Phenethylamine in chlorella alleviates high-fat diet-induced mouse liver damage by regulating generation of methylglyoxal

AbstractThis study examined the effects of oral administration of water extract of chlorella (WEC) (100 mg/kg bodyweight) and phenethylamine (10 μg/kg bodyweight) on high-fat diet (HFD)-induced liver damage in mice. Phenethylamine significantly mitigated HFD-induced lipid oxidation (generation of malondialdehyde) and liver damage without markedly decreasing hepatic lipid accumulation. WEC exerted similar effects although with decreased efficacy. In addition, WEC and phenethylamine decreased the methylglyoxal levels and increased the glyceraldehyde 3-phosphate dehydrogenase (GAPDH) protein levels in the liver. Methylglyoxal is generated from substrates of GAPDH, dihydroxyacetone phosphate and glyceraldehyde 3-phosphate. These facts indicate that methylglyoxal triggers oxidation of accumulated lipid, which generates malondialdehyde and consequently induces liver damage. Suppression of generation of toxic aldehydes by WEC and phenethylamine was also confirmed by maintaining hepatic cysteine, highly reactive to aldehydes. Thus, trace amounts of phenethylamine alleviate HFD-induced liver damage by regulating methylglyoxal via increase of GAPDH.

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Oral Administration of CardioAid and Lunasin Alleviates Liver Damage in a High-Fat Diet Nonalcoholic Steatohepatitis Model

Digestion ◽

10.1159/000479734 ◽

2017 ◽

Vol 96 (2) ◽

pp. 110-118 ◽

Cited By ~ 5

Author(s):

Ariel Drori ◽

Dvorah Rotnemer-Golinkin ◽

Lidya Zolotarov ◽

Yaron Ilan

Keyword(s):

Oral Administration ◽

Liver Damage ◽

Nonalcoholic Steatohepatitis ◽

High Fat Diet ◽

High Fat

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BL153 Partially Prevents High-Fat Diet Induced Liver Damage Probably via Inhibition of Lipid Accumulation, Inflammation, and Oxidative Stress

Oxidative Medicine and Cellular Longevity ◽

10.1155/2014/674690 ◽

2014 ◽

Vol 2014 ◽

pp. 1-10 ◽

Cited By ~ 8

Author(s):

Jian Wang ◽

Chi Zhang ◽

Zhiguo Zhang ◽

Qiang Chen ◽

Xuemian Lu ◽

...

Keyword(s):

Oxidative Stress ◽

Body Weight ◽

Growth Factor ◽

Liver Damage ◽

Lipid Accumulation ◽

High Fat Diet ◽

Liver Weight ◽

High Fat ◽

Hepatic Lipid Accumulation ◽

And Oxidative Stress

The present study was to investigate whether amagnoliaextract, named BL153, can prevent obesity-induced liver damage and identify the possible protective mechanism. To this end, obese mice were induced by feeding with high fat diet (HFD, 60% kcal as fat) and the age-matched control mice were fed with control diet (10% kcal as fat) for 6 months. Simultaneously these mice were treated with or without BL153 daily at 3 dose levels (2.5, 5, and 10 mg/kg) by gavage. HFD feeding significantly increased the body weight and the liver weight. Administration of BL153 significantly reduced the liver weight but without effects on body weight. As a critical step of the development of NAFLD, hepatic fibrosis was induced in the mice fed with HFD, shown by upregulating the expression of connective tissue growth factor and transforming growth factor beta 1, which were significantly attenuated by BL153 in a dose-dependent manner. Mechanism study revealed that BL153 significantly suppressed HFD induced hepatic lipid accumulation and oxidative stress and slightly prevented liver inflammation. These results suggest that HFD induced fibrosis in the liver can be prevented partially by BL153, probably due to reduction of hepatic lipid accumulation, inflammation and oxidative stress.

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Exercise Alleviates the Apolipoprotein A5-Toll-Like Receptor 4 Axis Impairment in Mice With High-Fat Diet-Induced Non-alcoholic Steatohepatitis

Frontiers in Physiology ◽

10.3389/fphys.2021.783341 ◽

2021 ◽

Vol 12 ◽

Author(s):

Yang Yu ◽

Lina Yu ◽

Nuo Cheng ◽

Xiaoguang Liu ◽

Chunlu Fang ◽

...

Keyword(s):

