Tumor Necrosis Factor-α Antagonism Improves Vasodilation During Hyperinsulinemia in Metabolic Syndrome
- Manfredi Tesauro, MD1,
- Francesca Schinzari, MD2,
- Valentina Rovella, MD1,
- Domenico Melina, MD2,
- Nadia Mores, MD2,
- Angela Barini, MD2,
- Marco Mettimano, MD2,
- Davide Lauro, MD1,
- Micaela Iantorno, MD3,
- Michael J. Quon, MD, PHD3 and
- Carmine Cardillo, MD2
- 1Università di Tor Vergata, Rome, Italy
- 2Università Cattolica del Sacro Cuore, Rome, Italy
- 3National Center for Complementary and Alternative Medicine, National Institutes of Health, Bethesda, Maryland
- Corresponding author: Carmine Cardillo, carmine.cardillo{at}rm.unicatt.it
Abstract
OBJECTIVE—Obesity is associated with chronic inflammation due to overproduction of proinflammatory cytokines, including tumor necrosis factor (TNF)-α. We assessed the effects of TNF-α neutralization by infliximab on vascular reactivity during hyperinsulinemia in obesity-related metabolic syndrome.
RESEARCH DESIGN AND METHODS—Vascular responses to intra-arterial infusion of acetylcholine (ACh) and sodium nitroprusside (SNP) were assessed in patients with metabolic syndrome, before and after administration of infliximab.
RESULTS—Patients had blunted vasodilator responses to ACh and SNP during hyperinsulinemia compared with control subjects; a potentiation of the responsiveness to both ACh and SNP, however, was observed in patients following infliximab. The antioxidant vitamin C improved the vasodilator response to ACh in patients with metabolic syndrome, but its effect was not further enhanced by concurrent administration of infliximab.
CONCLUSIONS—TNF-α neutralization ameliorates vascular reactivity in metabolic syndrome during hyperinsulinemia, likely in relation to decreased oxidative stress, thereby suggesting an involvement of inflammatory cytokines in vascular dysfunction of these patients.
Footnotes
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Published ahead of print at http://care.diabetesjournals.org on 4 April 2008.
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- Accepted March 30, 2008.
- Received January 31, 2008.
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