Long-Term Effects of Bariatric Surgery on Meal Disposal and β-Cell Function in Diabetic and Nondiabetic Patients
- Stefania Camastra1⇑,
- Elza Muscelli1,
- Amalia Gastaldelli2,
- Jens J. Holst3,
- Brenno Astiarraga1,
- Simona Baldi1,
- Monica Nannipieri1,
- Demetrio Ciociaro2,
- Marco Anselmino4,
- Andrea Mari5 and
- Ele Ferrannini1,2
- 1Department of Internal Medicine, University of Pisa, Pisa, Italy
- 2CNR Institute of Clinical Physiology, Pisa, Italy
- 3Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen, Denmark
- 4Division of Bariatric Surgery, Santa Chiara Hospital, Pisa, Italy
- 5CNR Institute of Biomedical Engineering, Padua, Italy.
- Corresponding author: Stefania Camastra, .
Gastric bypass surgery leads to marked improvements in glucose tolerance and insulin sensitivity in obese type 2 diabetes (T2D); the impact on glucose fluxes in response to a physiological stimulus, such as a mixed meal test (MTT), has not been determined. We administered an MTT to 12 obese T2D patients and 15 obese nondiabetic (ND) subjects before and 1 year after surgery (10 T2D and 11 ND) using the double-tracer technique and modeling of β-cell function. In both groups postsurgery, tracer-derived appearance of oral glucose was biphasic, a rapid increase followed by a sharp drop, a pattern that was mirrored by postprandial glucose levels and insulin secretion. In diabetic patients, surgery lowered fasting and postprandial glucose levels, peripheral insulin sensitivity increased in proportion to weight loss (∼30%), and β-cell glucose sensitivity doubled but did not normalize (compared with 21 nonsurgical obese and lean controls). Endogenous glucose production, however, was less suppressed during the MMT as the combined result of a relative hyperglucagonemia and the rapid fall in plasma glucose and insulin levels. We conclude that in T2D, bypass surgery changes the postprandial response to a dumping-like pattern and improves glucose tolerance, β-cell function, and peripheral insulin sensitivity but worsens endogenous glucose output in response to a physiological stimulus.
This article contains Supplementary Data online at http://diabetes.diabetesjournals.org/lookup/suppl/doi:10.2337/db13-0321/-/DC1.
See accompanying commentary, p. 3671.
- Received February 25, 2013.
- Accepted June 14, 2013.
- © 2013 by the American Diabetes Association.
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