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The distinction of metabolically healthy from unhealthy obese individuals

Blüher, Matthias

Current Opinion in Lipidology:
doi: 10.1097/MOL.0b013e3283346ccc
Nutrition and metabolism: Edited by Paul Nestel and Ronald P. Mensink
Abstract

Purpose of review: The prevalence and severity of obesity are dramatically increasing throughout the world. Obesity causes a decline in life expectancy due to its associated metabolic and cardiovascular comorbid disorders. Therefore, it will become more important to distinguish obese individuals at high risk for obesity-related metabolic diseases from those who are metabolically ‘healthy’. This review focuses on recent evidence suggesting that normal adipose tissue function contributes to the healthy obese phenotype.

Recent findings: The majority of individuals with obesity develop insulin resistance, type 2 diabetes, dyslipidemia, gout, hypertension and cardiovascular disease. However, approximately 10–25% of obese individuals are metabolically healthy most likely due to preserved insulin sensitivity. Recent studies suggest that inflammation of visceral adipose tissue, ectopic fat deposition and adipose tissue dysfunction mediate insulin resistance in human obesity independently of total body fat mass. This suggests that mechanisms beyond a positive caloric balance such as inflammation and adipokine release determine the pathological metabolic consequences in patients with obesity.

Summary: Recommendations for obesity treatment should distinguish the metabolically ‘healthy’ from ‘unhealthy’ obese phenotype to identify early the obese person who will benefit the most from losing weight. In addition, novel antiobesity treatment strategies targeting adipose tissue dysfunction are needed.

Author Information

Department of Medicine, University of Leipzig, Leipzig, Germany

Correspondence to Matthias Blüher, MD, University of Leipzig, Department of Medicine, Liebigstr. 20, 04103 Leipzig, Germany Tel: +49 341 97 15984; fax: +49 341 97 22439; e-mail: bluma@medizin.uni-leipzig.de

© 2010 Lippincott Williams & Wilkins, Inc.