Architecture and the extracellular matrix: the still unappreciated components of the adipose tissue

• Published in: Obesity reviews Vol. 12; no. 5; pp. e494 - e503
• Main Authors: Divoux, A, Clément, K
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.05.2011
• Subjects: adipocytes; adipose tissue; Adipose Tissue - metabolism; Adipose Tissue - pathology; animal models; Animals; collagen; cysteine; Disease Models, Animal; Extracellular matrix; Extracellular Matrix - physiology; Fibrosis; human adipose tissue; Humans; hypertrophy; hypoxia; hypoxia-inducible factor 1; kidneys; liver; metabolic diseases; mice; obesity; Obesity - metabolism; Obesity - pathology; pancreas
• ISSN: 1467-7881; 1467-789X
• DOI: 10.1111/j.1467-789X.2010.00811.x

Fibrosis is usually characterized by the modification of both the amount and composition of a wide panel of extracellular matrix (ECM) proteins. In the liver, pancreas, kidney and lung the accumulation of fibrosis disrupts cellular processes and appears detrimental for organ function. This review highlights the available evidence supporting an important ECM remodelling in adipose tissue (AT) and, in particular, during the development of obesity. The modifications and occurrence of new adipose ECM components leads to an abnormal accumulation of fibrosis in this tissue. This phenomenon was well described in rodent models and evidence is beginning to emerge in humans; however, the origin and potential impact of these depots in AT biology are unclear. Two animal models with disruptions in ECM components (secreted proteins acidic in nature rich in cysteine null mice and ob/ob collagen VI null mice) suggest that fibrosis limits adipocyte hypertrophy and may cause the metabolic disorders associated with obesity. Over-expression of Hypoxia-inducible factor 1 leading to an increase in collagen expression suggests a role for hypoxia in fibrosis development. We conclude this review with possible hypotheses regarding the cellular and molecular contributors of fibrosis initiation.