Leptin and the proinflammatory state associated with human obesity

article
It has been suggested that elevated leptin levels underlie the low grade proinflammatory state in human obesity. We reasoned that if elevated leptin levels are an important factor in the proinflammatory state in obesity, then exogenous leptin administration during weight loss should counteract the concurrent beneficial effects of weight loss on the proinflammatory state. We therefore determined whether long-acting pegylated recombinant leptin (PEG-OB) prevents the decrease in cellular and humoral inflammation parameters during a very low calorie diet in healthy overweight young men. Except for B cells, PEG-OB treatment did not influence the decline in total leukocyte count and mononuclear subtractions during the diet. Weight loss decreased the humoral inflammation parameters TNFα, tissue plasminogen activator, and von Willebrand factor (P < 0.05), but in combination with PEG-OB treatment, a significant decrease was shown for inflammation markers as a whole (P < 0.014) and that of the individual parameters tissue plasminogen activator, von Willebrand factor, plasminogen activator inhibitor type 1, and intercellular adhesion molecule-1 (P < 0.05). The increase in C-reactive protein levels (P < 0.05) was the sole indication for a humoral proinflammatory action of leptin. Although PEG-OB treatment significantly increased weight loss (P < 0.03), the data do not support a proinflammatory role of leptin in human obesity. Chemicals / CAS: intercellular adhesion molecule 1, 126547-89-5; plasminogen activator inhibitor 1, 140208-23-7; tissue plasminogen activator, 105913-11-9; von Willebrand factor, 109319-16-6; Intercellular Adhesion Molecule-1, 126547-89-5; Leptin; pegylated leptin; Plasminogen Activator Inhibitor 1; Polyethylene Glycols; Recombinant Proteins; Tissue Plasminogen Activator, EC 3.4.21.68; Tumor Necrosis Factor-alpha; von Willebrand Factor
TNO Identifier
237685
ISSN
0021972X
Source
Journal of Clinical Endocrinology and Metabolism, 89(4), pp. 1773-1778.
Pages
1773-1778
Files
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