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Inflammatory mediators in morbidly obese subjects; associations with glucose abnormalities and changes after oral glucose

D Hofsø, Morbid Obesity Centre, Vestfold Hospital trust, Tønsberg, 3103, Norway
T Ueland, Research Institute of Internal Medicine, Rikshospitalet University Hospital, Oslo, Norway
H Hager, Department of Clinical Chemistry, Vestfold Hospital Trust, Oslo, Norway
T Jenssen, Department of Medicine, Rikshospitalet University Hospital, Oslo, Norway
J Bollerslev, Department of Medicine, Rikshospitalet University Hospital, Oslo, Norway
K Godang, Research Institute of Internal Medicine, Rikshospitalet University Hospital, Oslo, Norway
P Aukrust, University of Oslo, Oslo, Norway
J Røislien, Morbid Obesity Centre, Vestfold Hospital Trust, Tønsberg, Norway
J Hjelmesæth, Morbid Obesity Centre, Vestfold Hospital Trust, Tønsberg, Norway

Correspondence: Dag Hofsø, Email: dag.hofso{at}siv.no

Objective: To explore inflammatory mediators in morbidly obese subjects with various categories of glucose tolerance and to study the changes in these mediators after an oral glucose load.

Design: Cross-sectional and experimental study.

Methods: One hundred and forty-four morbidly obese subjects classified into three categories; normal glucose tolerance (NGT), pre-diabetes and new onset diabetes; were included, as were 27 normal weight normoglycemic controls. Serum osteoprotegerin (OPG), visfatin, leptin, adiponectin, interleukin-1 receptor antagonist (IL-1Ra) and C-reactive protein (CRP) were analyzed during an oral glucose tolerance test (OGTT).

Results: Fasting levels of leptin and IL-1Ra were consistently higher in obese persons (p<0.001 and p<0.05). Morbidly obese subjects with NGT had higher CRP levels (p<0.001) and lower adiponectin levels compared to controls (p<0.05). Yet when compared to morbidly obese subjects with new onset diabetes, those with NGT had lower CRP levels and higher adiponectin levels (both p<0.05). Baseline OPG and visfatin levels did not differ between the groups (p=0.326 and p=0.198). During OGTT OPG levels decreased (p<0.001) and visfatin levels increased transiently (p=0.018). The response in OPG and visfatin did not differ between the groups (p=0.690 and p=0.170). There were minor changes in adiponectin and leptin levels.

Conclusions: Morbid obesity and glucose intolerance were associated with lower adiponectin levels and higher CRP levels, thus supporting a relationship between obesity, glucose homeostasis and inflammation. Oral glucose suppressed OPG levels and transiently enhanced visfatin levels independent of obesity and glucose tolerance status, indicating that glucose may be involved in the acute regulation of these proteins.