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Research Progress on Prevention and Treatment of Glucolipid metabolic disease with Integrated Traditional Chinese and Western Medicine

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Chinese Journal of Integrative Medicine 2017年第6期23卷 403-409页

作者： GUO Jiao Guangdong metabolic disease Research Center of Integrated Chinese and Western Medicine Guangdong Key Laboratory of metabolic disease Prevention and Treatment of Traditional Chinese Medicine Key Unit of Modulating Liver in Treating Hyperlipidemia SACM Institute of Traditional Chinese Medicine Research InstituteGuangdong Pharmaceutical UniversityGuangzhou 510006China

Hyperlipidemia, type 2 diabetes mellitus, nonalcoholic fatty liver and many other metabolic disorder are frequently co-existing in patients. In addition, these diseases are closely related in pathophysiological settings. However, increasing of the disease incidence, lacking of comprehensive prevention and control measurements against the key pathology point concomitant occurrence with the pattem of the single disease, single target therapy, that is leading therapeutic strategy for these metabolic disorders in the setting of Western medicine （WM）. On the basis of the combination of the advantages of integrated Chinese medicine （CM） and WM, with unified understanding of such diseases, the new concept of glucolipid metabolic disease （GLMD） is introduced. In this new concept, disorders in glucose and lipid metabolism are recognized as the key trigger and major driving force for the progress of GLMD. The key points of pathology included dysfunction of neuronal-endocrine-immune system,insulin resistance, oxidative stress, inflammation and intestinal flora imbalance. In the core pathogenic perspective of CM, it can be explained as ＂Gan （Liver） Shi Shu Xie＂（dysfunction of Gan in metabolism and emotion regulation） that will lead to the occurence/production of endogenous dampness and phlegm, blood stasis and turbid. This leads to the new concept of ＂Liver-based regulatory system for metabolic homeostasis＂ to be introduced further. The comprehensive prevention and control strategy ＂Tiao Gan Qi Shu Hua Zhuo＂（modulating Gan, trigging key metabolic system to resolve pathogenic factors such as phlegm retention and dampness）. Its representative formula Fufang Zhenzhu Tiaozhi Capsule （复方贞术调脂胶囊） is innovated under such rationales. Comment for some commonly-used CM GLMD therapeutic drugs was presented. High-level evidence-based and epidemiological and mechanism studies should be carded out to further interpret and explain of the scientific connotation of GLMD.

关键词： glucolipid metabolic disease liver-based regulatory system for metabolic homeostasis Tiao Gan （Liver） Qi Shu Hua Zhuo （modulating Gan trigging key metabolic system to resolve pathogenic factors such as phlegm retention and dampness） Chinese medicine

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metabolic regulation by protein tyrosine phosphatases

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The Journal of Biomedical Research 2014年第3期28卷 157-168页

作者： Hilla Knobler Ari Elson Diabetes and metabolic disease Unit Kaplan Medical Center Department of Molecular Genetics the Weizmann Institute of Science

Obesity and the metabolic syndrome and their associated morbidities are major public health issues, whose prevalence will continue to increase in the foreseeable future. Aberrant signaling by the receptors for leptin and insulin plays a pivotal role in development of the metabolic syndrome. More complete molecular-level understanding of how both of these key signaling pathways are regulated is essential for full characterization of obesity, the metabolic syndrome, and type lI diabetes, and for developing novel treatments for these diseases. Phosphorylation of proteins on tyrosine residues plays a key role in mediating the effects of leptin and insulin on their target cells. Here, we discuss the molecular methods by which protein tyrosine phosphatases, which are key physiological regulators of protein phosphorylation in vivo, affect signaling by the leptin and insulin receptors in their major target tissues.

