Obesity and its associated comorbidities are an ongoing health care problem worldwide. It is well known that obese patients are at increased risk for the development of diabetes, hypertension, hyperlipidemia, sleep apnea, osteoarthritis, and other degenerative diseases. Bariatric surgery has demonstrated to achieve, on top of significant weight reduction, also long-term control of metabolic comorbidities in morbidly obese patients.

In particular, glycemic control in morbidly obese diabetic patients improves markedly within days of bariatric surgery, which suggests that the procedures have a specific effect on glucose metabolism, which is likely to be independent from weight loss per se. Restrictive and malabsorptive procedures seem to work differently and apparently do achieve a different degree of control on glucose metabolism and the different aspects of metabolic syndrome. Still, in-depth knowledge of the mechanisms underlying the effects of bariatric surgery on the metabolic comorbidities of obese patients, especially on diabetes mellitus type 2, is lacking.

We invite authors to present original research articles as well as review articles that will stimulate the continuing efforts in understanding the pathophysiology of bariatric surgery in the different aspects of metabolic syndrome.

We are particularly interested in manuscripts that investigate the mechanisms involved in glycemic control after bariatric surgery in morbidly obese, diabetic patients, with a particular emphasis on the recent developments undergone also in diabetic patients with a BMI below 35 kg/m2.

Potential topics include, but are not limited to:

• Clinical long-term efficacy of bariatric surgery on the metabolic syndrome
• Clinical data on long-term control of glucose metabolism after bariatric surgery
• Efficacy of bariatric surgery on glycemic control in nonmorbidly obese, diabetes type 2 patients
• Studies on the physiology of glucose metabolism in diabetic patients submitted to bariatric surgery

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