Up-regulation of the Sirtuin 1 (Sirt1) and Peroxisome Proliferator-activated Receptor γ Coactivator-1α (PGC-1α) Genes in White Adipose Tissue of Id1 Protein-deficient Mice

Zhao, Ying; Ling, Flora; Griffin, Timothy M.; He, Ting; Towner, Rheal A.; Ruan, Hong; Sun, Xiao Hong

doi:10.1074/jbc.m114.571679

Cited by 22 publications

(18 citation statements)

References 49 publications

(61 reference statements)

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“…SIRT1 can maintain the oxidation of fatty acid at low glucose concentrations. SIRT1 is a regulator of PGC-1 α that induces the transcription of metabolic relevant genes for the oxidation of mitochondrial fatty acid [ 75 ]. Furthermore, the intake of high-fat diets can increase the level of PGC-1 α in rats [ 76 ].…”

Section: Discussionmentioning

confidence: 99%

Dietary Blueberry and Bifidobacteria Attenuate Nonalcoholic Fatty Liver Disease in Rats by Affecting SIRT1-Mediated Signaling Pathway

Ren¹,

Huang²,

Cheng³

2014

Oxidative Medicine and Cellular Longevity

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NAFLD model rats were established and divided into NAFLD model (MG group), SIRT1 RNAi (SI group), blueberry juice (BJ group), blueberry juice + bifidobacteria (BJB group), blueberry juice + SIRT1 RNAi (BJSI group), and blueberry juice + bifidobacteria + SIRT1 RNAi groups (BJBSI group). A group with normal rats was a control group (CG). BJB group ameliorated NAFLD, which was better than BJ group (P < 0.05). The lipid accumulation was lower in CG, BJ, and BJB groups than that in MG, SI, BJSI, and BJBSI groups (P < 0.05). The levels of SIRT1 and PPAR-α were higher in CG, BJ, and BJB groups than those in MG, SI, BJSI, and BJBSI groups (P < 0.05). The levels of SREBP-1c were lower in CG, BJ, and BJB groups than those in MG, SI, BJSI, and BJBSI groups (P < 0.05). The biochemical indexes SOD, GSH, and HDL-c were improved from CG to BJB group (P < 0.05). Inversely, the levels of AST and ALT, TG, TC, LDL-c, and MDA were decreased from CG to BJB group (P < 0.05). These changes enhance antioxidative capability and biochemical index of rats. Blueberry juice and bifidobacteria improve NAFLD by activating SIRTI-mediating signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Dietary Blueberry and Bifidobacteria Attenuate Nonalcoholic Fatty Liver Disease in Rats by Affecting SIRT1-Mediated Signaling Pathway

Ren¹,

Huang²,

Cheng³

2014

Oxidative Medicine and Cellular Longevity

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“…Id1 −/− mice show less insulin resistance in skeletal muscle, liver and white adipose tissue, and increased Uncoupling Protein 1 and Peroxisome proliferator-activated receptor gamma coactivator 1 in brown adipose tissue (corresponding to increased energy expenditure) (Satyanarayana et al, 2012). Mice over-expressing E-proteins revealed similar phenotypes (Zhao et al, 2014). …”

Section: Diabetes Glucose and Lipid Metabolismmentioning

confidence: 97%

E Proteins and ID Proteins: Helix-Loop-Helix Partners in Development and Disease

2015

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The basic Helix-Loop-Helix (bHLH) proteins represent a well-known class of transcriptional regulators. Many bHLH proteins act as heterodimers with members of a class of ubiquitous partners, the E-proteins. A widely-expressed class of inhibitory heterodimer partners- the Inhibitor of DNA-binding (ID) proteins- also exists. Genetic and molecular analyses in humans and in knockout mice implicate E-proteins and ID-proteins in a wide variety of diseases, belying the notion that they are non-specific partner proteins. Here, we explore relationships of E-proteins and ID-proteins to a variety of disease processes and highlight gaps in knowledge of disease mechanisms.

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“…Furthermore, hepatic TG accumulation may occur as a result of increased fat synthesis and delivery, as well as decreased export and/or oxidation of fat ( 6 ). Additionally, inflammatory cytokines, including tumour necrosis factor (TNF)-α, interleukin (IL)-6 and IL-8, mediate steatohepatitis in patients with NAFLD ( 7 ) and may be regulated by the peroxisome proliferator-activated receptor (PPAR)-γ. PPAR-γ may be activated by the PPARγ coactivator (PGC)-1α following sirtuin (Sirt)-1 activation ( 8 ).…”

Section: Introductionmentioning

confidence: 99%

Targeting Sirt1 in a rat model of high‑fat diet‑induced non‑alcoholic fatty liver disease: Comparison of Gegen Qinlian decoction and resveratrol

Guo

Mao

et al. 2017

Exp Ther Med

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The present study aimed to explore the mechanism of action of Gegen Qinlian decoction (GGQLD) in experimental non-alcoholic fatty liver disease (NAFLD). A total of 30 rats were randomly divided into five groups: The chow, model, high- and low-dose GGQLD (GGQLD-H and GGQLD-L, respectively) and resveratrol (Resl) groups, and were treated with saline, GGQLD and Resl when a model of high-fat diet (HFD)-induced NAFLD was established. Blood lipid and liver enzymes were detected following treatment for 8 weeks and liver tissue pathology was observed using Oil Red O and haematoxylin and eosin staining. Furthermore, the liver protein and mRNA expression of sirtuin (Sirt)1, peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α and nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) were measured using western blotting and reverse transcription-quantitative polymerase chain reaction. Compared with the chow group, the model group demonstrated significantly increased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels (P<0.01). GGQLD doses and Resl attenuated the elevated serum ALT and AST levels. GGQLD-H and Resl significantly increased the serum high-density lipoprotein cholesterol level compared with that in the model group (P<0.01), while GGQLD-L and Resl significantly decreased serum low-density lipoprotein cholesterol levels (P<0.01). The GGQLDs and Resl groups revealed an evident improvement in Sirt1 protein and mRNA expression. Although GGQLD and Resl significantly decreased NF-κB gene expression compared with the model group (P<0.01), the effect on NF-κB protein expression was not significant. Furthermore, the PGC-1α gene and protein expression in the HFD rat group slightly decreased compared to the levels in the chow group, but the decrease was insignificant. However, an evident increase in PGC-1α mRNA expression was observed in the GGQLD-H group compared with the model group (P<0.01). Histological staining revealed that GGQLD and Resl decreased the lipid droplets in hepatocytes and normalized steatosis in rats fed with a HFD. The results indicated that GGQLD treatment may be a potent strategy for managing NAFLD by managing lipid metabolism and inflammatory and histological abnormalities by triggering the Sirt1 pathway.

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Up-regulation of the Sirtuin 1 (Sirt1) and Peroxisome Proliferator-activated Receptor γ Coactivator-1α (PGC-1α) Genes in White Adipose Tissue of Id1 Protein-deficient Mice

Cited by 22 publications

References 49 publications

Dietary Blueberry and Bifidobacteria Attenuate Nonalcoholic Fatty Liver Disease in Rats by Affecting SIRT1-Mediated Signaling Pathway

Dietary Blueberry and Bifidobacteria Attenuate Nonalcoholic Fatty Liver Disease in Rats by Affecting SIRT1-Mediated Signaling Pathway

E Proteins and ID Proteins: Helix-Loop-Helix Partners in Development and Disease

Targeting Sirt1 in a rat model of high‑fat diet‑induced non‑alcoholic fatty liver disease: Comparison of Gegen Qinlian decoction and resveratrol

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