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Abdominal Obesity and Type 2 Diabetes

European Endocrinology, 2008; 4:26-28; DOI: http://doi.org/10.17925/EE.2008.04.00.26

Epidemiology

Recent statistics from the World Health Organization (WHO) indicate that in 2005 approximately 1.6 billion adults (aged 15 years and over) were overweight worldwide, while at least 400 million adults were obese. Furthermore, the WHO predicts that by 2015 approximately 2.3 billion adults will be overweight and more than 700 million will be obese.1 At the same time, diabetes currently affects 246 million people worldwide. It is expected to affect 380 million by 2025, with the largest increases in diabetes prevalence in developing countries; most of the cases will be type 2 diabetes.2,3

Excess weight is the most important modifiable risk factor for the development of type 2 diabetes because 85–90% of people with type 2 diabetes are either overweight or obese.4 The term ‘diabesity’ has been coined to express that type 2 diabetes is obesity-dependent and that obesity is the main aetiological cause of type 2 diabetes.5 Epidemiological studies have shown that body mass index (BMI) is a powerful predictor of type 2 diabetes:6 Field et al. reported that both men and women with BMI >35kg/m2 were approximately 20 times more likely to develop type 2 diabetes compared with controls.7 However, obesity is remarkably heterogeneous and some obese patients are insulin-sensitive, and even some massively obese patients show a normal plasma lipoprotein–lipid profile despite their significant excess of body fat.8

Fat Topography

Waist circumference as a measure of abdominal obesity was proposed as a better predictor of risk of type 2 diabetes development.9 However, total body fat is not the only source of adverse health complications of obesity; in fact, fat distribution and the relative portion of lipids in various insulinsensitive tissues (skeletal muscle and liver), which affects their normal metabolic pathways, actually determine metabolic risk.10 Accumulation of intra-abdominal or visceral fat is associated with insulin resistance and is a major feature of metabolic syndrome, which confers a 1.5–2-fold increased risk of developing diabetes and cardiovascular disease (CVD).11

Abdominal obesity as a clinical feature of excessive accumulation of visceral fat is usually associated with a cluster of cardiovascular risk factors, defined by the WHO as ‘metabolic syndrome’. This syndrome is characterised by abdominal obesity, insulin resistance, dyslipidaemia (high triglyceride level and low high-density lipoprotein [HDL] cholesterol level), hypertension, high fasting glucose, procoagulant (elevated plasminogen activator inhibitor [PAI-1] levels) and pro-inflammatory state, i.e. elevated tumour necrosis factor (TNF), C-reactive protein (CRP) and interleukin (IL)-6.12 Insulin resistance is thought to be provoked by visceral obesity due to increased flux of free fatty acids (FFAs) to the liver and increased secretion of inflammatory mediators. It was shown that abdominally obese patients have about 50% increased FFA lipolysis and 50% lower FFA turnover compared with lean individuals.13 At the same time, abdominally obese patients have a greater FFA lipolysis rate compared with non-abdominally obese patients.13
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