1,2,3,4,6 penta-O-galloyl-β-D-glucose ameliorates high-fat diet-induced nonalcoholic fatty liver disease and maintains the expression of genes involved in lipid homeostasis in mice

Kant, Rajni; Lu, Chung‐Kuang; Nguyen, Hien Minh; Hsiao, Hui‐Hua; Chen, Chao-Ju; Hsiao, Hui‐Pin; Lin, Kuo‐Cherng; Fang, Cheng-Chieh; Yen, Chia‐Hung

doi:10.1016/j.biopha.2020.110348

Cited by 14 publications

(9 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…20 As we know, obesity can lead to NAFLD, which is characterized by an increase in the intrahepatic TG content. 21 It is reported that HFD induces NAFLD by inducing insulin resistance, which impaires the glucose-lowering effect of insulin and causes the increased TG and TC levels in serum, 14 and it also increases body and liver weights and elevates the levels of hepatic injury markers in mice, thus resulting in the development of hepatic steatosis and injury. 22 In this study, Herp knockout effectively reversed the highly elevated serum levels of TG, TC, HDL, LDL, glucose, insulin, and HOMA-IR in HFD-fed mice with reduction in the body weight, liver weight and liver/body weight ratio in mice, indicating that Herp knockout could improve hepatic lipid profiles, glucose tolerance and insulin sensitivity in HFD-fed mice with the decreased body weight and live weight.…”

Section: Discussionmentioning

confidence: 99%

“…Currently, studies on NASH pathogenesis and therapeutic efficacy have been mainly conducted by using animal models, and HFD-induced NAFLD model is most similar to human NAFLD, which could increase the body weight and body fat content, as well as induce insulin resistance. 13,14 Thus, we detected the Herp expression in the liver tissues of HFD-induce NFALD mice and then investigated the effect of Herp knockout on NAFLD by feeding mice with HFD/NFD in this work.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Herp knockout protects against nonalcoholic fatty liver disease in mice on a high fat diet

Lei

Wang

et al. 2021

The Kaohsiung J of Med Scie

View full text Add to dashboard Cite

This study aims to discover the role of Homocysteine-induced ER protein (Herp) deficiency in high-fat diet (HFD)-induced nonalcoholic fatty liver disease (NAFLD). After 8 weeks of feeding with normal-fat diet (NFD) or HFD, WT (wild type) and Herp −/− mice were measured for the body weight, liver weight and serum biochemical parameters. HE, Oil Red O, and Sirius red stainings were used to evaluate the histopathological changes of liver tissues. QRT-PCR, Western blotting and Immunohistochemistry were employed to detect the mRNA and protein expression. TUNEL staining was used to observe the hepatocyte apoptosis. Herp knockout reduced the liver/body weight ratio of mice fed with HFD with the decreased serum levels of TG, TC, HDL, LDL, GGT, Hcy, ALT, and AST. Besides, WT mice fed with HFD presented obvious steatosis, inflammation and hepatocytes ballooning, which was relieved in Herp −/− mice. HFD-induce NFALD mice demonstrated increased Oil Red, Sirius red, and α-SMA staining than NFD-induced mice, but mice in the Herp −/− + HFD group was lower than the WT + HFD group. HFD-induce NFALD mice showed upregulated expression of Grp78, Chop, and Atf4 in liver tissues when compared with NFD fed mice. However, regarding to the mice fed with HFD, Herp deficiency decrease in the expression of Grp78, Chop, and Atf4 in liver tissues with the reduced hepatocyte apoptosis. Herp was highly expressed in HFD-induced NAFLD mice. Herp knockout improved liver function and histopathological conditions with the decreased hepatocyte apoptosis and endoplasmic reticulum stress (ERS) of HFDinduce NFALD mice.

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Herp knockout protects against nonalcoholic fatty liver disease in mice on a high fat diet

Lei

Wang

et al. 2021

The Kaohsiung J of Med Scie

View full text Add to dashboard Cite

show abstract

“…Other small-molecules have been reported to act as ABCA1 / Abca1 downregulators, acting independently of the previously mentioned LXR, RXR, PPAR, and HMG-CoA-reductase pathways. Natural compounds such as α,β-unsaturated carbonyl derivative acrolein, 442 the polyphenol bisphenol A, 443 and the polyphenol 1,2,3,4,6 penta- O -galloyl-β- d -glucose 444 demonstrated an Abca1 mRNA 443 , 444 and ABCA1 protein 442 downregulation in vitro 443 , 442 and in vivo . 444 The effect of acrolein could be abrogated by 3-hydroxytyrosol, 442 an inducer of ABCA1 protein content.…”

