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Circulating leptin levels predict the development of metabolic syndrome in middle-aged men: an 8-year follow-up study

Galletti, Ferruccioa; Barbato, Antonioa; Versiero, Marcoa; Iacone, Robertoa; Russo, Ornellaa; Barba, Gianvincenzob; Siani, Alfonsob; Cappuccio, Francesco Pc; Farinaro, Eduardod; Valle, Elisabetta dellad; Strazzullo, Pasqualea

Journal of Hypertension:
doi: 10.1097/HJH.0b013e3281afa09e
Original papers: Metabolic syndrome
Abstract

Background: Because high circulating plasma leptin is associated with many features of the metabolic syndrome (MS), such as abdominal obesity, insulin resistance and high blood pressure (BP), we analysed the ability of plasma leptin concentration to predict the risk of developing MS in a prospective investigation of adult male participants of the Olivetti Heart Study (OHS).

Methods and results: Three hundred and sixty out of 907 men participating in the 1994–95 and 2002–04 OHS examinations (mean age at baseline 50.4 years, range 25–73 years) were free of MS at first visit according to NCEP-ATP III criteria (modified for the lack of high-density lipoprotein cholesterol measurement at baseline). During an average follow-up period of 8 years, there were 52 incident cases of MS (14.5%) due, in particular, to a rise in the prevalence of high BP (+42.4%), abdominal obesity (+16.4%) and impaired fasting glucose (IFG, +6.1%). In multivariate analyses, a one standard deviation difference in baseline plasma leptin concentration was associated with a 1.58-fold greater risk of developing MS (95% confidence interval = 1.10–2.30, P = 0.016) accounting for age, waist circumference, homeostatic assessment model index, smoking, alcohol consumption and physical activity. In particular, plasma leptin was positively associated with the risk of developing high BP (0.006) and IFG (0.014), after adjustment for confounders.

Conclusion: In this sample of an adult male population free of MS at baseline, circulating plasma leptin was a significant predictor of the risk of MS and, in particular, of its high BP and IFG components, independently of potential confounders.

Author Information

aDepartment of Clinical and Experimental Medicine, Federico II University of Naples Medical School, Naples, Italy

bEpidemiology and Population Genetics, Institute of Food Science, CNR, Avellino, Italy

cClinical Sciences Research Institute, Warwick Medical School, Coventry, UK

dDepartments of Preventive Medical Sciences, Federico II University of Naples, Medical School, Naples, Italy

Received 22 September, 2006

Revised 28 February, 2007

Accepted 30 March, 2007

Correspondence to Dr Ferruccio Galletti and Dr Pasquale Strazzullo, Department of Clinical & Experimental Medicine, ‘Federico II’ University of Naples Medical School, Via S. Pansini 5, 80131 Naples, Italy Tel: +39 0817 464301; fax: +39 0815 466152; e-mail: galletti@unina.it, strazzul@unina.it

© 2007 Lippincott Williams & Wilkins, Inc.