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Polystyrene nanoplastics induce glycolipid metabolism disorder via NF-κB and MAPK signaling pathway in mice

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Journal of Environmental Sciences 2024年第3期137卷 553-566页

作者： Xingpei Fan Xiaoyan Li Jiaxin Li Yuxia Zhang Xiangjuan Wei Hailong Hu Boya Zhang Haining Du Meimei Zhao Ruijiao Zhu Daqian Yang Yuri Oh Ning Gu School of Life Science and Technology Harbin Institute of TechnologyHarbin 150001China State Key Laboratory of Urban Water Resource and Environment Harbin Institute of TechnologyHarbin 150006China department of Medicine Renal Electrolyte and Hypertension DivisionDepartment of GeneticsPerelman School of MedicineUniversity of PennsylvaniaPhiladelphia 19104USA Faculty of education Wakayama UniversityWakayama 640-8441Japan

Nanoplastics-induced developmental and reproductive toxicity,neurotoxicity and immunotoxicity are a focus of widespread attention.However,the effects of nanoplastics(NPs)on glycolipid metabolism and the precise underlying mechanisms are unclear at present.Here,we showed that oral administration of polystyrene nanoparticles(PS-NPs)disrupts glycolipid metabolism,with reactive oxygen species(ROS)identified as a potential key signaling molecule.After PS-NPs treatment,excessive production of ROS induced the infammatory response and activated the antioxidant pathway through nuclear factor-erythroid factor 2-related factor 2.The activation of nuclear factor-κB(NFκB)signaling pathway induced the phosphorylation of the mitogen-activated protein kinases(MAPK)signaling pathway,which induced the activation of extracellular regulated kinases(ERK)and p38.Constitutive activation of the MAPK signaling proteins induced high continued phosphorylation of insulin receptor substrate-1,in turn,leading to decreased protein kinase B(Akt)activity,which weakened the sensitivity of liver cells to insulin signals and induced insulin resistance.In parallel,phosphorylation of Akt led to loss of control of Fo XO1,a key gene of gluconeogenesis,activating transcription of glucose-6-phosphatase(G6PC)and phosphoenolpyruvate carboxykinase(PEPCK)in a manner dependent on PGC1α.Moreover,the activated ERK promoted lipid accumulation through ERK-PPARγcascades.Therefore,sterol regulatory element-binding protein-1 and levels of its downstream lipogenic enzymes,ACC-1,were up-regulated.Upon treatment with the antioxidant resveratrol,PS-NPs-induced glucose and lipid metabolic disorders were improved by inhibiting ROS-induced activation of NFκB and MAPK signaling pathway in mice.Based on above,PS-NPs exposure disrupts glycolipid metabolism in mice,with ROS identified as a potential key signaling molecule.

关键词： Nanoplastics Resveratrol Hyperglycemia Lipid metabolism Infammatory response Reactive oxygen species(ROS)

Gut microbiota remodeling drived by dietary millet protein prevents the metabolic syndrome

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Food Science and Human Wellness 2024年第4期13卷 1987-2001页

作者： Shuhua Shan Ruopeng Yin Jiangying Shi Lizhen Zhang Jiaqi Zhou Qinqin Qiao Xiushan Dong Wenjing Zhao Zhuoyu Li Institute of Biotechnology Key Laboratory of Chemical Biology and Molecular Engineering of National Ministry of EducationShanxi UniversityTaiyuan 030006China School of Life Science Shanxi UniversityTaiyuan 030006China Shanxi Bethune Hospital Shanxi Academy of Medical SciencesTongji Shanxi HospitalThird Hospital of Shanxi Medical UniversityTaiyuan 030032China department of Biology Biological Science and Technology CollegeTaiyuan Normal UniversityJinzhong 030619China

