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Frankó, A. ; Huypens, P. ; Neschen, S. ; Irmler, M. ; Rozman, J. ; Rathkolb, B. ; Neff, F. ; Prehn, C. ; Dubois, G. ; Baumann, M. ; Massinger, R. ; Gradinger, D. ; Przemeck, G.K.H. ; Repp, B. ; Aichler, M. ; Feuchtinger, A. ; Schommers, P.* ; Stöhr, O.* ; Sanchez-Lasheras, C.* ; Adamski, J. ; Peter, A. ; Prokisch, H. ; Beckers, J. ; Walch, A.K. ; Fuchs, H. ; Wolf, E.* ; Schubert, M.* ; Wiesner, R.J.* ; Hrabě de Angelis, M.

Bezafibrate improves insulin sensitivity and metabolic flexibility in STZ-treated diabetic mice.

Diabetes 65, 2540-2552 (2016)
Verlagsversion Postprint DOI PMC
Open Access Green
Bezafibrate (BEZ), a pan activator of peroxisome proliferator-activated receptors (PPARs), has been generally used to treat hyperlipidemia for decades. Clinical trials with type 2 diabetes patients indicated that BEZ also has beneficial effects on glucose metabolism, although the underlying mechanisms of these effects remain elusive. Even less is known about a potential role for BEZ in treating type 1 diabetes. Here we show that BEZ markedly improves hyperglycemia and glucose and insulin tolerance in streptozotocin (STZ)-treated mice, an insulin-deficient mouse model of type 1 diabetes. BEZ treatment of STZ mice significantly suppressed the hepatic expression of genes that are annotated in inflammatory processes, whereas the expression of PPAR and insulin target gene transcripts was increased. Furthermore, BEZ-treated mice also exhibited improved metabolic flexibility as well as an enhanced mitochondrial mass and function in the liver. Finally, we show that the number of pancreatic islets and the area of insulin positive cells tended to be higher in BEZ-treated mice. Our data suggest that BEZ may improve impaired glucose metabolism by augmenting hepatic mitochondrial performance, suppressing hepatic inflammatory pathways, and improving insulin sensitivity and metabolic flexibility. Thus, BEZ treatment might also be useful for patients with impaired glucose tolerance or diabetes.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Complex I Deficiency; Mitochondrial Myopathy; Clinical-implications; Respiratory-chain; Beta-oxidation; Resistance; Mellitus; Glucose; Liver; Activation
Sprache deutsch
Veröffentlichungsjahr 2016
HGF-Berichtsjahr 2016
ISSN (print) / ISBN 0012-1797
e-ISSN 1939-327X
Zeitschrift Diabetes
Quellenangaben Band: 65, Heft: 9, Seiten: 2540-2552 Artikelnummer: , Supplement: ,
Verlag American Diabetes Association
Verlagsort Alexandria, VA.
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Experimental Genetics (IEG)
Institute of Pathology (PATH)
Molekulare Endokrinologie und Metabolismus (MEM)
Research Unit Analytical Pathology (AAP)
Institute of Human Genetics (IHG)
German Center for Diabetes Reseach (DZD)
POF Topic(s) 30201 - Metabolic Health
90000 - German Center for Diabetes Research
30502 - Diabetes: Pathophysiology, Prevention and Therapy
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
30205 - Bioengineering and Digital Health
30501 - Systemic Analysis of Genetic and Environmental Factors that Impact Health
Forschungsfeld(er) Genetics and Epidemiology
Enabling and Novel Technologies
Helmholtz Diabetes Center
PSP-Element(e) G-500600-003
G-501900-063
G-500600-004
G-500600-005
G-500600-006
G-501900-062
G-500692-001
G-500300-001
G-505600-003
G-500390-001
G-500700-001
G-500600-001
G-501900-002
G-501900-022
DOI 10.2337/db15-1670
WOS ID WOS:000382099800011
Scopus ID 84987657521
PubMed ID 27284107
Erfassungsdatum 2016-06-13
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