In recent years, the link between obesity, inflammation and atherosclerosis has attracted increasing interest. Recently, besides the classical inflammatory markers, the competitive nitric oxide synthase antagonist asymmetric dimethylarginine (ADMA) has been shown to be involved in the pathogenesis of atherosclerosis and cardiovascular diseases. Since obese people present a condition of chronic low-grade inflammation and endothelial dysfunction, in the present study we quantified ADMA levels in uncomplicated obese women (with no clinical, cardiac or metabolic complications) and normal-weight control subjects. We investigated the relationship of ADMA with some anthropometric measurements, abdominal visceral and subcutaneous adipose tissue accumulation, and biochemical and proinflammatory factors of the subjects [interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6R), IL6-R/IL-6 ratio, tumor necrosis factor alpha (TNFα), homocysteine (Hcy) and plasminogen activator inhibitor-1 (PAI-1)]. ADMA and all the other pro-inflammatory parameters resulted higher in obese patients than in healthy subjects. ADMA significantly correlated with Hcy, PAI-1, TNFα and with sIL-6R/IL-6 ratio but not with other anthropometric and biochemical parameters. In a stepwise regression analysis ADMA correlated most closely with Hcy and TNFα. In conclusion, in our obese uncomplicated patients TNFα and Hcy emerged as strong predictors of ADMA which might be a potential mediator of the effects of different risk factors affecting the cardiovascular system.

Asymmetric dimethylarginine: relationship with circulating biomarkers of inflammation and cardiovascular disease risk in uncomplicated obese women / E. Dozio, A.E. Malavazos, G. Dogliotti, S. Goggi, E. Galliera, U. Solimene, P. Magni, E. Costa, L. Morricone, M.M. Corsi Romanelli. - In: EUROPEAN JOURNAL OF INFLAMMATION. - ISSN 1721-727X. - 9:3(2011), pp. 249-255. [10.1177/1721727X1100900305]

Asymmetric dimethylarginine: relationship with circulating biomarkers of inflammation and cardiovascular disease risk in uncomplicated obese women

E. Dozio
;
A.E. Malavazos;G. Dogliotti;E. Galliera;U. Solimene;P. Magni;M.M. Corsi Romanelli
Ultimo
2011

Abstract

In recent years, the link between obesity, inflammation and atherosclerosis has attracted increasing interest. Recently, besides the classical inflammatory markers, the competitive nitric oxide synthase antagonist asymmetric dimethylarginine (ADMA) has been shown to be involved in the pathogenesis of atherosclerosis and cardiovascular diseases. Since obese people present a condition of chronic low-grade inflammation and endothelial dysfunction, in the present study we quantified ADMA levels in uncomplicated obese women (with no clinical, cardiac or metabolic complications) and normal-weight control subjects. We investigated the relationship of ADMA with some anthropometric measurements, abdominal visceral and subcutaneous adipose tissue accumulation, and biochemical and proinflammatory factors of the subjects [interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6R), IL6-R/IL-6 ratio, tumor necrosis factor alpha (TNFα), homocysteine (Hcy) and plasminogen activator inhibitor-1 (PAI-1)]. ADMA and all the other pro-inflammatory parameters resulted higher in obese patients than in healthy subjects. ADMA significantly correlated with Hcy, PAI-1, TNFα and with sIL-6R/IL-6 ratio but not with other anthropometric and biochemical parameters. In a stepwise regression analysis ADMA correlated most closely with Hcy and TNFα. In conclusion, in our obese uncomplicated patients TNFα and Hcy emerged as strong predictors of ADMA which might be a potential mediator of the effects of different risk factors affecting the cardiovascular system.
asymmetric dimethylarginine; cardiovascular risk; obesity; inflammation
Settore MED/05 - Patologia Clinica
Settore MED/04 - Patologia Generale
Settore MED/13 - Endocrinologia
Settore MED/46 - Scienze Tecniche di Medicina di Laboratorio
2011
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/198470
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