metabolic syndrome(Met S)is a chronic disease associated with the disturbance of gut microbiota homeostasis.Metabolites derived from gut microbes play essential roles in Met S prevention and therapy.Here,we focused on the inhibitory effect of the extract of millet bran protein(EMBP)on a high-fat diet(HFD)-induced Met S,aiming to identify gut microbiota and their metabolites that involve in the anti-Met S activity of EMBP.The obesity,chronic inflammation,insulin resistance in Met S mouse models were abolished after EMBP treatment.The protective mechanism of EMBP against HFD-induced Met S may depend on improved gut barrier function.Using microbiome analysis,we found that EMBP supplementation improved gut microbiome dysbiosis in Met S mice,specifically upregulating Bacteroides acidifaciens.The fecal microbiota transplantation(FMT)also demonstrated this phenomenon.In addition,metabolomic analysis showed that EMBP mediates metabolic profiling reprogramming in Met S mice.Notably,a microbiota-derived metabolite,gamma-aminobutyric acid(GABA),is enriched by EMBP.In addition,exogenous GABA treatment produced a similar protective effect to EMBP by improving NRF2-dependent gut barrier function to protect HFDinduced Met S.The results suggest that EMBP suppress host Met S by remodeling of gut microbiota as an effective candidate for next-generation medicine food dual purpose dietary supplement to intervene in MetS.

关键词： metabolic syndrome Gut microbiota Extract of millet bran protein Gamma-aminobutyric acid Gut barrier function

Reconsidering the role of depression and common psychiatric disorders as partners in the type 2 diabetes epidemic

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World Journal of Diabetes 2024年第6期15卷 1374-1380页

作者： Angelo Emilio Claro Clelia Palanza Marianna Mazza Alessandro Rizzi Andrea Corsello Linda Tartaglione Giuseppe Marano Giovanna Elsa Ute Muti Schuenemann Marta Rigoni Alfredo Pontecorvi Luigi Janiri Paola Muti Dario Pitocco Diabetes Care Unit Department of Medical and Surgical SciencesFondazione Policlinico Universitario A Gemelli IRCCSRome 00168Italy department of Biomedical Surgical and Dental SciencesUniversity of MilanMilan 20122Italy Istituto Italiano di Antropologia ISItARome 00100Italy Unit of Psychiatry Department of NeurosciencesFondazione Policlinico Universitario A Gemelli IRCCSUniversitàCattolica del Sacro CuoreRome 00168Italy Dipartimento di Medicina e Chirurgia Traslazionale UniversitàCattolica del Sacro CuoreRome 00168Italy Health Research Methods Evidence and Impact DepartmentMcMaster UniversityOntario 1280Canada department of Endocrine-metabolic and Dermo-Rheumatology Fondazione Policlinico Universitario A Gemelli IRCCSUniversitàCattolica del Sacro CuoreRome 00168Italy

Common psychiatric disorders(CPDs)and depression contribute significantly to the global epidemic of type 2 diabetes(T2D).We postulated a possible pathophysiological mechanism that through Bridge-Symptoms present in depression and CPDs,promotes the establishment of emotional eating,activation of the reward system,onset of overweight and obesity and,ultimately the increased risk of developing T2D.The plausibility of the proposed pathophysiological mechanism is supported by the mechanism of action of drugs such as naltrexonebupropion currently approved for the treatment of both obesity/overweight with T2D and as separate active pharmaceutical ingredients in drug addiction,but also from initial evidence that is emerging regarding glucagon-like peptide 1 receptor agonists that appear to be effective in the treatment of drug addiction.We hope that our hypothesis may be useful in interpreting the higher prevalence of CPDs and depression in patients with T2D compared with the general population and may help refine the integrated psychiatric-diabetic therapy approach to improve the treatment and or remission of T2D.

