Long-term effects of bariatric surgery on meal disposal and ß-cell function in diabetic and nondiabetic patients

  1. Ele Ferrannini1,2
  1. 1Department of Internal Medicine University of Pisa, Italy,
  2. 2C.N.R. Institute of Clinical Physiology, Pisa, Italy
  3. 3NNF Center for Basic Metabolic Research, University of Copenhagen, Denmark,
  4. 4Division of Bariatric Surgery, Santa Chiara Hospital, Pisa, Italy,
  5. 5C.N.R. Institute of Biomedical Engineering, Padua, Italy.
  1. Corresponding authors: Stefania Camastra E-mail: stefania.camastra{at}med.unipi.it

Abstract

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.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

Articles citing this article

This Article

  1. Diabetes
  1. Supplementary Data
  2. All Versions of this Article:
    1. db13-0321v1
    2. 62/11/3709 most recent