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hepatic steatosis is associated with dysregulated cholesterol metabolism and altered protein acetylation dynamics in chickens

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Journal of Animal Science and Biotechnology 2024年第1期15卷 53-67页

作者： Xiaoli Guo Qianqian Zhou Jiaming Jin Fangren Lan Chaoliang Wen Junying Li Ning Yang Congjiao Sun National Engineering Laboratory for Animal Breeding and Key Laboratory of Animal Genetics Breeding and ReproductionMinistry of Agriculture and Rural AffairsChina Agricultural UniversityBeijing 100193China

Background hepatic steatosis is a prevalent manifestation of fatty liver, that has detrimental effect on the health and productivity of laying hens, resulting in economic losses to the poultry industry. Here, we aimed to systematically investigate the genetic regulatory mechanisms of hepatic steatosis in laying hens.Methods Ninety individuals with the most prominent characteristics were selected from 686 laying hens according to the accumulation of lipid droplets in the liver, and were graded into three groups, including the control, mild hepatic steatosis and severe hepatic steatosis groups. A combination of transcriptome, proteome, acetylome and lipidome analyses, along with bioinformatics analysis were used to screen the key biological processes, modifications and lipids associated with hepatic steatosis.Results The rationality of the hepatic steatosis grouping was verified through liver biochemical assays and RNA-seq. hepatic steatosis was characterized by increased lipid deposition and multiple metabolic abnormalities. Integration of proteome and acetylome revealed that differentially expressed proteins(DEPs) interacted with differentially acetylated proteins(DAPs) and were involved in maintaining the metabolic balance in the liver. Acetylation alterations mainly occurred in the progression from mild to severe hepatic steatosis, i.e., the enzymes in the fatty acid oxidation and bile acid synthesis pathways were significantly less acetylated in severe hepatic steatosis group than that in mild group(P hepatic steatosis(r ≤-0.5, P hepatic steatosis was associated with a decrease in cholesterol and bile acid synthesis and an increase in exogenous cholesterol transport.Conclusions In addition to acquiring a global and thorough picture of hepatic steatosis in laying hens, we were able to reveal the role of acetylation in hepatic steatosis and depict the ch

关键词： Acetylation Cholesterol metabolism hepatic steatosis Laying hens Multiomics

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hepatic steatosis with mass effect:A case report

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World Journal of Clinical Cases 2022年第30期10卷 11066-11073页

作者： Na Hu Shi-Jun Su Jin-Ye Li Hui Zhao Shan-Feng Liu Lin-Sheng Wang Ruo-Zhen Gong Chuan-Ting Li Department of Radiology Shandong Provincial ENT HospitalShandong UniversityJinan 250023Shandong ProvinceChina Department of Radiology The Fifth People's Hospital of JinanJinan 250022Shandong ProvinceChina Innovation Studio Shandong Provincial ENT HospitalShandong UniversityJinan 250023Shandong ProvinceChina Department of Radiology Shandong Provincial HospitalShandong UniversityJinan 250021Shandong ProvinceChina

BACKGROUND hepatic steatosis is a common radiologic finding.Some imaging inklings are the absence of a mass effect,and there is currently no report of hepatic steatosis with mass effect.CASE SUMMARY A 23-year-old female was admitted due to a liver mass for half a month.No obvious abnormalities were found in physical and laboratory examinations.Ultrasound,computed tomography,and magnetic resonance imaging showed a huge mass between the liver and stomach with a significant mass effect,and the caudate lobe and left lobe of the liver were involved.The signal on T2-and T1-weighted fat-saturated images of the mass was significantly reduced,and the enhanced scan showed inhomogeneous enhancement.Surgical and pathological findings indicated the diagnosis of hepatic steatosis.The operation and re-review of the patient’s images showed that the lesion was supplied by the branch of the hepatic artery.The signal on T1-weighted out-of-phase images of the lesion was lower than on in-phase images,and there was no black rim cancellation artifact around the hepatic steatosis area on T1-weighted out-of-phase images.The dynamic enhancement pattern of the lesion was similar to that of the adjacent normal liver parenchyma.The above characteristics suggested that the lesion was hepatic steatosis.However,in this case,the lesion showed exogenous growth and was mass-like,with an obvious mass effect,which has not been reported previously.CONCLUSION hepatic steatosis could grow exogenously and has an obvious mass effect.It needs to be distinguished from fat-rich tumors.The T1-weighted in-and out-of-phase images and dynamic enhanced scanning are valuable for differential diagnosis of this lesion.

