Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
Volume 1822, Issue 2, Pages 185-195Publisher
ELSEVIER
DOI: 10.1016/j.bbadis.2011.10.008
Keywords
Metabolic syndrome; Berberine; Mitochondria; SIRT1; AMPK; NAMPT
Funding
- Portuguese Foundation for Science and Technology [PTDC/SAU-OSM/72443/2006, SFRH/BD/44674/2008, SFRH/BD/38372/2007, SFRH/BD/38467/2007, SFRH/BD/44796/2008]
- NSERC
- Ellison Medical Foundation
- Paul F. Glenn Foundation for medical research
- NIH/NIA [RO1 AG 028730]
- Fundação para a Ciência e a Tecnologia [SFRH/BD/44796/2008, PTDC/SAU-OSM/72443/2006] Funding Source: FCT
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Berberine (BBR) has recently been shown to improve insulin sensitivity in rodent models of insulin resistance. Although this effect was explained partly through an observed activation of AMP-activated protein kinase (AMPK), the upstream and downstream mediators of this phenotype were not explored. Here, we show that BBR supplementation reverts mitochondrial dysfunction induced by High Fat Diet (HFD) and hyperglycemia in skeletal muscle, in part due to an increase in mitochondrial biogenesis. Furthermore, we observe that the prevention of mitochondrial dysfunction by BBR, the increase in mitochondrial biogenesis, as well as BBR-induced AMPK activation, are blocked in cells in which SIRT1 has been knocked-down. Taken together, these data reveal an important role for SIRT1 and mitochondrial biogenesis in the preventive effects of BBR on diet-induced insulin resistance. (C) 2011 Elsevier B.V. All rights reserved.
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