Enhancement of mitochondrial gene expression in the liver of primary biliary cirrhosis

Chen, Cheng‐Hsin; Nagayama, Kazuyoshi; Enomoto, Nobuyuki; Miyasaka, Yuka; Kurosaki, Masayuki; Sakamoto, Naoya; Maekawa, Shinya; Kakinuma, Sei; Ikeda, Takaaki; Izumi, Namiki; Sato, Chifumi; Watanabe, Mamoru

doi:10.1016/j.hepres.2004.09.007

Cited by 5 publications

(4 citation statements)

References 42 publications

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“…SIRT1 regulates a range of cellular functions affecting metabolic homeostasis and the link between metabolism and INS secretion depends on mitochondrial function (34). PGC-1α is a mitochondrial regulator that serves an essential role in cellular energy metabolism and the ectopic expression of PGC-1α induces the expression of NRFs and mtTFA prior to mitochondrial biogenesis (35). The results of the present study demonstrate that SIRT1 knockdown modulates NRFs and mtTFA levels in cells treated with PA and RSV.…”

Section: Discussionsupporting

confidence: 52%

Resveratrol attenuates type 2 diabetes mellitus by mediating mitochondrial biogenesis and lipid metabolism via Sirtuin type 1

Cao

Liu

et al. 2017

Exp Ther Med

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Abstract. The rising incidence of type 2 diabetes mellitus (T2DM) is a major public health problem and novel therapeutic strategies are required to prevent and treat T2DM. It has been demonstrated that resveratrol (RSV) may prevent T2DM by targeting Sirtuin type 1 (SIRT1), indicating that SIRT1 may be a novel therapeutic target for T2DM prevention. In the present study, a T2DM rat model was established by administering a high fat diet and streptozotocin (STZ) injections. Measurements of blood glucose and insulin confirmed successful establishment of the T2DM model. RSV was used to treat rats with STZ-induced T2DM and the results indicated that RSV reversed the STZ-induced downregulation of peroxisome proliferator-activated receptor-γ coactivator-1α, SIRT1 and forkhead box protein O 3a. Furthermore, RSV modulated the activity of superoxide dismutase and malondialdehyde, which are associated with oxidative stress. In vitro, cells from the insulinoma cell line clone 1E were pretreated with palmitic acid (PA) to simulate a high fat environment. The results of reverse transcription-quantitative polymerase chain reaction indicated that PA suppressed the expression of SIRT1 in a dose-and time-dependent manner. Furthermore, PA modulated the expression of mitochondrial biogenesis-associated, lipid metabolism-associated and β-cell-associated genes, whereas RSV treatment ameliorated the PA-induced changes in the expression of these genes via SIRT1. The results of the present study suggest that RSV participates in the prevention of T2DM by regulating the expression of mitochondrial genes associated with biogenesis, lipid metabolism and β-cells via SIRT1. The results of the current study provide an insight into the mechanisms by which SIRT1 inhibits T2DM and may be used as a basis for future studies.

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Section: Discussionsupporting

confidence: 52%

Resveratrol attenuates type 2 diabetes mellitus by mediating mitochondrial biogenesis and lipid metabolism via Sirtuin type 1

Cao

Liu

et al. 2017

Exp Ther Med

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“…An alternative possibility is that NRF1 and NRF2α genes were stimulated by other transcriptional regulators. A similar dysynchrony is seen in liver disease, in which NRF1 increases despite decreases in PGC-1α (Chen et al 2005).…”

Section: Mitochondrial Enzymessupporting

confidence: 55%

Control of mitochondrial gene expression in the aging rat myocardium

LeMoine¹,

McClelland²,

Lyons³

et al. 2006

Biochem. Cell Biol.

