FOXO transcription factors in non-alcoholic fatty liver disease.

@article{Dong2017FOXOTF,
  title={FOXO transcription factors in non-alcoholic fatty liver disease.},
  author={X. Charlie Dong},
  journal={Liver research},
  year={2017},
  volume={1 3},
  pages={
          168-173
        }
}
  • X. Dong
  • Published 1 September 2017
  • Medicine, Biology
  • Liver research
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doi.org
27 Citations
Highly Influential Citations
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Background Citations
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27 Citations

Transcriptional Regulation in Non-Alcoholic Fatty Liver Disease

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MicroRNA-122-5p Inhibition Improves Inflammation and Oxidative Stress Damage in Dietary-Induced Non-alcoholic Fatty Liver Disease Through Targeting FOXO3

It is reported that the high-fat diet (HFD) or palmitic acid (PA) significantly upregulated the hepatic miR-122-5p expression in vivo and in vitro, and a novel finding is provided that FOXO3 was the target gene of miR+5p to attenuate inflammatory response and oxidative stress damage in dietary-induced NAFLD.

FOXO4 ameliorates alcohol-induced chronic liver injury via inhibiting NF-κB and modulating gut microbiota in C57BL/6J mice.

Phytochemicals targeting NAFLD through modulating the dual function of forkhead box O1 (FOXO1) transcription factor signaling pathways

The findings of this review confirm that polyphenols, flavonoids, alkaloids, terpenoids, and anthocyanins are capable of modulating FOXO1 and associated signaling pathways, and they are potential therapeutic agents for NAFLD and related complications.

Emerging targets and potential therapeutic agents in non-alcoholic fatty liver disease treatment.

The adipokine sFRP4 induces insulin resistance and lipogenesis in the liver.

AMPK activation by AICAR reduces diet induced fatty liver in C57BL/6 mice.

FoxO3 Modulates LPS-Activated Hepatic Inflammation in Turbot (Scophthalmus maximus L.)

The results indicated that foxo3 might modulate LPS-activated hepatic inflammation in turbot by decreasing the proinflammatory cytokines, the levels of GOT and GPT as well as activating JNK/caspase-3 and tlr-2/myd88/nf-κb pathways.

FoxO1 Knockdown Promotes Fatty Acid Synthesis via Modulating SREBP1 Activities in the Dairy Goat Mammary Epithelial Cells.

The data reveal that FoxO1 plays critical roles in regulating the synthesis of the fatty acid and triacylglycerol (TAG) in GMECs.

Role of FoxO transcription factors in aging and age-related metabolic and neurodegenerative diseases

The complex role of FoxO in aging and age-related diseases, with focus on type 2 diabetes and Alzheimer’s disease is reviewed, and the possibility ofFoxO as a molecular link between aging and disease risks is discussed.

73 References

FOXO transcription factors protect against the diet-induced fatty liver disease

Examination of the effects of two different diets on wildtype and liver-specific Foxo1/3/4 triple knockout mice suggests that FOXO transcription factors play a salutary role in the protection against the diet-induced fatty liver disease.

Increased Expression and Activity of the Transcription Factor FOXO1 in Nonalcoholic Steatohepatitis

FoxO1 expression and activity are increased in patients with steatohepatitis, and mRNA levels are correlated with hepatic insulin resistance, and FOXO1 mRNA levels correlated with nonalcoholic steato hepatitis activity score.

Foxo1 integrates insulin signaling with mitochondrial function in the liver

Foxo1 integrates insulin signaling with mitochondrial function, and inhibition of Foxo1 can improve hepatic metabolism during insulin resistance and the metabolic syndrome.

Pharmacological promotion of autophagy alleviates steatosis and injury in alcoholic and non-alcoholic fatty liver conditions in mice.

Forkhead box class O transcription factors in liver function and disease

This review summarizes emerging knowledge of FOXO function in the liver, FOXO changes in liver disease, and the posttranslational modifications responsible for these effects.

Hepatic FoxO1 Ablation Exacerbates Lipid Abnormalities during Hyperglycemia*

The hypothesis that FoxO1 controls aspects of lipid metabolism in the diabetic liver and protects against excessive hepatic lipid production during hyperglycemia is addressed and its inhibition by intensive insulin treatment may exacerbate paradoxically the lipid abnormalities of diabetes.

Hepatic suppression of Foxo1 and Foxo3 causes hypoglycemia and hyperlipidemia in mice.

Findings indicate that Foxo1 and Foxo3 inactivation serves as a potential mechanism by which insulin reduces hepatic glucose production and increases hepatic lipid synthesis and secretion in healthy and diabetic states.

Aberrant Forkhead box O1 function is associated with impaired hepatic metabolism.

Data indicate that hepatic FoxO1 deregulation impairs the ability of insulin to regulate hepatic metabolism, contributing to the development of hepatic steatosis and abnormal metabolism in diabetes.

FoxO1 Regulates Multiple Metabolic Pathways in the Liver

Results indicate that FoxO proteins promote hepatic glucose production through multiple mechanisms and contribute to the regulation of other metabolic pathways important in the adaptation to fasting and feeding in the liver, including glycolysis, the pentose phosphate shunt, and lipogenic and sterol synthetic pathways.

Forkhead Box O6 (FoxO6) Depletion Attenuates Hepatic Gluconeogenesis and Protects against Fat-induced Glucose Disorder in Mice*

The data indicate that FoxO6 depletion protected against diet-induced glucose intolerance and insulin resistance by attenuating hepatic gluconeogenesis and curbing macrophage infiltration in liver and adipose tissues in mice.
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