关键词： obesity diabetes metabolic syndrome insulin resistance leptin resistance tyrosine phosphatase PTP

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Endothelin-1-induced mini-stroke in the dorsal hippocampus or lateral amygdala results in deficits in learning and memory

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The Journal of Biomedical Research 2015年第5期29卷 362-369页

作者： Tao Sheng Xueting Zhang Shaoli Wang Jingyun Zhang Wei Lu Yifan Dai The Center of metabolic disease Research Nanjing Medical University The Key Laboratory of Developmental Genes and Human disease Institute of Life SciencesSoutheast University Department of Neurobiology Nanjing Medical University

Functional and structural alterations in brain connectivity associated with brain ischemia have been extensively studied. However, the mechanism whereby local ischemia in deep brain region affect brain functions is still unknown. Here, we first established a mini-stroke model by infusion of endothelin-1 （ET-1） into the dorsal hippo- campus or the lateral amygdala, and then investigated how these mini-infarcts affected brain functions associated with these regions. We found that rats with ET-1 infusion showed deficit in recall of contextual fear memory, but not in learning process and recall of tone fear memory. In novel object task, ET-1 in the hippocampus also elimi- nated object identity memory. ET-1 in the lateral amygdale affected acquisition of fear conditioning and disrupted retention of tone-conditioned fear, but did not impair retention of contextual fear. These findings suggest that ET-1- induced mini-infarct in deep brain area leads to functional deficits in learning and memory associated with these regions.

关键词： endothelin-1 dorsal hippocampus lateral amygdala fear conditioning

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CCAAT/Enhancer-Binding Proteins in Fibrosis:Complex Roles Beyond Conventional Understanding

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Research 2023年第1期2022卷 231-272页

作者： Lexun Wang Jiaojiao Feng Yanyue Deng Qianqian Yang Quxing Wei Dewei Ye Xianglu Rong Jiao Guo Guangdong metabolic diseases Research Center of Integrated Chinese and Western Medicine China Key Laboratory of Glucolipid metabolic Disorder Ministry of Education of ChinaChina Guangdong Key Laboratory of metabolic disease Prevention and Treatment of Traditional Chinese Medicine China institute of Chinese Medicine Guangdong Pharmaceutical UniversityGuangzhouChina

CCAAT/enhancer-binding proteins(C/EBPs)are a family of at least six identified transcription factors that contain a highly conserved basic leucine zipper domain and interact selectively with duplex DNA to regulate target gene expression.C/EBPs play important roles in various physiological processes,and their abnormal function can lead to various diseases.Recently,accumulating evidence has demonstrated that aberrant C/EBP expression or activity is closely associated with the onset and progression of fibrosis in several organs and tissues.During fibrosis,various C/EBPs can exert distinct functions in the same organ,while the same C/EBP can exert distinct functions in different organs.Modulating C/EBP expression or activity could regulate various molecular processes to alleviate fibrosis in multiple organs;therefore,novel C/EBPs-based therapeutic methods for treating fibrosis have attracted considerable attention.In this review,we will explore the features of C/EBPs and their critical functions in fibrosis in order to highlight new avenues for the development of novel therapies targeting C/EBPs.

关键词： organs expression Complex

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Novel insights into immune-related genes associated with type 2 diabetes mellitus-related cognitive impairment

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World Journal of Diabetes 2024年第4期15卷 735-757页

作者： Jing Gao Ying Zou Xiao-Yu Lv Li Chen Xin-Guo Hou Department of Endocrinology Qilu Hospital of Shandong UniversityCheeloo College of MedicineShandong UniversityJinan 250012Shandong ProvinceChina institute of Endocrine and metabolic diseases Shandong UniversityJinan 250012Shandong ProvinceChina Key Laboratory of Endocrine and metabolic diseases Shandong Province Medicine&HealthJinan 250012Shandong ProvinceChina Department of Endocrinology Jinan Clinical Research Center for Endocrine and Metabolic DiseaseJinan 250012Shandong ProvinceChina

BACKGROUND The cognitive impairment in type 2 diabetes mellitus(T2DM)is a multifaceted and advancing state that requires further exploration to fully comprehend.Neu-roinflammation is considered to be one of the main mechanisms and the immune system has played a vital role in the progression of the disease.AIM To identify and validate the immune-related genes in the hippocampus associated with T2DM-related cognitive impairment.METHODS To identify differentially expressed genes(DEGs)between T2DM and controls,we used data from the Gene Expression Omnibus database GSE125387.To identify T2DM module genes,we used Weighted Gene Co-Expression Network Analysis.All the genes were subject to Gene Set Enrichment Analysis.Protein-protein interaction network construction and machine learning were utilized to identify three hub genes.Immune cell infiltration analysis was performed.The three hub genes were validated in GSE152539 via receiver operating characteristic curve analysis.Validation experiments including reverse transcription quantitative real-time PCR,Western blotting and immunohistochemistry were conducted both in vivo and in vitro.To identify potential drugs associated with hub genes,we used the Comparative Toxicogenomics Database(CTD).RESULTS A total of 576 DEGs were identified using GSE125387.By taking the intersection of DEGs,T2DM module genes,and immune-related genes,a total of 59 genes associated with the immune system were identified.Afterward,machine learning was utilized to identify three hub genes(H2-T24,Rac3,and Tfrc).The hub genes were associated with a variety of immune cells.The three hub genes were validated in GSE152539.Validation experiments were conducted at the mRNA and protein levels both in vivo and in vitro,consistent with the bioinformatics analysis.Additionally,11 potential drugs associated with RAC3 and TFRC were identified based on the CTD.CONCLUSION Immune-related genes that differ in expression in the hippocampus are closely linked to microglia.We validated the expression of three hub genes

