To investigate the rate of type 2 diabetes remission after gastric bypass and banding and establish the mechanism leading to remission of type 2 diabetes after bariatric surgery.
Glycemic control in type 2 diabetic patients is improved after bariatric surgery.
In study 1, 34 obese type 2 diabetic patients undergoing either gastric bypass or gastric banding were followed up for 36 months. Remission of diabetes was defined as patients not requiring hypoglycemic medication, fasting glucose below 7 mmol/L, 2 hour glucose after oral glucose tolerance test below 11.1 mmol/L, and glycated haemoglobin (HbA1c) <6%. In study 2, 41 obese type 2 diabetic patients undergoing either bypass, banding, or very low calorie diet were followed up for 42 days. Insulin resistance (HOMA-IR), insulin production, and glucagon-like peptide 1 (GLP-1) responses after a standard meal were measured.
In study 1, HbA1c as a marker of glycemic control improved by 2.9% after gastric bypass and 1.9% after gastric banding at latest follow-up (P < 0.001 for both groups). Despite similar weight loss, 72% (16/22) of bypass and 17% (2/12) of banding patients (P = 0.001) fulfilled the definition of remission at latest follow-up. In study 2, within days, only bypass patients had improved insulin resistance, insulin production, and GLP-1 responses (all P < 0.05).
With gastric bypass, type 2 diabetes can be improved and even rapidly put into a state of remission irrespective of weight loss. Improved insulin resistance within the first week after surgery remains unexplained, but increased insulin production in the first week after surgery may be explained by the enhanced postprandial GLP-1 responses.
Gastric bypass surgery induces greater diabetes remission than restrictive surgery in spite of identical weight loss and leads to improved glycemic control in the first week after surgery through a dual mechanism of increased insulin production and reduced insulin resistance. Glucagon like peptide 1 (GLP-1) is associated with the increased insulin production, but not the reduced insulin resistance.
*Department of Bariatric Surgery, Musgrove Park Hospital, Taunton, Somerset, United Kingdom;
†Department of Investigative Medicine, Imperial Weight Centre, Imperial College London, United Kingdom.
Authors D.J.P. and A.O. contributed equally to this article.
Supported by a Royal College of Surgeons Research Fellowship (to D.J.P.), Department of Health Clinician Scientist Award (to C.l.R.), programme grants from the MRC (G7811974), Wellcome Trust (072643/Z/03/Z), an EU FP6 Integrated Project Grant LSHM-CT-2003–503041, and the NIHR Biomedical Research Centre funding scheme.
Reprints: Richard Welbourn, MD, FRCS, Department of Bariatric Surgery, Musgrove Park Hospital, Taunton, Somerset, TA1 5DA United Kingdom. E-mail: firstname.lastname@example.org.