Chapter 4. Pathophysiology of Obesity-Induced T2DM

  1. Anthony H. Barnett3,4,5 and
  2. Sudhesh Kumar6
  1. Konstantinos Lois1,
  2. Phillip McTernan2 and
  3. Sudhesh Kumar6

Published Online: 24 APR 2009

DOI: 10.1002/9780470741474.ch4

Obesity and Diabetes, Second Edition

Obesity and Diabetes, Second Edition

How to Cite

Lois, K., McTernan, P. and Kumar, S. (2009) Pathophysiology of Obesity-Induced T2DM, in Obesity and Diabetes, Second Edition (eds A. H. Barnett and S. Kumar), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/9780470741474.ch4

Editor Information

  1. 3

    Department of Medicine, University of Birmingham, UK

  2. 4

    Birmingham Heartlands and Solihull NHS Trust, UK

  3. 5

    Birmingham Heartlands Hospital, Undergraduate Centre, Bordesley Green East, Birmingham, B9 5SS, UK

  4. 6

    Warwick Medical School, University of Warwick, Coventry, CV4 7AL, UK

Author Information

  1. 1

    Clinical Sciences Research Institute, Clinical Sciences Building, University Hospitals of Coventry, and Warwickshire, Clifford Bridge Road, Coventry, CV2 2DX, UK

  2. 2

    WISDEM, University Hospital, Coventry and CSRI, Warwick Medical School, Coventry, UK

  3. 6

    Warwick Medical School, University of Warwick, Coventry, CV4 7AL, UK

Publication History

  1. Published Online: 24 APR 2009
  2. Published Print: 20 MAR 2009

ISBN Information

Print ISBN: 9780470519813

Online ISBN: 9780470741474

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Keywords:

  • pathophysiology of obesity-induced T2DM;
  • sources of increased plasma NEFA in obesity;
  • ‘Randle's glucose-fatty acid’ hypothesis;
  • ectopic fat storage hypothesis;
  • oxidative stress in pathogenesis of insulin resistance and b-cell dysfunction in obese individuals;
  • role of adipose tissue as ‘endocrine organ’ in pathogenesis of T2DM;
  • obesity as low-grade inflammatory state

Summary

This chapter contains sections titled:

  • Introduction

  • Potential mechanisms linking central obesity to T2DM

  • Sources of increased plasma NEFA in obesity

  • ‘Randle's glucose-fatty acid’ hypothesis

  • Ectopic fat storage hypothesis

  • ‘Oxidative stress’

  • The role of adipose tissue as an ‘endocrine organ’ in the pathogenesis of T2DM

  • Obesity as a low-grade inflammatory state

  • Summary

  • References