Long-term effects of bariatric surgery on meal disposal and ß-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, Italy,
- 2C.N.R. Institute of Clinical Physiology, Pisa, Italy
- 3NNF Center for Basic Metabolic Research, University of Copenhagen, Denmark,
- 4Division of Bariatric Surgery, Santa Chiara Hospital, Pisa, Italy,
- 5C.N.R. Institute of Biomedical Engineering, Padua, Italy.
- Corresponding authors: Stefania Camastra E-mail:
Gastric bypass surgery leads to marked improvements in glucose tolerance and insulin sensitivity in obese type 2 diabetes; the impact on glucose fluxes in response to a physiological stimulus – such as a mixed meal (MTT) – has not been determined. We administered an MTT to 12 obese type 2 diabetic patients (T2D) and 15 obese nondiabetic subjects (ND) before and one year after surgery (10 T2D and 11 ND) using the double-tracer technique and modeling of ß-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%), ß-cell glucose sensitivity doubled but did not normalize (viz. 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 type 2 diabetes bypass surgery changes the postprandial response to a dumping-like pattern, improves glucose tolerance, ß-cell function, and peripheral insulin sensitivity but worsens endogenous glucose output in response to a physiological stimulus.
- Received February 25, 2013.
- Accepted June 12, 2013.
- © 2013 by the American Diabetes Association.
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