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IJUP08 - Universidade do Porto

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Possible correlation between morbid obesity and inflammation: a<br />

peripheral leukocyte study<br />

A. Meneses 1* , I. Maio 1* , D. Pestana 1 , P. Freitas 2 , R. Monteiro 1 , I. Azeve<strong>do</strong> 1 , C.<br />

Calhau 1 , R. Soares 1<br />

1 Department of Biochemistry, Faculty of Medicine, University of <strong>Porto</strong>, Portugal.<br />

2 Department of En<strong>do</strong>crinology, S. João Hospital<br />

* The two authors contributed equally to the present study<br />

Obesity has emerged as a major public health problem in the western world. Recently,<br />

more than an inactive bystander, adipose tissue is actually a dynamic and metabolically<br />

active one, since it releases a huge number of inflammatory cytokines [1,2]. Large size<br />

adipocytes mainly in visceral adipose tissue are prone to rupture, therefore evoking an<br />

inflammatory reaction [3].<br />

Nuclear factor kappa-B (NF-kappaB), a transcription factor, is a primary event in<br />

inflammation. NF-kappaB is a crucial molecule regulating the expression and function of a<br />

wide spectrum of inflammatory genes [2]. Alkaline phosphatase (ALP) is a membranebound<br />

enzyme playing a role in lipids transport and storage, two processes occuring in<br />

adipose tissue [4]. In addition, ALP was reported to be associated with inflammation [5].<br />

The purpose of our work was to examine the presence and activity of NFkappaB and ALP<br />

isoforms in peripheral leukocytes in morbid obese patients.<br />

Blood samples were collected from 50 obese patients and 20 volunteers age- and sexmatched.<br />

Proteins were isolated from peripheral leukocytes by the TriPure method. ELISA<br />

assays were performed for NF-kappaB activity and intestinal and tissue-nonspecific<br />

isoforms of alkaline phosphatase (I-ALP and TNS-ALP) expression. Clinical data, such as<br />

weight, height, diet and BMI, were obtained and crossed with lab findings.<br />

Two subgroups of patients were identified: the first presenting NFkappaB activity mean<br />

values identical to controls and another exhibiting significantly higher NFkappaB activity.<br />

I-ALP and TNS-ALP isoforms expression were also increased in the subgroup presenting<br />

higher NFkappaB activity.<br />

In conclusion, two distinct groups of obese patients were identified according to the<br />

presence of inflammatory markers. Clinical parameters of these patients are now being<br />

evaluated in order to investigate the causes behind these distinct inflammatory profiles.<br />

References:<br />

[1] Charo IF, Ransohoff RM (2006) The many roles of chemokines and chemokine receptors in<br />

inflammation. N Engl J Med 354:610-621.<br />

[2] Stienstra R, Duval C, M 252 Ller M, Kersten S (2006) PPARs, Obesity, and Inflammation.<br />

PPAR Res 23;2007:95974.<br />

[3] Rosario Monteiro, Paulo M. S. T. de Castro, Conceição Calhau, Isabel Azeve<strong>do</strong> (2006)<br />

Adipocyte size and liability to cell death. Obes Surg 16(6):804-806.<br />

[4] Ali AT, Penny CB, Paiker JE, Psaras G, Ikram F, Crowther NJ (2006) The relationship between<br />

alkaline phosphatase activity and intracellular lipid accumulation in murine 3T3-L1 cells and<br />

human preadipocytes. Anal Biochem 15;354(2):247-54.<br />

[5] Shanmugham LN, Petrarca C, Castellani ML, Symeoni<strong>do</strong>u I, Frydas S, Vecchiet J, Falasca K,<br />

Tete S, Conti P, Salini V (2007) IL-1beta induces alkaline phosphatase in human phagocytes. Arch<br />

Med Res 38(1):39-44.<br />

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