关键词： Depression Glucagon-like peptide-1 receptor agonists Diabetes mellitus type 2 Stress psychological Sleep wake disorders Food addiction

Hereditary severe insulin resistance syndrome:Pathogenesis,pathophysiology,and clinical management

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Genes & Diseases 2023年第5期10卷 1846-1856页

作者： Junaid Iqbal Hong-Li Jiang Hui-Xuan Wu Long Li Ying-Hui Zhou Nan Hu Fen Xiao Ting Wang Shi-Na Xu Hou-De Zhou National Clinical Research Center for metabolic Diseases Hunan Provincial Key Laboratory for Metabolic Bone Diseasesand Department of Endocrinology and MetabolismThe Second XiangYa Hospital of Central South UniversityChangshaHunan 410011China

Severe insulin resistance has been linked to some of the most globally prevalent disorders,such as diabetes mellitus,nonalcoholic fatty liver disease,polycystic ovarian syndrome,and hypertension.Hereditary severe insulin resistance syndrome(H-SIRS)is a rare disorder classified into four principal categories:primary insulin receptor defects,lipodystrophies,complex syndromes,and obesity-related H-SIRS.Genes such as INSR,AKT2,TBC1D4,AGPAT2,BSCL2,CAV1,PTRF,LMNA,PPARG,PLIN1,CIDEC,LIPE,PCYT1A,MC4R,LEP,POMC,SH2B1,RECQL2,RECQL3,ALMS1,PCNT,ZMPSTE24,PIK3R1,and POLD1 have been linked to H-SIRS.Its clinical features include insulin resistance,hyperglycemia,hyperandrogenism,severe dyslipidemia,fatty liver,abnormal topography of adipose tissue,and low serum leptin and adiponectin levels.Diagnosis of H-SIRS is based on the presence of typical clinical features associated with the various H-SIRS forms and the identification of mutations in H-SIRS-linked genes by genetic testing.Diet therapy,insulin sensitization,exogenous insulin therapy,and leptin replacement therapy have widely been adopted to manage H-SIRS.The rarity of H-SIRS,its highly variable clinical presentation,refusal to be tested for genetic mutations by patients’family members who are not severely sick,unavailability of genetic testing,and testing expenses contribute to the delayed or underdiagnoses of H-SIRS.Early diagnosis facilitates early management of the condition,which results in improved glycemic control and delayed onset of diabetes and other complications related to severe insulin resistance.The use of updated genetic sequencing technologies is recommended,and long-term studies are required for genotype–phenotype differentiation and formulation of diagnostic and treatment protocols.

关键词： Diabetes Genetics Insulin resistance Lipodystrophy Pathophysiology Therapy

Protein neddylation and its role in health and diseases

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Signal Transduction and Targeted Therapy 2024年第5期9卷 1869-1904页

作者： Shizhen Zhang Qing Yu Zhijian Li Yongchao Zhao Yi Sun department of Breast Surgery the Second Affiliated HospitalZhejiang University School of MedicineHangzhou 310029China Cancer Institute(Key Laboratory of Cancer Prevention and Intervention China National Ministry of Education)the Second Affiliated HospitalZhejiang University School of MedicineHangzhou 310029China Institute of Translational Medicine Zhejiang University School of MedicineHangzhou 310029China department of Thyroid Surgery Zhejiang Cancer HospitalInstitute of Basic Medicine and Cancer(IBMC)Chinese Academy of SciencesHangzhou 310022China Key Laboratory of Head&Neck Cancer Translational Research of Zhejiang Province Hangzhou 310022China department of Hepatobiliary and Pancreatic Surgery Zhejiang University School of MedicineHangzhou 310029China Zhejiang Provincial Key Laboratory of Pancreatic Disease The First Affiliated HospitalZhejiang University School of MedicineHangzhou 310029China Zhejiang University Cancer Center Hangzhou 310029China Leading Innovative and Entrepreneur Team Introduction Program of Zhejiang Hangzhou 310024China Research Center for Life Science and Human Health Binjiang Institute of Zhejiang UniversityHangzhou 310053China

