Molecular mechanisms involved in obesity-associated insulin resistance: Therapeutical approach

Insulin resistance is an important contributor to the pathogenesis of T2D and obesity is a risk factor for its development. It has been demonstrated that these obesity-related metabolic disorders are associated with a state of chronic low-intensity inflammation. Several mediators released from adipo...

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Bibliographic Details
Published in:Archives of physiology and biochemistry 2009-10, Vol.115 (4), p.227-239
Main Authors: Fernández-Veledo, Sonia, Nieto-Vazquez, Iria, Vila-Bedmar, Rocio, Garcia-Guerra, Lucia, Alonso-Chamorro, Maria, Lorenzo, Margarita
Format: Article
Language:English
Subjects:
Adipose Tissue - physiopathology
Biological and medical sciences
cytokines
Fundamental and applied biological sciences. Psychology
GLUT4
Humans
hyperinsulinemia
Inflammation Mediators - physiology
Insulin Resistance
Interleukin-6 - physiology
Islets of Langerhans - physiopathology
nuclear receptor agonists
obesity
Obesity - physiopathology
PTP1B
stress and proinflammatory kinases
Tumor Necrosis Factor-alpha - physiology
Vertebrates: anatomy and physiology, studies on body, several organs or systems
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Summary:Insulin resistance is an important contributor to the pathogenesis of T2D and obesity is a risk factor for its development. It has been demonstrated that these obesity-related metabolic disorders are associated with a state of chronic low-intensity inflammation. Several mediators released from adipocytes and macrophages, such as the pro-inflammatory cytokines TNF-alpha and IL-6, have been suggested to impair insulin action in peripheral tissues, including fat and skeletal muscle. Such insulin resistance can initially be compensated by increased insulin secretion, but the prolonged presence of the hormone is detrimental for insulin sensitivity. Stress and pro-inflamatory kinases as well as more recent players, phosphatases, seem to be involved in the molecular mechanisms by which pro-inflammatory cytokines and hyperinsulinemia disrupt insulin signalling at the level of IRSs. Pharmacological approaches, such as treatment with PPAR and LXR agonists, overcome such insulin resistance, exerting anti-inflamatory properties as well as controlling the expression of cytokines with tissular specificity.
ISSN:1381-3455
1744-4160
DOI:10.1080/13813450903164330