Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2010) 22 S23.3

Department of Clinical Science and Education, Karolinska Institutet, Stockholm South Hospital, Stockholm, Sweden.

A better understanding of the endocrine changes following bariatric surgery becomes increasingly important as the prevalence of obesity and obesity-related diseases is rising worldwide. Bariatric surgery is the most effective therapy for severe obesity in terms of weight loss, quality of life improvement, reduction of mortality and morbidity. Gastric procedures for severe obesity can yield dramatic and long-term weight reduction with an average weight loss of two-thirds of excess weight within 1–2 years. Weight becomes stable at this level and is well maintained at long-term follow-up. Improvement of the carbohydrate metabolism following gastric bypass surgery occurs within a few days and is partially independent of weight loss and caloric restriction and sustained. The effects of weight reduction by different types of bariatric surgery on islet function and on leptin have been studied by our group and others over the past years.

The mechanism allowing massive weight reduction and diabetes resolution after bariatric surgery is only partially understood but there is little doubt that the gastrointestinal incretin hormones glucagon-like-peptide-1 (GLP-1) and gastric inhibitory peptide/glucose-dependent insulinotropic peptide (GIP) are important and exciting contributors. The GLP-1 response to oral glucose or meal ingestion increase after gastric bypass and jejunoileal bypass (JIB) surgery, but not after restrictive bariatric surgery, such as vertical banded gastroplasty (VBG). Because the changes in incretin hormones after bariatric surgery seem to be different after different types of surgery we have compared the GLP-1 and GIP responses after VBG and JIB. Malabsorptive and restrictive surgical procedures will be presented in short for a better understanding of the ‘foregut and hindgut hypothesis’ as to why bariatric surgery ameliorates type 2 diabetes. Finally, we will discuss the implications of the hindgut hypothesis for GLP-1 and for the appetite-suppressant hormone peptide YY (PYY) and their contribution to satiety after bariatric surgery.

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