname: Kawiecki
authors.forename: Kevin
authors.initials: K
authors.lastname: Ballard
authors.forename: Yi
authors.initials: Y
authors.lastname: Guo
authors.forename: Jeff S
authors.initials: JS
authors.lastname: Volek
authors.forename: Richard S
authors.initials: RS
authors.lastname: Bruno
mesh_terms: D000975:Antioxidants / Q000008:administration & dosage / Q000378:metabolism; D001205:Ascorbic Acid / Q000008:administration & dosage* / Q000097:blood*; D001783:Blood Flow Velocity; D001916:Brachial Artery / Q000000981:diagnostic imaging; D002097:C-Reactive Protein / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000378:metabolism; D003430:Cross-Sectional Studies; D016207:Cytokines / Q000097:blood; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology*; D006801:Humans; D007249:Inflammation / Q000097:blood*; D008297:Male; D009752:Nutritional Status; D009765:Obesity / Q000097:blood*; D009195:Peroxidase / Q000378:metabolism; D013851:Thinness / Q000097:blood*; D014463:Ultrasonography; D014810:Vitamin E / Q000097:blood; D055815:Young Adult
chemical_list: D000975:Antioxidants; D015815:Cell Adhesion Molecules; D016207:Cytokines; D014810:Vitamin E; D002097:C-Reactive Protein; D009195:Peroxidase; D001205:Ascorbic Acid