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Lingguizhugan decoction attenuates diet-induced obesity and Hepatosteatosis via gut microbiota

World Journal of Gastroenterology 2019年第27期25卷 3590-3606页

作者： Meng-Ting Liu Ying-Juan Huang Ting-Ying Zhang Lun-Bo Tan Xi-Feng Lu Jian Qin Department of Traditional Chinese Medicine the First Affiliated Hospital of Sun Yat-Sen UniversityGuangzhou 510080Guangdong ProvinceChina Department of Traditional Chinese Medicine the Seventh Affiliated Hospital of Sun Yat-Sen UniversityShenzhen 518107Guangdong ProvinceChina Department of Physiology Shenzhen University Health Science CenterShenzhen UniversityShenzhen 518060Guangdong ProvinceChina

BACKGROUND Obesity is a major risk factor for a variety of diseases such as diabetes,nonalcoholic fatty liver disease, and cardiovascular diseases. Restricting energy intake, or caloric restriction(CR), can reduce body weight and improve metabolic parameters in overweight or obese patients. We previously found that Lingguizhugan decoction(LZD) in combination with CR can effectively lower plasma lipid levels in patients with metabolic syndrome. However, the mechanism underlying CR and LZD treatment is still unclear.AIM To investigate whether CR and LZD improve metabolic parameters by modulating gut microbiota.METHODS We extracted the water-soluble components out of raw materials and dried as LZD extracts. Eight-week old male C57 BL/6 mice were treated with a 3-d treatment regime that included 24 h-fasting followed by gavage of LZD extracts for 2 consecutive days, followed by a normal diet(ND) ad libitum for 16 wk. To test the effects of gut microbiota on diet-induced obesity, 8-wk old male C57 BL/6 mice received fecal microbiota transplantation(FMT) from CR and LZD-treated mice every 3 d and were fed with high-fat diet(HFD) ad libitum for 16 wk.Control mice received either saline gavage or FMT from ND-fed mice receiving saline gavage as mentioned above. Body weight was monitored bi-weekly. Food consumption of each cage hosting five mice was recorded weekly. To monitor blood glucose, total cholesterol, and total triglycerides, blood samples were collected via submandibular bleeding after 6 h fasting. Oxygen consumption rate was monitored with metabolic cages. Feces were collected, and fecal DNA was extracted. Profiles of gut microbiota were mapped by metagenomic sequencing.RESULTS We found that CR and LZD treatment significantly reduced the body weight of mice fed with ND(28.71 ± 0.29 vs 28.05 ± 0.15, P < 0.05), but did not affect plasma total cholesterol or total triglyceride levels. We then transplanted the fecal microbiota collected from CR and LZD-treated mice under ND feeding to HFDfed mice. Intriguingly, tran

关键词： Obesity Diabetes Lipid metabolism Hepatosteatosis Gut microbiota

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The deubiquitinating enzyme 13 retards non-alcoholic steatohepatitis via blocking inactive rhomboid protein 2-dependent pathway

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Acta Pharmaceutica Sinica B 2023年第3期13卷 1071-1092页

作者： Minxuan Xu Jun Tan Liancai Zhu Chenxu Ge Wei Dong Xianling Dai Qin Kuang Shaoyu Zhong Lili Lai Chao Yi Qiang Li Deshuai Lou Linfeng Hu Xi Liu Gang Kuang Jing Luo Jing Feng Bochu Wang Chongqing Key Laboratory of Medicinal Resources in the Three Gorges Reservoir Region School of Biological and Chemical EngineeringChongqing University of EducationChongqing 400067China College of Modern Health Industry Chongqing University of EducationChongqing 400067China Key Laboratory of Biorheological Science and Technology(Chongqing University) Ministry of EducationCollege of BioengineeringChongqing UniversityChongqing 400030China Shandong Cancer Hospital and Institute Shandong First Medical University&Shandong Academy of Medical SciencesJinan 250117China

Nowadays potential preclinical drugs for the treatment of nonalcoholic steatohepatitis(NASH)have failed to achieve expected therapeutic efficacy because the pathogenic mechanisms are underestimated.Inactive rhomboid protein 2(IRHOM2),a promising target for treatment of inflammation-related diseases,contributes to deregulated hepatocyte metabolism-associated nonalcoholic steatohepatitis(NASH)progression.However,the molecular mechanism underlying Irhom2 regulation is still not completely understood.In this work,we identify the ubiquitin-specific protease 13(USP13)as a critical and novel endogenous blocker of IRHOM2,and we also indicate that USP13 is an IRHOM2-interacting protein that catalyzes deubiquitination of Irhom2 in hepatocytes.Hepatocyte-specific loss of the Usp13 disrupts liver metabolic homeostasis,followed by glycometabolic disorder,lipid deposition,increased inflammation,and markedly promotes NASH development.Conversely,transgenic mice with Usp13 overexpression,lentivirus(LV)-or adeno-associated virus(AAV)-driven Usp13 gene therapeutics mitigates NASH in 3 models of rodent.Mechanistically,in response to metabolic stresses,USP13 directly interacts with IRHOM2 and removes its K63-linked ubiquitination induced by ubiquitin-conjugating enzyme E2N(UBC13),a ubiquitin E2 conjugating enzyme,and thus prevents its activation of downstream cascade pathway.USP13 is a potential treatment target for NASH therapy by targeting the Irhom2 signaling pathway.