Section: Part I: Status Quomentioning

confidence: 99%

Strategies to gain novel Alzheimer’s disease diagnostics and therapeutics using modulators of ABCA transporters

Pahnke

Bascuñana

Brackhan

et al. 2021

Free Neuropathology

View full text Add to dashboard Cite

Adenosine-triphosphate-(ATP)-binding cassette (ABC) transport proteins are ubiquitously present membrane-bound efflux pumps that distribute endo- and xenobiotics across intra- and intercellular barriers. Discovered over 40 years ago, ABC transporters have been identified as key players in various human diseases, such as multidrug-resistant cancer and atherosclerosis, but also neurodegenerative diseases, such as Alzheimer’s disease (AD). Most prominent and well-studied are ABCB1, ABCC1, and ABCG2, not only due to their contribution to the multidrug resistance (MDR) phenotype in cancer, but also due to their contribution to AD. However, our understanding of other ABC transporters is limited, and most of the 49 human ABC transporters have been largely neglected as potential targets for novel small-molecule drugs. This is especially true for the ABCA subfamily, which contains several members known to play a role in AD initiation and progression. This review provides up-to-date information on the proposed functional background and pathological role of ABCA transporters in AD. We also provide an overview of small-molecules shown to interact with ABCA transporters as well as potential in silico , in vitro , and in vivo methodologies to gain novel templates for the development of innovative ABC transporter-targeting diagnostics and therapeutics.

show abstract

“…In addition, β-PGG inhibits the expression of IL-6 and MCP-1 in mature 3T3-L1 cells induced by TNF-α, followed by improving the inflammatory response [ 187 ]. Animal studies have also revealed that β-PGG significantly improves hypertriglyceridemia, hyperglycemia, and NAFLD induced by HFD [ 188 , 189 ]. Mechanistically, β-PGG reverses HFD-induced alterations in lipid-associated genes such as CD36, ABCA1, ACACA, cluster of differentiation 11c (CD11c), HMGCR, and microsomal triglyceride transfer protein (MTTP) [ 188 ].…”

Section: Non-flavonoidsmentioning

confidence: 99%

“…Animal studies have also revealed that β-PGG significantly improves hypertriglyceridemia, hyperglycemia, and NAFLD induced by HFD [ 188 , 189 ]. Mechanistically, β-PGG reverses HFD-induced alterations in lipid-associated genes such as CD36, ABCA1, ACACA, cluster of differentiation 11c (CD11c), HMGCR, and microsomal triglyceride transfer protein (MTTP) [ 188 ]. Moreover, β-PGG inhibits the activity of 11β-hydroxysteroid dehydrogenases (11β-HSD-1), which participates in the regulation of the levels of glucocorticoids in the body [ 189 ].…”

Section: Non-flavonoidsmentioning

confidence: 99%

Natural Polyphenols in Metabolic Syndrome: Protective Mechanisms and Clinical Applications

Zhang

et al. 2021

IJMS

View full text Add to dashboard Cite

Metabolic syndrome (MetS) is a chronic disease, including abdominal obesity, dyslipidemia, hyperglycemia, and hypertension. It should be noted that the occurrence of MetS is closely related to oxidative stress-induced mitochondrial dysfunction, ectopic fat accumulation, and the impairment of the antioxidant system, which in turn further aggravates the intracellular oxidative imbalance and inflammatory response. As enriched anti-inflammatory and antioxidant components in plants, natural polyphenols exhibit beneficial effects, including improving liver fat accumulation and dyslipidemia, reducing blood pressure. Hence, they are expected to be useful in the prevention and management of MetS. At present, epidemiological studies indicate a negative correlation between polyphenol intake and MetS incidence. In this review, we summarized and discussed the most promising natural polyphenols (including flavonoid and non-flavonoid drugs) in the precaution and treatment of MetS, including their anti-inflammatory and antioxidant properties, as well as their regulatory functions involved in glycolipid homeostasis.

show abstract

1,2,3,4,6 penta-O-galloyl-β-D-glucose ameliorates high-fat diet-induced nonalcoholic fatty liver disease and maintains the expression of genes involved in lipid homeostasis in mice

Cited by 14 publications

References 56 publications

Herp knockout protects against nonalcoholic fatty liver disease in mice on a high fat diet

Herp knockout protects against nonalcoholic fatty liver disease in mice on a high fat diet

Strategies to gain novel Alzheimer’s disease diagnostics and therapeutics using modulators of ABCA transporters

Natural Polyphenols in Metabolic Syndrome: Protective Mechanisms and Clinical Applications

Contact Info

Product

Resources

About