关键词： hepatic steatosis Computed tomography Magnetic resonance imaging In-phase and out-of-phase imaging Case report

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hepatic DDAH1 mitigates hepatic steatosis and insulin resistance in obese mice: Involvement of reduced S100A11 expression

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Acta Pharmaceutica Sinica B 2023年第8期13卷 3352-3364页

作者： Xiyue Shen Kai Luo Juntao Yuan Junling Gao Bingqing Cui Zhuoran Yu Zhongbing Lu College of Life Science University of Chinese Academy of SciencesBeijing 100049China Institute of Respiratory Medicine Tongji University School of MedicineShanghai 200433China

Dimethylarginine dimethylaminohydrolase 1(DDAH1)is an important regulator of plasma asymmetric dimethylarginine(ADMA)levels,which are associated with insulin resistance in patients with nonalcoholic fatty liver disease(NAFLD).To elucidate the role of hepatic DDAH1 in the pathogenesis of NAFLD,we used hepatocyte-specific Ddah1-knockout mice(Ddah1HKO)to examine the progress of high-fat diet(HFD)-induced NAFLD.Compared to diet-matched flox/flox littermates(Ddah1f/f),Ddah1HKO mice exhibited higher serum ADMA levels.After HFD feeding for 16 weeks,Ddah1HKO mice developed more severe liver steatosis and worse insulin resistance than Ddah1f/f mice.On the contrary,overexpression of DDAH1 attenuated the NAFLD-like phenotype in HFD-fed mice and ob/ob mice.RNA-seq analysis showed that DDAH1 affects NF-kB signaling,lipid metabolic processes,and immune system processes in fatty livers.Furthermore,DDAH1 reduces S100 calcium-binding protein A11(S100A11)possibly via NF-kB,JNK and oxidative stress-dependent manner in fatty livers.Knockdown of hepatic S100a11 by an AAV8-shS100a11 vector alleviated hepatic steatosis and insulin resistance in HFD-fed Ddah1HKO mice.In summary,our results suggested that the liver DDAH1/S100A11 axis has a marked effect on liver lipid metabolism in obese mice.Strategies to increase liver DDAH1 activity or decrease S100A11 expression could be a valuable approach for NAFLD therapy.

关键词： ADMA DDAH1 hepatic steatosis Insulinresistance S100A11 Oxidativestress Inflammation Highfat diet

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Anthelmintics nitazoxanide protects against experimental hyperlipidemia and hepatic steatosis in hamsters and mice

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Acta Pharmaceutica Sinica B 2022年第3期12卷 1322-1338页

作者： Fengfeng Li Man Jiang Minghui Ma Xuyang Chen Yidan Zhang Yixin Zhang Yuanyuan Yu Yunfeng Cui Jiahui Chen Hui Zhao Zhijie Sun Deli Dong Department of Pharmacology(the State-Province Key Laboratories of Biomedicine-Pharmaceutics of China Key Laboratory of Cardiovascular ResearchMinistry of Education)College of PharmacyHarbin Medical UniversityHarbin 150086China Translational Medicine Research and Cooperation Center of Northern China Heilongjiang Academy of Medical SciencesHarbin Medical UniversityHarbin 150086China Department of Pharmacology China Pharmaceutical UniversityNanjing 211198China

Lipid metabolism disorders contribute to hyperlipidemia and hepatic steatosis.It is ideal to develop drugs simultaneous improving both hyperlipidemia and hepatic steatosis.Nitazoxanide is an FDA-approved oral antiprotozoal drug with excellent pharmacokinetic and safety profile.We found that nitazoxanide and its metabolite tizoxanide induced mild mitochondrial uncoupling and subsequently activated AMPK in Hep G2 cells.Gavage administration of nitazoxanide inhibited high-fat diet(HFD)-induced increases of liver weight,blood and liver lipids,and ameliorated HFD-induced renal lipid accumulation in hamsters.Nitazoxanide significantly improved HFD-induced histopathologic changes of hamster livers.In the hamsters with pre-existing hyperlipidemia and hepatic steatosis,nitazoxanide also showed therapeutic effect.Gavage administration of nitazoxanide improved HFD-induced hepatic steatosis in C57BL/6J mice and western diet(WD)-induced hepatic steatosis in Apoe-/-mice.The present study suggests that repurposing nitazoxanide as a drug for hyperlipidemia and hepatic steatosis treatment is promising.