关键词： Usp13 Irhom2 NASH Hepatosteatosis Ubc13 NAFLD Ubiquitination Liver inflammation

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C-peptide as a key risk factor for non-alcoholic fatty liver disease in the United States population

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World Journal of Gastroenterology 2018年第32期24卷 3663-3670页

作者： Amporn Atsawarungruangkit Jirat Chenbhanich George Dickstein Department of Medicine MetroWest Medical CenterFraminghamMA 01702United States Department of Medicine Tufts University School of MedicineBostonMA 02111United States

AIM To determine whether fasting C-peptide is an independent predictor for non-alcoholic fatty liver disease(NAFLD) in United States population.METHODS Using the National Health and Nutrition Examination Survey(NHANES) 1988-1994, NAFLD participants aged 20 or greater without any other liver diseases were included in this study. Excessive alcohol intake is defined as > 2 drinks per day for males and > 1 drink per day for females. C-peptide and 27 other factors known to be associated with NAFLD(e.g., age, gender, body mass index, waist circumference, race/ethnicity, liver chemistries, and other diabetes tests) were tested in both univariate and multivariate level using logistic regression with a P-value 0.05.RESULTS Of 18825 participants aged ≥ 20, 3235 participants(n = 3235) met inclusion criteria. There were 23 factors associated with NAFLD by univariate analysis. 9 factors, ranked by the highest change in pseudo R2, were found to be significant predictors of NAFLD in multivariate model: waist circumference, fasting C-peptide, natural log of alanine aminotransferase(ALT), total protein, beingMexican American, natural log of glycated hemoglobin, triglyceride level, being non-Hispanic white, and ferritin level. CONCLUSION Together with waist circumference and ALT, fasting C-peptide is among three most important predictors of NAFLD in United States population in the NHANES data set. Further study is needed to validate the clinical utility of fasting C-peptide in diagnosis or monitoring insulin resistance in NAFLD patients.

关键词： Insulin resistance Fatty liver Hepatosteatosis Metabolic syndrome C-peptide

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Relationship between non-alcoholic fatty liver disease and coronary heart disease

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World Journal of Clinical Cases 2020年第20期8卷 4688-4699页

作者： Ugur Arslan Mustafa Yenerçağ Department of Cardiology University of Health Sciences Samsun Training and Research HospitalSamsun 55400Turkey

Non-alcoholic fatty liver disease(NAFLD)is the leading cause of chronic liver disease and considered a liver manifestation of metabolic syndrome.It is in close relationship with insulin resistance,obesity,diabetes mellitus,all of which increase risk of cardiovascular disease(CVD).Besides,many studies point out that NAFLD independently contributes to the development of atherosclerosis and CHD.On the other hand,CVDs are the leading cause of death in NAFLD patients.Many pathophysiological changes and molecular mechanisms play an important role in NAFLD for CVD formation.Atherosclerosis is common in NAFLD,which also mainly contributes to the CVD formation and CHD.Many studies linking atherosclerotic CHD and NAFLD are present in the literature.Subclinical CHD,mainly detected by coronary computed tomography views,have been detected more common in NAFLD patients.Presence of NAFLD has been found to be more common in patients with severe CHD and in stable CHD,NAFLD has been found to be associated with more diffuse disease.In acute coronary syndromes,especially in acute myocardial infarction,patients with NAFLD have been found to have poor prognosis when compared with NAFLD free patients.In this review,our aim is to evaluate the relationship between NAFLD and CHD in detail and go over the pathophysiological mechanisms underlying this relationship.

关键词： Fatty liver Hepatosteatosis Coronary heart disease Atherosclerosis Cardiovascular Artery

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Ganoderma lucidum polysaccharide peptide alleviates hepatoteatosis via modulating bile acid metabolism dependent on FXR-SHP/FGF

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中国药理学与毒理学杂志 2019年第9期33卷 703-704页

作者： ZHONG Dan-dan YANG Bao-xue State Key Laboratory of Natural and Biomimetic Drugs Department of PharmacologySchool of Basic Medical SciencesPeking University

OBJECTIVE Ganoderma lucidum polysaccharide peptide(GLPP)is a group of extract from Ganoderma lucidum with a molecular mass of approximately 5×10^5,which ratio of polysaccharide to peptide is approximately 95%/5%.The purpose of this study was to determine whether GLPP has therapeutic effect on Non-alcoholic fatty liver disease(NAFLD).METHODS Ob/ob mouse model and ApoC3 transgenic mouse model were used for exploring the effect of GLPP on NAFLD.Key metabolic pathways and enzymes were identified by metabolomics combining with KEGG and PIUmet analyses and key enzymes were detected by Western blotting.Hepatosteatosis models of HepG2 cells and primary hepatocytes were used to further confirm the therapeutic effect of GLPP on NAFLD.RESULTS GLPP administrated for a month alleviated Hepatosteatosis,dyslipidemia,liver dysfunction and liver insulin resistance.Pathways of glycerophos⁃pholipid metabolism,fatty acid metabolism and primary bile acid biosynthesis were involved in the therapeutic effect of GLPP on NAFLD.Detection of key enzymes revealed that GLPP reversed low expression of CYP7A1,CYP8B1,FXR,SHP and high expression of FGFR4 in ob/ob mice and ApoC3 mice.Besides,GLPP inhibited fatty acid synthesis by reducing the expression of SREBP1c,FAS and ACC via a FXR-SHP dependent mechanism.Additionally,GLPP reduced the accumulation of lipid droplets and the content of TG in HepG2 cells and primary hepatocytes induced by oleic acid and palmitic acid.CONCLUSION GLPP significantly improves NAFLD via regulating bile acid synthesis dependent on FXR-SHP/FGF pathway,which finally inhibits fatty acid synthesis,indicating that GLPP might be developed as a ther⁃apeutic drug for NAFLD.

关键词： Ganoderma lucidum polysaccharide peptide NAFLD insulin resistance Hepatosteatosis metabolo⁃mics bile acid synthesis nuclear receptors fatty acid synthesis

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