Original articleChanges in post-prandial glucose and pancreatic hormones, and steady-state insulin and free fatty acids after gastric bypass surgery
Section snippets
Methods
Morbidly obese nondiabetic patients, selected to undergo RYGB, were recruited at the University of California San Francisco’s (UCSF) Bariatric Surgery Program. They met the National Institutes of Health and UCSF Bariatric Surgery Program eligibility criteria for bariatric surgery as described previously [10]. Exclusion criteria included previous weight loss, foregut and/or hindgut surgery, and diagnosis of endocrine or chronic renal disease. This project was approved by the UCSF Committee on
Baseline evaluation (V1)
Before surgical and diet interventions, glucose and pancreatic hormone concentrations during the MTT and insulin and FFA concentrations during the clamp were generally similar for both groups (Fig. 1, Fig. 2), with the exception of C-peptide concentrations, which were slightly higher in the Diet group. Changes at 14 days (RYGB and Diet, V2) and at 6 months (RYGB, V3) are described below.
Glucose concentrations during the MTT
After 14 days, the early increase of plasma glucose concentrations (slope 0–15 min) was significantly greater
Discussion
In this study, RYGB accompanied by caloric restriction was associated with changes in postprandial glucose kinetics and concentrations of C-peptide, glucagon, and PP in response to a meal, as well as changes in steady-state insulin concentrations during a clamp that were not observed after caloric restriction alone. After substantial weight loss had occurred, there were further changes of postprandial glucose kinetics and glucagon responses; the augmented postprandial C-peptide responses
Conclusions
Despite these limitations, we conclude that, in morbidly obese nondiabetics, RYGB is associated with early and persistent changes in postprandial glucose kinetics and pancreatic hormone concentrations. In addition, our data suggest enhanced hepatic insulin clearance early after RYGB, as well as improved insulin sensitivity in adipose tissue at 6 months. These findings, taken together with the other documented changes in GI hormones concentrations, hepatic glucose metabolism, and hepatic and
Disclosures
The authors have no commercial associations that might be a conflict of interest in relation to this article.
Acknowledgments
This research was supported by Grant Number KL2 RR024130 from the National Center for Research Resources (NCRR), a component of the NIH and NIH Roadmap for Medical Research (GMC), and by NIH/NCRR UCSF-CTSI Grant Number UL1 RR024131. Dr. Havel’s research program receives support from NIH grants HL-075675, HL-091333, AT-003545, DK-097307, DK-095980 and a Multicampus Award (#142691) from the University of California, Office of the President. We are also grateful for the assistance of the SFGH-CRC
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