关键词： Nitazoxanide Tizoxanide Hyperlipidemia hepatic steatosis AMPK Autophagy SQSTM1/P62 Mitochondrial uncoupling

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An early screening model of pulse detection technology for hepatic steatosis

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Intelligent Medicine 2023年第4期3卷 280-286页

作者： Wenjie Wu Chunke Zhang Xiaotian Ma Rui Guo Jianjun Yan Yiqin Wang Haixia Yan Yeqing Zhang Department of Basic Medical Science Shanghai University of Traditional Chinese MedicineShanghai 201203China Institute of Intelligent Perception and Diagnosis School of Mechanical and Power EngineeringEast China University of Science and TechnologyShanghai 200237China Department of Chinese Internal Medicine Shanghai Municipal Hospital of Traditional Chinese MedicineShanghai University of Traditional Chinese MedicineShanghai 200071China

Background The increasing prevalence of hepatic steatosis presents a considerable challenge to public health.There is a critical need for the development of novel preventive and screening strategies for this condition.Thisstudy evaluated the potential applications of wrist pulse detection technology for the early detection of liverdiseases.The pulse time-domain features of a medical exam population with and without hepatic steatosis wereassessed to develop a screening model for this disease.Methods Participants were consecutively recruited from March 2021 to March 2022 in the medical examinationcenters of the Yueyang Hospital of Integrated Traditional Chinese and Western Medicine and the Shanghai Municipal Hospital of Traditional Chinese Medicine.Clinical data from 255 participants,including general information(sex,age,and body mass index),and data related to glucose and blood lipids(fasting plasma glucose,triglyceride,total cholesterol,high-density lipoprotein,and low-density lipoprotein levels)were collected.Wrist pulse signalswere acquired using a pulse detection device,and the pulse time-domain features,including t_(1),t_(4),t_(5),T,w_(1),w_(2),h_(2)/h_(1),h_(3)/h_(1),and h5/h_(1) were extracted.Participants were assigned to hepatic steatosis and non-hepatic steatosisgroups according to their abdominal ultrasound examination results.Their clinical data and pulse time-domainfeatures were compared using chi-square and parametric or non-parametric statistical methods.Three datasetswere used to construct screening models for hepatic steatosis based on the random forest algorithm.The datasetsfor modeling were defined as Dataset 1,containing blood glucose and lipid data and general information;Dataset2,containing time-domain features and general information;Dataset 3,containing time-domain features,bloodglucose and lipid data,and general information.The evaluation metrics,accuracy,precision,recall,F1-score,andareas under the receiver operating characteristic curve(AUC)were compared for each model.Results The time-d

关键词： Pulse detection technology Time-domain method hepatic steatosis Early screening Random forest

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Activation of NLRP3 Inflammasome via Drp1 Overexpression in Kupffer Cells Aggravates Ischemia-reperfusion Injury in hepatic steatosis

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Journal of Clinical and Translational Hepatology 2023年第5期11卷 1069-1078页

作者： Lu Zhang Mingfu Wang Ran An Jun Dai Shujun Liu Ming Chen Haoran Ding Department of Hepatobiliary Surgery Affiliated Drum Tower Hospital of Nanjing University Medical SchoolNanjingJiangsuChina Surgery Department I Zhangjiagang Traditional Chinese Medicine HospitalSuzhouJiangsuChina Department of Hepatobiliary Surgery The First Affiliated Hospital of Wannan Medical CollegeWuhuAnhuiChina Department of Hepatobiliary Surgery Nanjing Drum Tower HospitalClinical College of Traditional Chinese and Western MedicineSchool of PharmacyNanjing University of Chinese MedicineNanjingJiangsuChina

Background and Aims:Donors with fatty livers are considered to address the shortage of livers for transplantation,but those livers are particularly sensitive to ischemia-reperfusion injury(IRI),and an increased incidence of graft failure is observed.Kupffer cells account for 20–35%of liver nonparenchymal cells,and have been shown to participate in the process of IRI and inflammatory reactions of hepatic steatosis.NOD-like receptor thermal protein domain-associated protein 3(NLRP3)is an intracellular sensor activated by Kupffer cells to promote generation and participates in IRI.Dynamics-associated protein 1(Drp1)is one of the main proteins regulating mitochondrial division and exacerbates IRI by affecting mitochondrial dynamics.The mechanism of interaction of Kupffer cells with Drp1 and NLRP3 to aggravate IRI has not been clarified.Methods:A mouse model of hepatic steatosis was established by feeding the mice with a high-fat diet.In vitro experiments were performed using AML12 normal mouse liver cells and RAW264.7 mononuclear macrophage cells cultured in medium with palmitate and oleic acid.Western blotting and immunohistochemical(IHC)staining were used to detect the expression of NLRPP3 and Drp1 in IRI in the control and high-fat diet groups.The expression of F4/80+cells during IRI in hepatic steatosis was verified by IHC staining,and the role of NLRPP3 and Drp1 in Kupffer-cell mediated IRI was investigated by targeting Drp-1 inhibition.Results:Drp1 and NLRP3 expression was increased during IRI in hepatic steatosis,and the expression of Drp1 and NLRP3 were decreased after the elimination of Kupffer cells.That indicated Kupffer cells were involved in the process of IRI in hepatic steatosis through the action of Drp1 and NLRP3.After Drp1 inhibition,liver function was restored and NLRP3 expression level was reduced.Conclusions:Kupffer cells aggravated IRI in hepatic steatosis via NLRP3 and Drp1.Drp1 inhibitors might be useful as specific therapeutics to alleviate IRI in hepatic steatosis and may have promise in cas

