Elevated soluble intercellular adhesion molecule-1 levels in obesity: Relationship to insulin resistance and tumor necrosis factor-[alpha ] system activity
Intercellular adhesion molecule-1 (ICAM-1) is 1 of the possible factors linking obesity and diabetes with cardiovascular disease, however, the mechanism of the increase in ICAM-1 concentration in obesity remains unclear. Therefore, the aim of the present study was to assess plasma soluble ICAM-1 (sI...
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Veröffentlicht in: | Metabolism, clinical and experimental clinical and experimental, 2002-01, Vol.51 (1), p.75-78 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Intercellular adhesion molecule-1 (ICAM-1) is 1 of the possible factors linking obesity and diabetes with cardiovascular disease, however, the mechanism of the increase in ICAM-1 concentration in obesity remains unclear. Therefore, the aim of the present study was to assess plasma soluble ICAM-1 (sICAM-1) levels in obese subjects with normal glucose tolerance and to evaluate whether those levels may be related to insulin resistance and tumor necrosis factor-[alpha ] (TNF[alpha ]) system activity. The study was performed in 8 lean and 15 obese subjects. Anthropometric and biochemical parameters were measured, and insulin sensitivity was evaluated using the euglycemic hyperinsulinemic clamp technique (insulin infusion, 50 mU [times ] kg[minus ]1 [times ] h[minus ]1). Obese subjects were markedly more hyperinsulinemic and insulin resistant and had higher plasma soluble TNF receptor 2 (sTNFR2) and sICAM-1 levels. sICAM-1 was related positively to body mass index (BMI), waist-to-hip ratio (WHR), percent of body fat, glycated hemoglobin (HbA1c), plasma insulin and triglycerides (TG), TNF[alpha ], and sTNFR2 and negatively to insulin sensitivity. Multiple regression analysis showed that only sTNFR2 and insulin sensitivity were independent predictors of sICAM-1 concentrations and were responsible for 66% of sICAM-1 variability. We conclude that an increase in plasma sICAM-1 concentration in obesity is related to TNF[alpha ] system activation and insulin resistance. |
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ISSN: | 0026-0495 1532-8600 |
DOI: | 10.1053/meta.2002.28095 |