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NUTRIM, Department of Human Biology, Maastricht University (C.J.H., W.H.M.S., M.S.W.-P.) 6200 MD Maastricht, The Netherlands; Gaubius Laboratory, TNO Prevention and Health (J.H.N.L., K.H.T., T.K.), 2301 CE Leiden, The Netherlands; and Departments of Vascular Surgery (J.H.N.L.) and Medical Statistics (P.H.C.E.), Leiden University Medical Center, 2300 RC Leiden, The Netherlands
Address all correspondence and requests for reprints to: Dr. Jan H. N. Lindeman, Department of Vascular Surgery, Leiden University Medical Center, P.O. Box 9600, 2300 RC Leiden, The Netherlands. E-mail: lindeman{at}lumc.nl.
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 subfractions during the diet. Weight loss decreased the humoral inflammation parameters TNF
, 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.
This work was supported by a grant from The Netherlands Heart Foundation (NHS 97.100).
C.J.H. and J.H.N.L. contributed equally to this work and should both be considered as first authors.
Abbreviations: CRP, C-Reactive protein; HDL, high-density lipoprotein; ICAM, intracellular adhesion molecular; LDL, low-density lipoprotein; PAI-1, plasminogen activator inhibitor type 1; PEG-OB, pegylated recombinant leptin; sTNFR, soluble TNF receptor; tPA, tissue plasminogen activator; VLCD, very low calorie diet; vWF, von Willebrand factor.
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