Original article
Changes in post-prandial glucose and pancreatic hormones, and steady-state insulin and free fatty acids after gastric bypass surgery

https://doi.org/10.1016/j.soard.2013.07.010Get rights and content

Abstract

Background

Changes in the multiple mechanisms that regulate glucose metabolism after gastric bypass (RYGB) are still being unveiled. The objective of this study was to compare the changes of glucose and pancreatic hormones [C-peptide, glucagon, and pancreatic polypeptide (PP)] during a meal tolerance test (MTT) and steady-state insulin and free fatty acid (FFA) concentrations during euglycemic–hyperinsulinemic clamp 14 days and 6 months after RYGB in morbidly obese nondiabetic patients.

Methods

Two groups were studied at baseline and at 14 days: the RYGB followed by caloric restriction group (RYGB, n = 12) and the equivalent caloric restriction alone group (Diet, n = 10), to control for energy intake and weight loss. The RYGB group was studied again at 6 months to assess the changes after substantial weight loss. During MTT, the early and overall changes in glucose and pancreatic hormone concentrations were determined, and during the clamp, steady-state insulin and FFA concentrations were assessed.

Results

After 14 days, RYGB patients had enhanced postprandial glucose, C-peptide, and glucagon responses, and decreased postprandial PP concentrations. Steady-state insulin concentrations were decreased at 14 days only in RYGB patients, and FFA increased in both groups. Six months after RYGB and substantial weight loss, the decrease in insulin concentrations during clamp persisted, and there were further changes in postprandial glucose and glucagon responses. FFA concentrations during clamp were significantly lower at 6 months, relative to presurgical values.

Conclusions

In morbidly obese nondiabetic patients, RYGB produces early changes in postmeal glucose, C-peptide, glucagon, and PP responses, and it appears to enhance insulin clearance early after RYGB and improve insulin sensitivity in adipose tissue at 6 months postsurgery. The early changes cannot be explained by caloric restriction alone.

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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