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P3.09 STIFFER ARTERIES IN “HEALTHY” SUBJECTS WITH COMPONENTS OF THE METABOLIC SYNDROME
oleh: O. Mac Ananey, B. Mc Loughlin, I. Abuzaid, A. Leonard, P. Gaffney, G. Boran, V. Maher
| Format: | Article |
|---|---|
| Diterbitkan: | BMC 2013-11-01 |
Deskripsi
Objectives: To compare indices of vascular stiffness and markers of adiposity and inflammation in “healthy” subjects with/without components of the metabolic syndrome (met-x). Methods: Subjects satisfying ≥1 (≥1 Met-X;) and no criteria (0 Met-X) were recruited (IDF 2006). All were lifelong non-smokers, normotensive, normolipidaemic and normoglycaemic. Augmentation index (AIx) and pulse wave velocity (PWV) were measured using applanation tonometry (Sphygmacor & Vicorder). Fasting leptin, adiponectin, IL-6, TNFα & MCP-1 were measured. Unpaired students t-test and Fischer’s exact test was used to detect differences. Results: Anthropometric, metabolic and haemodynamic indices of the met-x syndrome were significantly higher in the ≥1 Met-X group (p<0.0001). AIx and PWV were higher in the ≥1 Met-X group. The adipose related hormones, leptin and adiponectin were higher and lower, respectively, in the ≥1 Met-X group but the pro-inflammatory markers, IL-6, TNFα & MCP-1 were not different (Table 1). 0 Met-X criteria ≥1 Met-X criteria P n 91 106 Age (years) 37±10 40±8 years 0.06 Body fat (%) 22.64±6.74 30.44±7.71 <0.0001 AIx (%) 12.83±13.60 19.28±13.34 <0.001 PWV (m.s−1) 6.82±0.85 7.14±1.20 <0.05 Leptin (pg.mL−1.10−2) 100.39±73.44 168.93±123.94 <0.001 Adiponectin (pg.mL−1.10−2) 77.54±41.10 53.91±31.98 <0.001 IL-6 (pg.ml−1) 1.59±0.96 2.08±3.01 0.27 TNFα (pg.ml−1) 2.98±1.10 3.29±1.50 0.21 MCP-1 (pg.ml−1) 214.26±96.85 204.51±80.15 0.55 Table 1Body fat composition, arterial stiffness and humoral adipose/pro-inflammatory markers in subjects with/without early signs of met-x. Results are mean±SD. Conclusion: Subjects with early met-x have stiffer arteries than those with normal metabolic function. These results suggest that premature arterial stiffening may be mediated via hormonal rather than inflammatory mechanisms.