Disclosure: The authors declared no conflict of interest.
Article first published online: 26 MAR 2013
Copyright © 2012 The Obesity Society
Volume 21, Issue 2, pages 361–366, February 2013
How to Cite
Dullaart, R. P. F., de Boer, J. F., Annema, W. and Tietge, U. J.F. (2013), The inverse relation of HDL anti-oxidative functionality with serum amyloid a is lost in metabolic syndrome subjects. Obesity, 21: 361–366. doi: 10.1002/oby.20058
Funding agencies: R.P.F. Dullaart, MD, PhD, is supported by the Dutch Diabetes Research Foundation, grant 2001.00.012. U.J.F. Tietge, MD, PhD, is supported by grants from the Top Institute (TI) Food and Nutrition and the Groningen Expert Center for Kids with Obesity.
- Issue published online: 26 MAR 2013
- Article first published online: 26 MAR 2013
- Accepted manuscript online: 3 OCT 2012 05:36PM EST
- Manuscript Accepted: 4 AUG 2012
- Manuscript Received: 1 FEB 2012
- Dutch Diabetes Research Foundation. Grant Number: 2001.00.012
- Top Institute (TI) Food and Nutrition and the Groningen Expert Center for Kids with Obesity
Anti-oxidative properties of high density lipoproteins (HDL) are relevant for atheroprotection. HDL carry serum amyloid A (SAA), which may impair HDL functionality. We questioned whether HDL anti-oxidative capacity is determined by SAA.
Design and Methods:
Relationships of HDL anti-oxidative capacity (% inhibition of low density lipoprotein oxidation in vitro) with SAA were determined in 54 non-diabetic subjects without metabolic syndrome (MetS) and 68 subjects with MetS (including 51 subjects with Type 2 diabetes mellitus).
SAA levels were higher in MetS subjects, coinciding higher high sensitive C-reactive protein (hs-CRP) and lower HDL cholesterol and apolipoprotein (apo) A-I levels (P<0.001 for all). HDL anti-oxidative capacity was not different between subjects with and without MetS (P=0.76), but the HDL anti-oxidation index (HDL anti-oxidative capacity multiplied by individual HDL cholesterol concentrations), as a measure of global anti-oxidative functionality of HDL, was lower in Mets subjects (P<0.001). HDL anti-oxidative capacity was correlated inversely with SAA levels in subjects without MetS (r=-0.286, P=0.036). Notably, this relationship was independent of HDL cholesterol or apoA-I (P<0.05 for both). In contrast, no relation of HDL anti-oxidative capacity with SAA was observed in MetS subjects (r=0.032, P=0.80). The relationship of SAA with HDL anti-oxidative capacity was different in subjects with MetS compared to subjects without MetS (P=0.039 for the interaction between the presence of MetS and SAA on HDL anti-oxidative capacity) taking age and diabetes status into account.
Higher SAA levels may impair HDL anti-oxidative functionality. The relationship of this physiologically relevant HDL functionality measure with circulating SAA levels is apparently disturbed in metabolic syndrome.