Accepted Preprint (first posted online 16 November 2012)

    Adipokine Inflammation and Insulin Resistance: The role of glucose, lipids and endotoxin

    1. Sudesh Kumar
    1. M Piya, Division of Metabolic and Vascular Health, Warwick Medical School, University of Warwick, Coventry, United Kingdom
    2. P McTernan, Division of Metabolic and Vascular Health, Warwick Medical School, University of Warwick, Coventry, United Kingdom
    3. S Kumar, Division of Metabolic and Vascular Health, Warwick Medical School, University of Warwick, Coventry, United Kingdom
    1. Correspondence: Milan Piya, Email: m.k.piya{at}warwick.ac.uk

    Abstract

    Adipose tissue is an active endocrine organ, and our knowledge of this secretory tissue, in recent years, has led us to completely rethink how our body functions and becomes dysregulated with weight gain. Human adipose tissue appears to act as a multi-functional secretory organ with the capacity to control energy homeostasis through peripheral and central regulation of energy homeostasis. It also plays an important role in innate immunity. However the capability to more than double its original mass to cope with positive energy balance in obesity leads to many pathogenic changes. These changes arise within the adipose tissue as well as inducing secondary detrimental effects on other organs like muscle and liver, including chronic low grade inflammation mediated by adipocytokines (adipokine inflammation). This inflammation is modulated by dietary factors and nutrients including glucose and lipids, as well as gut bacteria in the form of endotoxin or lipopolysaccharide. The aim of this current review is to consider the impact of nutrients such as glucose and lipids on inflammatory pathways, specifically within adipose tissue. Furthermore, to discuss how nutrients such as these can influence adipokine inflammation and consequently insulin resistance, directly through their effects on secretion of adipocytokines (TNFa, IL-6, and resistin) as well as indirectly through increases in endotoxin.

    • Received 13 August 2012
    • Accepted 16 November 2012
    • Accepted Preprint first posted online on 16 November 2012

    This Article

    1. J Endocrinol JOE-12-0498
    1. Abstract
    2. All Versions of this Article:
      1. JOE-12-0498v1
      2. 216/1/T1 most recent