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Adipokine dysregulation, adipose tissue inflammation and metabolic syndrome.

Abstract
Obesity plays a causative role in the pathogenesis of the metabolic syndrome. Adipokines may link obesity to its co-morbidities. Most adipokines with pro-inflammatory properties are overproduced with increasing adiposity, while some adipokines with anti-inflammatory or insulin-sensitizing properties, like adiponectin are decreased. This dysregulation of adipokine production may promote obesity-linked metabolic disorders and cardiovascular disease. Besides considering adipokines, this review will also highlight the cellular key players and molecular mechanisms involved in adipose inflammation. Targeting the changes in the cellular composition of adipose tissue, the underlying molecular mechanisms, and the altered production of adipokines may have therapeutic potential in the management of the metabolic syndrome.
AuthorsE Maury, S M Brichard
JournalMolecular and cellular endocrinology (Mol Cell Endocrinol) Vol. 314 Issue 1 Pg. 1-16 (Jan 15 2010) ISSN: 1872-8057 [Electronic] Ireland
PMID19682539 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Chemical References
  • APLN protein, human
  • Adipokines
  • Adiponectin
  • Apelin
  • Chemokines
  • Cytokines
  • Insulin
  • Intercellular Signaling Peptides and Proteins
  • Tumor Necrosis Factor-alpha
  • Nicotinamide Phosphoribosyltransferase
  • nicotinamide phosphoribosyltransferase, human
Topics
  • Adipocytes (cytology, metabolism)
  • Adipokines (immunology)
  • Adiponectin (metabolism)
  • Adipose Tissue (immunology, pathology)
  • Apelin
  • Body Fat Distribution
  • Chemokines (immunology)
  • Cytokines (immunology, metabolism)
  • Humans
  • Inflammation (immunology, pathology)
  • Insulin (metabolism)
  • Intercellular Signaling Peptides and Proteins (metabolism)
  • Macrophages (cytology, immunology)
  • Metabolic Syndrome (immunology, physiopathology)
  • Nicotinamide Phosphoribosyltransferase (metabolism)
  • Obesity (metabolism)
  • Signal Transduction (physiology)
  • Tumor Necrosis Factor-alpha (immunology)

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