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Graja, A.* ; Garcia-Carrizo, F.* ; Jank, A.* ; Gohlke, S.* ; Ambrosi, T.H.* ; Jonas, W.* ; Ussar, S. ; Kern, M.J.* ; Schürmann, A.* ; Aleksandrova, K.* ; Blüher, M.* ; Schulz, T.J.*

Loss of periostin occurs in aging adipose tissue of mice and its genetic ablation impairs adipose tissue lipid metabolism.

Aging Cell 17:e12810 (2018)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Remodeling of the extracellular matrix is a key component of the metabolic adaptations of adipose tissue in response to dietary and physiological challenges. Disruption of its integrity is a well-known aspect of adipose tissue dysfunction, for instance, during aging and obesity. Adipocyte regeneration from a tissue-resident pool of mesenchymal stem cells is part of normal tissue homeostasis. Among the pathophysiological consequences of adipogenic stem cell aging, characteristic changes in the secretory phenotype, which includes matrix-modifying proteins, have been described. Here, we show that the expression of the matricellular protein periostin, a component of the extracellular matrix produced and secreted by adipose tissue-resident interstitial cells, is markedly decreased in aged brown and white adipose tissue depots. Using a mouse model, we demonstrate that the adaptation of adipose tissue to adrenergic stimulation and high-fat diet feeding is impaired in animals with systemic ablation of the gene encoding for periostin. Our data suggest that loss of periostin attenuates lipid metabolism in adipose tissue, thus recapitulating one aspect of age-related metabolic dysfunction. In human white adipose tissue, periostin expression showed an unexpected positive correlation with age of study participants. This correlation, however, was no longer evident after adjusting for BMI or plasma lipid and liver function biomarkers. These findings taken together suggest that age-related alterations of the adipose tissue extracellular matrix may contribute to the development of metabolic disease by negatively affecting nutrient homeostasis.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Adipogenic Progenitor Cells ; Adipose Tissue ; Aging ; Extracellular Matrix ; Fatty Acid Metabolism ; Periostin; Extracellular-matrix; Fat; Differentiation; Cell; Adipocytes; Fibrillogenesis; Proliferation; Accumulation; Expression; Osteoblast
Sprache
Veröffentlichungsjahr 2018
HGF-Berichtsjahr 2018
ISSN (print) / ISBN 1474-9718
e-ISSN 1474-9726
Zeitschrift Aging Cell
Quellenangaben Band: 17, Heft: 5, Seiten: , Artikelnummer: e12810 Supplement: ,
Verlag Wiley
Verlagsort 111 River St, Hoboken 07030-5774, Nj Usa
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Obesity (IDO)
POF Topic(s) 30502 - Diabetes: Pathophysiology, Prevention and Therapy
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-508600-009
DOI 10.1111/acel.12810
WOS ID WOS:000445599100006
PubMed ID 30088333
Erfassungsdatum 2018-10-19
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