Format

Send to

Choose Destination
See comment in PubMed Commons below
Scand J Clin Lab Invest. 2005;65(4):283-90.

Changes in serum levels of E-selectin correlate to improved glycaemic control and reduced obesity in subjects with the metabolic syndrome.

Author information

1
Centre for Clinical Research, Ullevål University Hospital, Oslo, Norway. troseid@hotmail.com

Abstract

OBJECTIVE:

Inflammation plays an essential role in the atherosclerotic process. Cellular adhesion molecules (CAMs) such as E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are involved in the rolling, adhesion and extravasation of monocytes and T-lymphocytes into the atherosclerotic plaque. In the present study the effect of physical exercise and pravastatin (40 mg daily) on serum levels of CAMs and a possible role of adipose tissue in regulating serum levels of CAMs were investigated.

MATERIAL AND METHODS:

The study was designed as an unmasked randomized 2x2 factorial trial of 12 weeks duration in 32 subjects with the metabolic syndrome. Changes from baseline were studied, and correlations between changes in CAMs, anthropometric measures, regional fat distribution, glycaemic control and the adipocytokine tumour necrosis factor-a (TNF-a) and adiponectin were investigated.

RESULTS:

No significant changes in CAMs were observed in any of the intervention groups. However, when examining the whole study population regardless of intervention, changes in serum E-selectin were significantly correlated to changes in body mass index (r=0.48, p=0.006), waist circumference (r=0.48, p=0.006), fasting glucose (r=0.43, p=0.02) and HbA1c (r=0.45, p=0.01), but not to changes in visceral fat, subcutaneous fat, TNF-a or adiponectin.

CONCLUSION:

Changes in glycaemic control and obesity, rather than regional fat distribution, seem to influence the levels of E-selectin in subjects with the metabolic syndrome.

PMID:
16076683
DOI:
10.1080/00365510510013811
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Taylor & Francis
    Loading ...
    Support Center