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Targeting Islets: Metabolic Surgery Is More than a Bariatric Surgery

  • Xi Chen
  • Jingjing Zhang
  • Zhiguang ZhouEmail author
Review Article
  • 52 Downloads

Abstract

Metabolic surgery is an effective therapy for diabetic patients with obesity. The main mechanisms underlying the effects of metabolic surgery include food intake restriction and the accompanying reduced daily caloric intake and changes in gut hormones and bile acid. Insulin resistance and impaired β-cell function contribute to the development of type 2 diabetes. An increasing number of studies have focused on the central role of islet function in type 2 diabetes. In this article, we review the related high-quality literature and summarize the following mechanisms and principles underlying metabolic surgery in the context of islet function protection: (1) reduced glucotoxicity and chronic inflammation help facilitate better β-cell function and the preservation of β-cell mass following metabolic surgery; (2) based on the increased levels of GLP-1 and PYY after metabolic surgery, gut hormones appear to play a significant role in improving β-cell function through the GLP-1R signaling pathways; (3) the bile acid signaling pathway could affect β-cell function; and (4) the GLP-1R and bile acid signaling pathways could also cause other endocrine cells to contribute to islet function.

Keywords

Metabolic surgery Islet function Obesity Type 2 diabetes mellitus Mechanisms 

Abbreviations

IDF

International Diabetes Federation

T2D

Type 2 diabetes

RYGB

Roux-en-Y gastric bypass

SG

Sleeve gastrostomy

BA

Bile acid

GPCRs

G protein-coupled receptors

PKC

Protein kinase C

PKA

Protein kinase A

IRS-2

Insulin receptor substrate-2

PKB

Protein kinase B

TGF-β

Transforming growth factor-β

FFA

Free fatty acid

GLP-1

Glucagon-like peptide 1

PYY

Peptide-YY

GIP

Gastric inhibitory polypeptide

FXR

Farnesoid X receptor

TGR5

G protein-coupled bile acid receptor 5

AUC

Area under the curve

FGF-19

Fibroblast growth factor-19

GLP-1R

GLP-1 receptor

IL-1β

Interleukin-1β

NF-κB

Nuclear factor-κB

Notes

Acknowledgements

This study was supported by the National Key R&D Program of China (2016YFC1305000, 2016YFC1305001), the National Science and Technology Infrastructure Program (2015BAI12B13), the National Natural Science Foundation of China (81770775, 91749118, 81370017, 81130015, and 81000316), the Planned Science and Technology Project of Hunan Province (2017RS3015) and Natural Science Foundation of Hunan Province, China (14JJ3034), and the National Basic Research Program of China (2014CB910500).

Compliance with Ethical Standards

Conflict of Interest

The authors declare that they have no conflicts of interest.

Ethical Approval Statement

This article does not contain any studies with human participants or animals performed by any of the authors.

Informed Consent Statement

Does not apply.

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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2019

Authors and Affiliations

  1. 1.Department of Metabolism and Endocrinology, The Second Xiangya Hospital and Diabetes Center, Institute of Metabolism and Endocrinology and National Clinical Research Center for Metabolic DiseasesCentral South UniversityChangshaChina
  2. 2.Key Laboratory of Diabetes Immunology (Central South University), Ministry of Education; National Clinical Research Center for Metabolic Diseases; Metabolic Syndrome Research Center, the Second Xiangya HospitalCentral South UniversityChangshaChina

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