NEDD8(Neural precursor cell expressed developmentally downregulated protein 8)is an ubiquitin-like protein that is covalently attached to a lysine residue of a protein substrate through a process known as neddylation,catalyzed by the enzyme cascade,namely NEDD8 activating enzyme(E1),NEDD8 conjugating enzyme(E2),and NEDD8 ligase(E3).The substrates of neddylation are categorized into cullins and non-cullin proteins.Neddylation of cullins activates CRLs(cullin RING ligases),the largest family of E3 ligases,whereas neddylation of non-cullin substrates alters their stability and activity,as well as subcellular localization.Significantly,the neddylation pathway and/or many neddylation substrates are abnormally activated or over-expressed in various human diseases,such as metabolic disorders,liver dysfunction,neurodegenerative disorders,and cancers,among others.Thus,targeting neddylation becomes an attractive strategy for the treatment of these diseases.In this review,we first provide a general introduction on the neddylation cascade,its biochemical process and regulation,and the crystal structures of neddylation enzymes in complex with cullin substrates;then discuss how neddylation governs various key biological processes via the modification of cullins and non-cullin substrates.We further review the literature data on dysregulated neddylation in several human diseases,particularly cancer,followed by an outline of current efforts in the discovery of small molecule inhibitors of neddylation as a promising therapeutic approach.Finally,few perspectives were proposed for extensive future investigations.

关键词： NEDD8 attached attractive

Hepatocellular Carcinoma in Non-alcoholic Fatty Liver Disease:Current Progresses and Challenges

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Journal of Clinical and Translational Hepatology 2022年第5期10卷 955-964页

作者： Yu-Xian Teng Si Xie Ping-Ping Guo Zhu-Jian Deng Zi-Yi Zhang Wei Gao Wan-Guang Zhang Jian-Hong Zhong Hepatobiliary Surgery department Guangxi Liver Cancer Diagnosis and Treatment Engineering and Technology Research CenterGuangxi Medical University Cancer HospitalNanningGuangxiChina Key Laboratory of Early Prevention and treatment for Regional High Frequency Tumor(Guangxi Medical University) Ministry of EducationGuangxi Key Laboratory of Early Prevention and Treatment for Regional High Frequency TumorNanningGuangxiChina Hepatic Surgery Center Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubeiChina

The rising global prevalence of metabolic diseases has increased the prevalence of non-alcoholic fatty liver disease(NAFLD),leading to an increase in cases of NAFLD-related hepatocellular carcinoma(HCC).To provide an updated literature review detailing epidemiology,risk factors,pathogenic pathways,and treatment strategies linked to NAFLD-related HCC,we conducted a literature search on PubMed from its inception to December 31,2021.About 25%of the global population suffers from NAFLD.The annual incidence of HCC among NAFLD patients is approximately 1.8 per 1,000 person-years.Older age,male sex,metabolic comorbidities,unhealthy lifestyle habits(such as smoking and alcohol consumption),physical inactivity,genetic susceptibility,liver fibrosis,and degree of cirrhosis in NAFLD patients are important risk factors for NAFLD-related HCC.Therefore,low-calorie diet,moderate-intensity exercise,treatment of metabolic comorbidities,and cessation of smoking and alcohol are the main measures to prevent NAFLD-related HCC.In addition,all patients with advanced NAFLD-related fibrosis or cirrhosis should be screened for HCC.Immune suppression disorders and changes in the liver microenvironment may be the main pathogenesis of NAFLD-related HCC.Hepatic resection,liver transplantation,ablation,transarterial chemoembolization,radiotherapy,targeted drugs,and immune checkpoint inhibitors are used to treat NAFLD-related HCC.Lenvatinib treatment may lead to better overall survival,while immune checkpoint inhibitors may lead to worse overall survival.Given the specific risk factors for NAFLD-related HCC,primary prevention is key.Moreover,the same treatment may differ substantially in efficacy against NAFLD-related HCC than against HCC of other etiologies.