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Aging induces complex changes in myocardium bioenergetic and contractile properties. Using F344BNF(1) rats, we examined age-dependent changes in myocardial bioenergetic enzymes (catalytic activities and transcript levels) and mRNA levels of putative transcriptional regulators of bioenergetic genes. Very old rats (35 months) showed a 22% increase in ventricular mass with no changes in DNA or RNA per gram. Age-dependent cardiac hypertrophy was accompanied by complex changes in mitochondrial enzymes. Enzymes of the Krebs cycle and electron transport system remained within 15% of the values measured in adult heart, significant decreases occurring in citrate synthase (10%) and aconitase (15%). Transcripts for these enzymes were largely unaffected by aging, although mRNA levels of putative transcriptional regulators of the enzymes (nuclear respiratory factor (NRF) 1 and 2 alpha subunit) increased by about 30%-50%. In contrast, enzymes of fatty acid oxidation exhibited a more diverse pattern, with a 50% decrease in beta-hydroxyacyl-CoA dehydrogenase (HOAD) and no change in long-chain acyl-CoA dehydrogenase or carnitine palmitoyltransferase. Transcript levels for fatty acid oxidizing enzymes covaried with HOAD, which declined significantly by 30%. There were no significant changes in the relative transcript levels of regulators of genes for fatty acid oxidizing enzymes: peroxisome proliferator-activated receptor-alpha (PPARalpha), PPARbeta, or PPARgamma coactivator-1alpha (PGC-1alpha). There were no changes in the mRNA levels of Sirt1, a histone-modifying enzyme that interacts with PGC-1alpha. Collectively, these data suggest that aging causes complex changes in the enzymes of myocardial energy metabolism, triggered in part by NRF-independent pathways as well as post-transcriptional regulation.

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“…On the other hand, by competitive reverse transcription PCR, an increased expression of mitochondrial transcriptional factor A (mtTFA) and mitochondrial nuclear respiratory factor 1 (NRF-1) mRNA was demonstrated in PBC liver compared with other liver diseases, whereas NRF-1 coactivator 1, PGC-1, was suppressed. 96 Other studies such as the analysis of endothelial nitric oxide synthase genetic polymorphisms (894G/T, À786T/C) and Eta-1/ osteopontin genetic polymorphism did not detect any differences in their allelic frequencies between PBC patients and controls. 97,98 Microchimerism has been implicated in the etiology of autoimmune diseases.…”

Section: Genetic Factorsmentioning

confidence: 82%

Etiology of Primary Biliary Cirrhosis: The Search for the Culprit

Leung¹,

Coppel²,

Gershwin³

2005

Semin Liver Dis

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Primary biliary cirrhosis (PBC) is an organ-specific autoimmune disease characterized by the presence of high titer antimitochondrial autoantibodies (AMAs) and destruction of intrahepatic small bile ducts. Despite vigorous efforts in the characterization of autoantibodies and bile duct histopathology, the etiology of this disease is unclear. Although there is no correlation between the titer of AMAs and disease severity, the presence of AMAs usually occurs before symptoms of liver abnormalities. We believe that the production of AMAs is not an epiphenomenon, and an understanding of the mechanism of AMA induction will shed light on the etiology of PBC. Recent studies have suggested that the induction of PBC is multifactorial, in which the primary player involves the xenobiotics modification of mitochondrial proteins or exposure to xenobiotic-modified bacterial mitochondrial protein homologs, leading to breaking of tolerance to the human mitochondrial autoantigens and eventually liver pathology in genetic susceptible individuals. We discuss the immunophysiological characteristics of biliary epithelial cells, biochemistry of the 2-oxo-acid dehydrogenase complex, and environmental and genetic factors relevant to PBC.

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Enhancement of mitochondrial gene expression in the liver of primary biliary cirrhosis

Cited by 5 publications

References 42 publications

Resveratrol attenuates type 2 diabetes mellitus by mediating mitochondrial biogenesis and lipid metabolism via Sirtuin type 1

Resveratrol attenuates type 2 diabetes mellitus by mediating mitochondrial biogenesis and lipid metabolism via Sirtuin type 1

Control of mitochondrial gene expression in the aging rat myocardium

Etiology of Primary Biliary Cirrhosis: The Search for the Culprit

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