The etiology of obesity-induced insulin resistance

Kyle L. Hoehn, William L. Holland, Trina A. Knotts, Scott A. Summers

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Insulin is an essential hormone with important roles in glucose homeostasis and anabolicmetabolism. Cellular and/or molecular defects in insulin action result in a state of insulinresistance, which is an essential feature of the diseases type 2 diabetes and the metabolicsyndrome. One of the largest correlations to insulin resistance is obesity; specifically theenlargement of adipose tissue in the abdomen. This correlation is unmistakably obvious todayas the twin epidemics of obesity and type 2 diabetes have co-emerged. One of the biggestchallenges in the field of diabetes research is to determine how the increase in visceraladiposity leads to impaired insulin action. Recently, two hypothetical mechanisms havetranspired: (a) obesity shifts the secretory profile of adipose tissue to favor a reduction innutrient uptake by creating insulin resistance, and/or (b) overloaded fat cells and increasedcaloric intake common in obesity leads to inappropriate storage of lipids in non-adiposetissues where they antagonize insulin action. This review summarizes findings implicatingeach mechanism, alone or in concert, in the etiology of obesity-induced insulin resistance.

Original languageEnglish (US)
Title of host publicationDiabetes Mellitus Research Advances
PublisherNova Science Publishers, Inc.
Pages99-132
Number of pages34
ISBN (Print)9781600217111
StatePublished - Feb 1 2009

Keywords

  • Adipose tissue
  • Insulin resistance
  • Metabolism
  • Obesity

ASJC Scopus subject areas

  • Medicine(all)

Fingerprint Dive into the research topics of 'The etiology of obesity-induced insulin resistance'. Together they form a unique fingerprint.

  • Cite this

    Hoehn, K. L., Holland, W. L., Knotts, T. A., & Summers, S. A. (2009). The etiology of obesity-induced insulin resistance. In Diabetes Mellitus Research Advances (pp. 99-132). Nova Science Publishers, Inc..