Limited Recovery of β-Cell Function After Gastric Bypass Despite Clinical Diabetes Remission

  1. Blandine Laferrère1,2,6,7
  1. 1Department of Medicine, St. Luke’s-Roosevelt Hospital Center, New York, NY
  2. 2New York Obesity Nutrition Research Center, St. Luke’s-Roosevelt Hospital Center, New York, NY
  3. 3Department of Medicine, Albert Einstein School of Medicine, New York, NY
  4. 4Department of Medicine, Centre de Recherche Clinique Etienne-Le Bel, Université de Sherbrooke, Sherbrooke, Quebec, Canada
  5. 5Division of Minimally Invasive Surgery, Department of Surgery, St. Luke’s-Roosevelt Hospital Center, New York, NY
  6. 6Columbia University College of Physicians and Surgeons, New York, NY
  7. 7Division of Endocrinology and Diabetes, St. Luke’s-Roosevelt Hospital Center, New York, NY
  1. Corresponding author: Blandine Laferrère, bbl14{at}columbia.edu.

Abstract

The mechanisms responsible for the remarkable remission of type 2 diabetes after Roux-en-Y gastric bypass (RYGBP) are still puzzling. To elucidate the role of the gut, we compared β-cell function assessed during an oral glucose tolerance test (OGTT) and an isoglycemic intravenous glucose clamp (iso-IVGC) in: 1) 16 severely obese patients with type 2 diabetes, up to 3 years post-RYGBP; 2) 11 severely obese normal glucose-tolerant control subjects; and 3) 7 lean control subjects. Diabetes remission was observed after RYGBP. β-Cell function during the OGTT, significantly blunted prior to RYGBP, normalized to levels of both control groups after RYGBP. In contrast, during the iso-IVGC, β-cell function improved minimally and remained significantly impaired compared with lean control subjects up to 3 years post-RYGBP. Presurgery, β-cell function, weight loss, and glucagon-like peptide 1 response were all predictors of postsurgery β-cell function, although weight loss appeared to be the strongest predictor. These data show that β-cell dysfunction persists after RYGBP, even in patients in clinical diabetes remission. This impairment can be rescued by oral glucose stimulation, suggesting that RYGBP leads to an important gastrointestinal effect, critical for improved β-cell function after surgery.

Footnotes

  • Received August 1, 2013.
  • Accepted November 22, 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.

| Table of Contents

This Article

  1. Diabetes vol. 63 no. 4 1214-1223
  1. Supplementary Data
  2. All Versions of this Article:
    1. db13-1176v1
    2. 63/4/1214 most recent