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Kunath, A.* ; Weiner, J.* ; Krause, K.* ; Rehders, M.* ; Pejkovska, A.* ; Gericke, M.* ; Biniossek, M.L.* ; Dommel, S.* ; Kern, M.* ; Ribas-Latre, A. ; Schilling, O.* ; Brix, K.* ; Stumvoll, M. ; Klöting, N. ; Heiker, J.T. ; Blüher, M.

Role of kallikrein 7 in body weight and fat mass regulation.

Biomedicines 9:131 (2021)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Increased plasma and adipose tissue protease activity is observed in patients with type 2 diabetes and obesity. It has been proposed that specific proteases contribute to the link between obesity, adipose tissue inflammation and metabolic diseases. We have recently shown that ablation of the serine protease kallikrein-related peptidase 7 (Klk7) specifically in adipose tissue preserves systemic insulin sensitivity and protects mice from obesity-related AT inflammation. Here, we investigated whether whole body Klk7 knockout (Klk7-/-) mice develop a phenotype distinct from that caused by reduced Klk7 expression in adipose tissue. Compared to littermate controls, Klk7-/- mice gain less body weight and fat mass both under chow and high fat diet (HFD) feeding, are hyper-responsive to exogenous insulin and exhibit preserved adipose tissue function due to adipocyte hyperplasia and lower inflammation. Klk7-/- mice exhibit increased adipose tissue thermogenesis, which is not related to altered thyroid function. These data strengthen our recently proposed role of Klk7 in the regulation of body weight, energy metabolism, and obesity-associated adipose tissue dysfunction. The protective effects of Klk7 deficiency in obesity are likely linked to a significant limitation of adipocyte hypertrophy. In conclusion, our data indicate potential application of specific KLK7 inhibitors to regulate KLK7 activity in the development of obesity and counteract obesity-associated inflammation and metabolic diseases.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Klk7 ; Adipose Tissue ; Inhibitor ; Kallikrein-related Peptidase 7 ; Metabolic Disease ; Obesity ; Protease ; Treatment
Sprache englisch
Veröffentlichungsjahr 2021
HGF-Berichtsjahr 2021
ISSN (print) / ISBN 2227-9059
e-ISSN 2227-9059
Zeitschrift Biomedicines
Quellenangaben Band: 9, Heft: 2, Seiten: , Artikelnummer: 131 Supplement: ,
Verlag MDPI
Verlagsort Basel, Switzerland
Begutachtungsstatus Peer reviewed
Institut(e) Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)
POF Topic(s) 30201 - Metabolic Health
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-506501-001
G-506500-001
G-554800-001
Förderungen Helmholtz Alliance ICEMED
Bundesministerium für Bildung und Forschung
Deutsche Forschungsgemeinschaft
DOI 10.3390/biomedicines9020131
WOS ID WOS:000622159400001
Scopus ID 85100583131
PubMed ID 33572949
Erfassungsdatum 2021-04-19
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