High Fat Diet ◽

Enzyme Linked Immunosorbent Assay ◽

Toll Like Receptor ◽

High Fat ◽

Toll Like Receptor 4 ◽

Alcoholic Fatty Liver ◽

Apolipoprotein A5 ◽

Hepatic Lipid Accumulation ◽

Protein Levels ◽

Alcoholic Steatohepatitis

Background: Apolipoprotein A5 (ApoA5), an important modulator of plasma and hepatic triglyceride metabolism, has been found to be downregulated by metformin to improve non-alcoholic fatty liver disease. Meanwhile, exercise has been recommended as a therapeutic strategy for non-alcoholic steatohepatitis (NASH). However, no study has yet determined whether exercise affects hepatic ApoA5 expression or the inhibition of ApoA5 to toll-like receptor 4 (TLR4). We herein examined the effects of exercise on hepatic ApoA5 expression and the relevance of ApoA5 and TLR4-mediated pathway in mice with high-fat diet (HFD)-induced NASH.Methods: Male C57BL/6J mice were built NASH model with high-fat diet for 12 weeks, and following mice were subjected to exercise for 12 weeks on a treadmill. Microscopy and enzyme-linked immunosorbent assay were used to measure histological analysis of liver and hepatic lipids, respectively. Quantitative real-time PCR and western blot were used to determined mRNA and protein levels of ApoA5 and TLR4-mediated nuclear factor kappa B (NF-κB) pathway components, respectively. ApoA5 overexpression plasmids transfected into mice to investigate the relevance of ApoA5 and TLR4.Results: 12 weeks of exercise remarkably alleviated HFD-induced hepatic lipid accumulation, inflammation, and fibrosis, as well as reduced serum lipopolysaccharide (LPS), hepatic TLR4, myeloid differentiation factor 88 (MyD88), and NF-κBp65 expression. Importantly, exercise did not reduce ApoA5 expression but instead enhanced its ability to suppress TLR4-mediated NF-κB pathway components by decreasing circulating LPS in our experiments involving transfection of ApoA5 overexpression plasmids and LPS interventions.Conclusion: The results demonstrated that exercise improved HFD-induced NASH by triggering the inhibitory effects of ApoA5 on the TLR4-mediated NF-κB pathway.

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Oral Administration of Acidophilus Milk Supplemented with Calcium Pyruvate Modulates some Biochemical Parameters and Weight Gain in Rats Fed High Fat Diet

Indian Journal of Dairy Science ◽

10.33785/ijds.2019.v72i04.008 ◽

2019 ◽

Vol 72 (04) ◽

pp. 397-402

Author(s):

Fouad Mahmoud Fouad Elshaghabee

Keyword(s):

Weight Gain ◽

Oral Administration ◽

High Fat Diet ◽

Biochemical Parameters ◽

High Fat

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Effect of Water Extract of Germinated Brown Rice on Adiposity and Obesity Indices in Mice Fed a High Fat Diet

Preventive Nutrition and Food Science ◽

10.3746/jfn.2005.10.3.251 ◽

2005 ◽

Vol 10 (3) ◽

pp. 251-256 ◽

Cited By ~ 5

Author(s):

Suk-Heung Oh ◽

Yeon-Jeong Moon ◽

Ju-Ryoun Soh ◽

Youn-Soo Cha

Keyword(s):

High Fat Diet ◽

Brown Rice ◽

Water Extract ◽

High Fat ◽

Germinated Brown Rice ◽

Effect Of Water ◽

Obesity Indices

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Uridine attenuates obesity, ameliorates hepatic lipid accumulation and modifies the gut microbiota composition in mice fed with a high-fat diet

Food & Function ◽

10.1039/d0fo02533j ◽

2021 ◽

Author(s):

Yilin Liu ◽

Chunyan Xie ◽

Zhenya Zhai ◽

Ze-yuan Deng ◽

Hugo R. De Jonge ◽

...

Keyword(s):

Gut Microbiota ◽

Lipid Accumulation ◽

High Fat Diet ◽

Microbiota Composition ◽

High Fat ◽

Fat Accumulation ◽

Hepatic Lipid ◽

Hepatic Lipid Accumulation ◽

Gut Microbiota Composition

This study aimed to investigate the effect of uridine on obesity, fat accumulation in liver, and gut microbiota composition in high-fat diet-fed mice.

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Maternal high-fat diet induces metabolic stress response disorders in offspring hypothalamus

Journal of Molecular Endocrinology ◽

10.1530/jme-17-0056 ◽

2017 ◽

Vol 59 (1) ◽

pp. 81-92 ◽

Cited By ~ 7

Author(s):

Long The Nguyen ◽

Sonia Saad ◽

Yi Tan ◽

Carol Pollock ◽

Hui Chen

Keyword(s):

Endoplasmic Reticulum ◽

Body Weight ◽

Er Stress ◽

High Fat Diet ◽

Maternal Obesity ◽

Mrna Level ◽

Metabolic Stress ◽

High Fat ◽

Chemical Chaperone ◽

Protein Levels

Maternal obesity has been shown to increase the risk of obesity and related disorders in the offspring, which has been partially attributed to changes of appetite regulators in the offspring hypothalamus. On the other hand, endoplasmic reticulum (ER) stress and autophagy have been implicated in hypothalamic neuropeptide dysregulation, thus may also play important roles in such transgenerational effect. In this study, we show that offspring born to high-fat diet-fed dams showed significantly increased body weight and glucose intolerance, adiposity and plasma triglyceride level at weaning. Hypothalamic mRNA level of the orexigenic neuropeptide Y (NPY) was increased, while the levels of the anorexigenic pro-opiomelanocortin (POMC), NPY1 receptor (NPY1R) and melanocortin-4 receptor (MC4R) were significantly downregulated. In association, the expression of unfolded protein response (UPR) markers including glucose-regulated protein (GRP)94 and endoplasmic reticulum DNA J domain-containing protein (Erdj)4 was reduced. By contrast, protein levels of autophagy-related genes Atg5 and Atg7, as well as mitophagy marker Parkin, were slightly increased. The administration of 4-phenyl butyrate (PBA), a chemical chaperone of protein folding and UPR activator, in the offspring from postnatal day 4 significantly reduced their body weight, fat deposition, which were in association with increased activating transcription factor (ATF)4, immunoglobulin-binding protein (BiP) and Erdj4 mRNA as well as reduced Parkin, PTEN-induced putative kinase (PINK)1 and dynamin-related protein (Drp)1 protein expression levels. These results suggest that hypothalamic ER stress and mitophagy are among the regulatory factors of offspring metabolic changes due to maternal obesity.

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