关键词： Drp1 Kupffer cells NLRP3 hepatic steatosis Ischemia-reperfusion

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Testosterone therapy reduces hepatic steatosis in men with type 2 diabetes and low serum testosterone concentrations

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World Journal of Hepatology 2022年第4期14卷 754-765页

作者： Ross Apostolov Emily Gianatti Darren Wong Numan Kutaiba Paul Gow Mathis Grossmann Marie Sinclair Department of Gastroenterology and Liver Transplant Unit Austin HealthHeidelberg 3084VICAustralia Department of Medicine University of MelbourneParkville 3010VICAustralia Department of Endocrinology Fiona Stanley HospitalMurdoch 6150WAAustralia Department of Radiology Austin HealthHeidelberg 3084VICAustralia Department of Endocrinology Austin HealthHeidelberg 3084VICAustralia

BACKGROUND Non-alcoholic fatty liver disease(NAFLD)is highly prevalent in people with diabetes with no available treatment.AIM To explore the effect of testosterone treatment on liver.Testosterone therapy improves insulin resistance and reduces total body fat,but its impact on the liver remains poorly studied.METHODS This secondary analysis of a 40 wk,randomised,double-blinded,placebocontrolled trial of intramuscular testosterone undecanoate in men with type 2 diabetes and lowered serum testosterone concentrations evaluated the change in hepatic steatosis as measured by liver fat fraction on magnetic resonance imaging(MRI).RESULTS Of 88 patients enrolled in the index study,39 had liver MRIs of whom 20 received testosterone therapy and 19 received placebo.All patients had>5%hepatic steatosis at baseline and 38 of 39 patients met diagnostic criteria for NAFLD.Median liver fat at baseline was 15.0%(IQR 11.5%-21.1%)in the testosterone and 18.4%(15.0%-28.9%)in the placebo group.Median ALT was 34units/L(26-38)in the testosterone and 32units/L(25-52)in the placebo group.At week 40,patients receiving testosterone had a median reduction in absolute liver fat of 3.5%(IQR 2.9%-6.4%)compared with an increase of 1.2%in the placebo arm(between-group difference 4.7%Phepatic steatosis in men with diabetes and low serum testosterone.Future randomised studies of testosterone therapy in men with NAFLD focusing on liver-related endpoints are therefore justified.

关键词： hepatic steatosis Non-alcoholic fatty liver disease Non-alcoholic steatohepatitis Testosterone therapy Testosterone undecanoate Type 2 diabetes

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Theasinensin A attenuated diabetic development by restoring glucose homeostasis, improving hepatic steatosis and modulating gut microbiota in high-fat-diet/streptozotocin-induced diabetic mice

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Food Science and Human Wellness 2023年第6期12卷 2073-2086页

作者： Weiqi Xu Yujie Huang Wangting Zhou Yujia Peng Xuhui Kan Wei Dong Guijie Chen Xiaoxiong Zeng Zhonghua Liu College of Food Science and Technology Nanjing Agricultural UniversityNanjing 210095China Key Laboratory of Ministry of Education for Tea Science Hunan Agricultural UniversityChangsha 410128China National Research Center of Engineering Technology for Utilization of Botanical Functional Ingredients Changsha 410128China

Theasinensin A(TSA),a dimer of epigallocatechin gallate,has been preliminarily demonstrated to have hypoglycemia and anti-inflammatory effects.However,little information is available on its potential mechanisms of anti-diabetes.Therefore,the present study aimed to investigate the influence of TSA on glucose and lipid metabolism and gut microbiota in high-fat-diet/streptozotocin-induced diabetic mice.As result,TSA improved polydipsia,polyphagia and impaired glucose tolerance of diabetic mice,declined the fasting blood glucose and hepatic triglyceride level,and enhanced the expression at mRNA level of insulin receptor substrate,phosphoinositide 3-kinase,protein kinase B and glucagon-like peptide 1 receptor(GLP-1R)in the diabetic liver.Moreover,TSA could restore the disorder of gut microbiota of diabetic mice.High-dose(100 mg/kg)TSA showed better benefi cial effects from the blood biochemical parameters,hepatic function and gut microbiota.In general,high-dose TSA significantly modulated gut microbiota by increasing the relative abundance of Akkermansia and decreasing the relative abundances of Acetatifactor,Anaerotruncus,Pseudofl avonifactor,Oscillibacter and Clostridium clusters.The results indicated that TSA could exert an anti-diabetes effect in diabetic mice through restoring glucose homeostasis,declining hepatic steatosis,activating insulin and GLP-1 signaling pathways,and ameliorating gut microbiota dysbiosis.