关键词： Epidemiology Hepatocellular carcinoma Non-alcoholic fatty liver disease Risk factor treatment strategy

Repurposing lansoprazole to alleviate metabolic syndrome via PHOSPHO1 inhibition

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Acta Pharmaceutica Sinica B 2024年第4期14卷 1711-1725页

作者： Yingting Wu Jiaqi Xin Xinyu Li Ting Yang Yi Liu Yongsheng Zhao Wen Xie Mengxi Jiang department of Pharmacology School of Basic Medical SciencesCapital Medical UniversityBeijing 100069China department of Traditional Chinese Medicine Capital Medical UniversityBeijing 100069China Center for Pharmacogenetics and department of Pharmaceutical Sciences University of PittsburghPittsburghPA 15261USA Advanced Innovation Center for Human Brain Protection Capital Medical UniversityBeijing 100069China

Drug repurposing offers an efficient approach to therapeutic development.In this study,our bioinformatic analysis first predicted an association between obesity and lansoprazole(LPZ),a commonly prescribed drug for gastrointestinal ulcers.We went on to show that LPZ treatment increased energy expenditure and alleviated the high-fat diet-induced obesity,insulin resistance,and hepatic stea-tosis in mice.treatment with LPZ elicited thermogenic gene expression and mitochondrial respiration in primary adipocytes,and induced cold tolerance in cold-exposed mice,suggesting the activity of LPZ in promoting adipose thermogenesis and energy metabolism.Mechanistically,LPZ is an efficient inhibitor of adipose phosphocholine phosphatase 1(PHOSPHOI)and produces metabolic benefits in a PHOS-PHO1-dependent manner.Our results suggested that LPZ may stimulate adipose thermogenesis by inhi-biting the conversion of 2-arachidonoylglycerol-lysophosphatidic acid(2-AG-LPA)to 2-arachidonoylglycerol(2-AG)and reduce the activity of the thermogenic-suppressive cannabinoid recep-tor signaling.In summary,we have uncovered a novel therapeutic indication and mechanism of LPZ in managing obesity and its related metabolic syndrome,and identified a potential metabolic basis by which LPZ improves energy metabolism.

关键词： Lansoprazole Proton pump inhibitors Adipose thermogenesis Energy expenditure metabolic syndrome PHOSPHO1 inhibitor Cannabinoid receptor signaling Drug repurposing

Adiponectin restores the obesity-induced impaired immunomodulatory function of mesenchymal stromal cells via glycolytic reprogramming

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Acta Pharmaceutica Sinica B 2024年第1期14卷 273-291页

作者： Duc-Vinh Pham Thi-Kem Nguyen Bao-Loc Nguyen Jong-Oh Kim Jee-Heon Jeong Inho Choi Pil-Hoon Park department of Pharmacology Hanoi University of PharmacyHanoi 100000Viet Nam College of Pharmacy Yeungnam UniversityGyeongsan 38541Republic of Korea department of Medical Biotechnology Yeungnam UniversityGyeongsan 38541Republic of Korea Research Institute of Cell Culture Yeungnam UniversityGyeongsan 38541Republic of Korea department of Precision Medicine School of MedicineSungkyunkwan UniversitySuwon 16419Republic of Korea

obesity has been known to negatively modulate the life-span and immunosuppressive potential of mesenchymal stromal cells(MSC).However,it remains unclear what drives the compromised potency of obese MSC.In this study,we examined the involvement of adiponectin,an adipose tissuederived hormone,in obesity-induced impaired therapeutic function of MSC.Diet-induced obesity leads to a decrease in serum adiponectin,accompanied by impairment of survival and immunomodulatory effects of adipose-derived MSC(ADSC).Interestingly,priming with globular adiponectin(gAcrp)improved the immunomodulatory potential of obese ADSC.Similar effects were also observed in lean ADSC.In addition,gAcrp potentiated the therapeutic effectiveness of ADSC in a mouse model of DSS-induced colitis.Mechanistically,while obesity inhibited the glycolytic capacity of MSC,gAcrp treatment induced a metabolic shift toward glycolysis through activation of adiponectin receptor type 1/p38 MAPK/hypoxia inducible factor-1a axis.These findings suggest that activation of adiponectin signaling is a promising strategy for enhancing the therapeutic efficacy of MSC against immune-mediated disorders.

