Cure of Type 2 Diabetes by Metabolic Surgery? A Critical Analysis of the Evidence in 2010

The prevalence of type 2 diabetes has markedly increased in the last decade worldwide, but in particular in Asian countries such as China and India (1–3), in strong correlation with a comparably steep increase in the prevalence of obesity (4). The primary risk factor for type 2 diabetes is obesity, and 90% of all patients with type 2 diabetes are overweight or obese. The relative risk of diabetes increases about 42-fold in men as the BMI increases from 35 kg/m2 (5) and approximately 93-fold in women as BMI increases from 35 kg/m2 (6). Type 2 diabetes is a complex major endocrine disorder in which insulin resistance in the muscle and liver as well as β-cell failure represent the core pathophysiological defects. In addition to the muscle, liver, and β-cell, the fat cell (accelerated lipolysis), gastrointestinal tract (incretin deficiency/resistance), α-cell (hyperglucagonemia), kidney (increased glucose reabsorption), and brain (insulin resistance) all play important roles in the development of type 2 diabetes (7). The development of type 2 diabetes is strongly associated with obesity and the accumulation of abdominal and ectopic fat, which are linked to peripheral and hepatic insulin resistance, inflammation, and subsequent “lipotoxicity” of β-cells (8,9). The adipose tissue of obese subjects is characterized by increased production and secretion of a wide panel of inflammatory molecules (10) such as tumor necrosis factor-α, interleukin-6, transforming growth factor-β, monocyte chemotactic protein-1, and plasminogen activator inhibitor-1. Evidence is increasing that chronic subclinical inflammation seems to be involved in the development of type 2 diabetes. Several prospective studies demonstrated that subjects who developed type 2 diabetes during the follow-up period had elevated levels of markers of inflammatory molecules at baseline compared with those who did not develop the disease. In …