关键词： Tea Theasinensin A Diabetes Glucose homeostasis Gut microbiota hepatic steatosis

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hepatic steatosis,low-grade chronic inflammation and hormone/growth factor/adipokine imbalance

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World Journal of Gastroenterology 2010年第38期16卷 4773-4783页

作者： Giovanni Tarantino Silvia Savastano Annamaria Colao Department of Clinical and Experimental Medicine Federico Ⅱ University Medical School of Naples Department of Molecular and Clinical Endocrinology and Oncology Section of EndocrinologyFederico Ⅱ University Medical School of Naples

Non-alcoholic fatty liver disease (NAFLD), a further expression of metabolic syndrome, strictly linked to obesity and diabetes mellitus, is characterized by insulin resistance (IR), elevated serum levels of free fatty acids and fatty infi ltration of the liver, which is known as hepatic steatosis. Hepatocyte apoptosis is a key feature of this disease and correlates with its severity. Free-fatty-acidinduced toxicity represents one of mechanisms for the pathogenesis of NAFLD and hormones, growth factors and adipokines influence also play a key role. This review highlights the various pathways that contribute to the development of hepatic steatosis. Circulating concentrations of inflammatory cytokines are reckoned to be the most important factor in causing and maintaining IR. Low-grade chronic inflammation is fundamental in the progression of NAFLD toward higher risk cirrhotic states.

关键词： hepatic steatosis Low-grade chronic inflammation Adipokines Hormones Growth factors

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Novel insights into the effect of Xiaoyao san on corticosterone-induced hepatic steatosis:inhibition of glucocorticoid receptor/perilipin-2 signaling pathway

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Acupuncture and Herbal Medicine 2022年第1期2卷 49-57页

作者： Lian Gong Guo-En Wang Qing-Yu Ma Wen-Zhi Hao Min-Hua Xian Yan-Ping Wu Hiroshi Kurihara Rong-Rong He Jia-Xu Chen Formula-Pattern Research Center School of Chinese MedicineJinan UniversityGuangzhouChina Guangdong Engineering Research Center of Chinese Medicine&Disease Susceptibility Jinan UniversityGuangzhouChina School of Traditional Chinese Medicine Guangdong Pharmaceutical UniversityGuangzhouChina

Objective:Xiaoyao san(XYS)is a classic traditional Chinese medicinal formula.It has been clinically administered to regulate liver function.However,its mechanisms in glucocorticoid-induced hepatic steatosis are unknown.This study aimed to investigate whether XYS protects against corticosterone(CORT)-induced hepatic steatosis,and to explore its mechanism.Methods:High-fat diet mice induced with hepatic steatosis by 2mg/kg CORT were administered 2.56 g/kg or 5.12 g/kg XYS daily for 7 weeks.The effects of XYS on hepatic steatosis in mice were evaluated by H&E and Oil Red O staining and by measuring their plasma lipids(triglyceride,total cholesterol,and free fatty acids).The mechanism of XYS against hepatic steatosis was investigated by network pharmacology,immunohistochemistry,western blotting,and gain-of-function/loss-offunction experiments.Results:XYS alleviated CORT-induced steatosis,decreased plasma lipids,and inhibited glucocorticoid receptor(GR)activation in the liver.Network pharmacology data indicated that XYS may have mitigated hepatic steatosis via GR which mediated adipose differentiation-related protein(ADFP).Gain-of-function/loss-of-function experiments in vitro confirmed that GR positively regulated ADFP expression.Conclusions:XYS ameliorated CORT-induced hepatic steatosis by downregulating the GR/ADFP axis and inhibiting lipid metabolism.Our studies implicate that XYS is promising as a therapy for CORT-induced hepatic steatosis,and lay the foundation for designing novel prophylactic and therapeutic strategies on CORT-induced hepatic steatosis.

关键词： Adipose differentiation-related protein Glucocorticoid receptor hepatic steatosis Network pharmacology Xiaoyao san

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