Berberine protects against high fat diet

Berberina reverte disfunção mitocondrial no músculo induzida por dieta rica em gordura :induz
biogênese mitocondrial via ativação da SIRT-1 : Efeito no câncer?
Berberina: Diminui o potencial de membrana mitocondrial (Delta-Psimt), Inibe
microorganismos tumorigênicos: bactérias, fungos e vírus, Interage com DNA e RNA
formando complexos, Ativa AMPK, Ativa p53, Inibe HIF-1, Inibe NAT – N-acetiltransferase,
Inibe a telomerase, Inibe a topoisomerase I, Inibe COOX-2, Inibe NOi (óxido nítrico
induzível), Inibe a 5 alfa-redutase tipo 2, Ativa p21, p27 e Wee1 e inibe Cdk1, Cdk2, Cdk4/6 e
Ciclinas A, E, D1 e D2, Aumenta expressão do Fas/FasL, Inibe fator nuclear NF-kappaB,Inibe
metaloproteinases: MMP-1, MMP-2 e MMP-9, Inibe vários fatores de crescimento, Reduz
resistência à insulina, Diminui a resistência do câncer MDR, Inibe a glicólise por inibir
extrusão do lactato (inibe CD147/Basigin - MCT1/4) . José de Felippe Junior
Berberine protects against high fat dietinduced dysfunction in muscle
mitochondria by inducing SIRT1dependent mitochondrial biogenesis.
Gomes AP, Duarte FV, Nunes P, Hubbard BP, Teodoro JS, Varela AT, Jones JG,
Sinclair DA, Palmeira CM, Rolo AP.
Biochim Biophys Acta. 2011 Oct 17;1822(2):185-195.
Source
Center for Neurosciences and Cell Biology, Department of Life Sciences, University of
Coimbra 3004-517 Coimbra, Portugal; Harvard Medical School Department of
Pathology/Genetics, Paul F. Glen Laboratories for the Biological mechanisms of Aging
77 Ave Louis Pasteur Boston, MA 02115, USA.
Abstract
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.
Copyright © 2011 Elsevier B.V. All rights reserved.
PMID:
22027215