关键词： Adiponectin Adipose-derived stromal cells Colitis Glycolytic induction HIF1a Immunomodulation Mesenchymal stromal cells obesity

Alisol B 23-acetate promotes white adipose tissue browning to mitigate high-fat diet-induced obesity by regulating mTOR-SREBP1 signaling

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Journal of Integrative Medicine 2024年第1期22卷 83-92页

作者： Lu-lu Han Xin Zhang Hui Zhang Ting Li Yi-chen Zhao Ming-hui Tian Feng-lei Sun Bo Feng department of Neurology Three The Fifth People’s Hospital of JinanJinan 250013Shandong ProvinceChina department of Gastroenterology Affiliated Hospital of Shandong University of Traditional Chinese MedicineJinan 250014Shandong ProvinceChina The First Clinical Medical College Shandong University of Traditional Chinese MedicineJinan 250014Shandong ProvinceChina department of Geriatrics the First Affiliated Hospital of Shandong First Medical University(Shandong Provincial Qianfoshan Hospital)Jinan 250014Shandong ProvinceChina Chinese Medicine Culture and Literature Research Institute Shandong University of Traditional Chinese MedicineJinan 250014Shandong ProvinceChina department of General Medicine Affiliated Hospital of Shandong University of Traditional Chinese MedicineJinan 250014Shandong ProvinceChina department of Traditional Chinese Medicine the Second People’s Hospital of Haibei PrefectureZangzu Autonomous Prefecture of Haibei810300Qinghai ProvinceChina

Objective obesity is a global health concern with management strategies encompassing bariatric surgery and anti-obesity drugs;however,concerns regarding complexities and side effects persist,driving research for more effective,low-risk strategies.The promotion of white adipose tissue(WAT)browning has emerged as a promising approach.Moreover,alisol B 23-acetate(AB23A)has demonstrated efficacy in addressing metabolic disorders,suggesting its potential as a therapeutic agent in obesity management.Therefore,in this study,we aimed to investigate the therapeutic potential of AB23A for mitigating obesity by regulating metabolic phenotypes and lipid distribution in mice fed a high-fat diet(HFD).Methods An obesity mouse model was established by administration of an HFD.Glucose and insulin metabolism were assessed via glucose and insulin tolerance tests.Adipocyte size was determined using hematoxylin and eosin staining.The expression of browning markers in WAT was evaluated using Western blotting and quantitative real-time polymerase chain reaction.metabolic cage monitoring involved the assessment of various parameters,including food and water intake,energy metabolism,respiratory exchange rates,and physical activity.Moreover,oil red O staining was used to evaluate intracellular lipid accumulation.A bioinformatic analysis tool for identifying the molecular mechanisms of traditional Chinese medicine was used to examine AB23A targets and associated signaling pathways.Results AB23A administration significantly reduced the weight of obese mice,decreased the mass of inguinal WAT,epididymal WAT,and perirenal adipose tissue,improved glucose and insulin metabolism,and reduced adipocyte size.Moreover,treatment with AB23A promoted the expression of browning markers in WAT,enhanced overall energy metabolism in mice,and had no discernible effect on food intake,water consumption,or physical activity.In 3T3-L1 cells,AB23A inhibited lipid accumulation,and both AB23A and rapamycin inhibited the mammalian target of rapamycin-sterol regulato

关键词： obesity Alisol B 23-acetate Adipose tissue mTOR-SREBP1 High-fat diet