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Monocyte Chemoattractant Protein-1 in Adipose Tissue

Endocrinology Unit (A.E.M., E.C., L.M., B.A.), Department of Medical and Surgical Sciences, University of Milano, Istituto Policlinico San Donato, 20097 San Donato Milanese, Italy; and Institute of General Pathology (M.M.C.), Laboratory of Clinical Pathology, 20133, University of Milano, Italy

Address correspondence to: Prof. Bruno Ambrosi, Endocrinology Unit, Dipartimento di Scienze Medico Chirurgiche, Università di Milano, Istituto Policlinico San Donato, Via Morandi 30, I-20097, San Donato Milanese, Italy. E-mail: bruno.ambrosi{at}unimi.it.

To the editor:

In their recent article to JCEM, Bruun et al. (1) demonstrated for the first time that monocyte chemoattractant protein 1 (MCP-1) release is higher in visceral adipose tissue (VAT) compared with sc adipose tissue.

It is well established that adipose tissue should be considered as an endocrine organ, able to produce and release a great variety of cytokines, and among these products the role of MCP-1 is emerging (2). Most of these mediators exert a systemic action as inflammatory pathway activators.

In a situation of expanded VAT, an enhancement of MCP-1 production by adipocytes may be hypothesized. Troseid et al. (3) observed a positive correlation between the reduction in MCP-1 and the decrease in visceral fat in patients affected by metabolic syndrome.

Because, to the best of our knowledge, literature about the correlation between MCP-1 and visceral adiposity is still inconsistent, we want to provide some additional information on visceral obesity, low-grade inflammatory state, and some cardiac complications. Recently, we evaluated (by ELISA kit) MCP-1 circulating levels in 20 uncomplicated women with severe obesity (body mass index, 43.9 ± 4.8 kg/m², mean ± SE). Female patients with a greater amount of visceral fat (VAT > 130 cm², as assessed by computed tomography) presented higher MCP-1 blood levels than those with a lower degree of abdominal adiposity (VAT < 130 cm²; MCP-1 = 77.3 ± 10.2 vs. 48.2 ± 1.9 pg/ml, respectively; P < 0.02). This finding supports the hypothesis that VAT may be a major source of this cytokine. Moreover, our preliminary data that MCP-1 levels and VAT were associated with some morphological and functional echocardiographic abnormalities, as previously observed in obesity (4), may also support a role of visceral fat in predisposing to cardiac dysfunction, possibly through a low-grade state of inflammation.

Therefore, we completely agree with the study of Bruun et al. (1) that opens new insights on the role of VAT in MCP-1 release and emphasizes the importance of macrophage infiltration in determining the low-grade inflammatory state associated with visceral obesity.

Footnotes

A response to this letter was invited, but the authors of the original article chose not to provide one.

Received February 28, 2005.

References

1. Bruun JM, Lihn AS, Pedersen SB, Richelsen B 2005 Monocyte chemoattractant protein-1 release is higher in visceral than subcutaneous human adipose tissue (AT): implication of macrophages resident in the AT. J Clin Endocrinol Metab 90:2282–2289[Abstract/Free Full Text]
2. Sartipy P, Loskutoff DJ 2003 Monocyte chemoattractant protein 1 in obesity and insulin resistance. Proc Natl Acad Sci USA 100:7265–7270[Abstract/Free Full Text]
3. Troseid M, Lappegard KT, Claudi T, Damas JK, Morkrid L, Brendberg R, Mollnes TE 2004 Exercise reduces plasma levels of the chemokines MCP-1 and IL-8 in subjects with the metabolic syndrome. Eur Heart J 25:349–355[Abstract/Free Full Text]
4. Morricone L, Malavazos AE, Coman C, Donati C, Hassan T, Caviezel F 2002 Echocardiographic abnormalities in normotensive obese patients: relationship with visceral fat. Obes Res 10:489–497[Medline]

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