关键词： Bioinformatics analysis Type 2 diabetes mellitus Cognitive impairment Hippocampus Immune Microglia

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Mechanism of depression as a risk factor in the development of Alzheimer’s disease: the function of AQP4 and the glymphatic system

Mechanism of depression as a risk factor in the development ...

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中国神经科学学会第十二届全国学术会议

作者： Baoman Li Laboratory of Brain metabolic diseases Institute of Metabolic Disease Research and Drug Development China Medical University

Background: Depression and Alzheimer’s disease（AD） are both common mental illnesses. Recently, many studies have reported a close link between these two diseases. Moreover, depression has a high risk for AD. It is known that the deposition of amyloid beta 42（Aβ42） is a key hallmark of AD. Currently, several studies demonstrate that a "cerebral lymphatic system" is also known as "glymphatic system", which is used to clear neuronal extracellular waste protein, including Aβ42 protein. And water channel aquaporin 4（AQP4） is essential for the function of glymphatic system. However, the function of glymphatic pathway has not been determined in depressive disorders. Therefore, our present study is aimed to investigate the pathogenetic relationship between depression and AD. Methods: According to whether the experimental mice were treated by chronic treatment with unpredictable mild stress（CUMS）, the experiment was divided into experimental group and control group. The glymphatic system function, AQP4 expression, and Aβ42 clearance were compared between the two groups. Then, CUMStreated mice were treated with or without antidepressant fluoxetine. Similarly, the glymphatic system function, AQP4 expression, and Aβ42 clearance in CUMS-treated mice with or without the treatment of antidepressant fluoxetine were measured. And the function of glymphatic pathway was determined through fluorescence tracers. Results: Fluorescence tracers penetration in the brain of the CUMS-treated mice were significantly decreased, glymphatic pathway circulation was impaired in mice treated with CUMS. Moreover, glymphatic pathway dysfunction suppressed Aβ42 metabolism, because the accumulation of endogenous and exogenous Aβ42 were increased in the brains of the CUMS-treated mice. In anhedonic mice, the expression of AQP4, a factor in glymphatic pathway dysfunction, was down-regulated in cortex and hippocampus. However, fluoxetine reversed these destructive effects of CUMS on glymphatic system. The expression of AQP4 was significantly increased b

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Association between Coronary Atherosclerotic Plaque Composition and Cardiovascular disease Risk

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Biomedical and Environmental Sciences 2019年第2期32卷 75-86页

作者： LI Lin WANG Long LIU Shan Shan ZHAO Zhi Yun LI Mian WANG Tian Ge XU Min LU Jie Li CHEN Yu Hong WANG Shuang Yuan DAI Meng HOU Ya Nan WU Xue Yan MA Li Na WANG Wei Qing XU Yu BI Yu Fang National Clinical Research Center for metabolic diseases Shanghai Institute of Endocrine and Metabolic Diseases and Department of Endocrine and Metabolic Diseases Rui-Jin Hospital Shanghai Jiao-Tong University School of Medicine

Objective The objective of this study is to determine whether coronary atherosclerotic plaque composition is associated with cardiovascular disease(CVD) risk in Chinese adults. Methods We performed a cross-sectional analysis in 549 subjects without previous diagnosis or clinical symptoms of CVD in a community cohort of middle-aged Chinese adults. The participants underwent coronary computed tomography(CT) angiography for the evaluation of the presence and composition of coronary plaques. CVD risk was evaluated by the Framingham risk score(FRS) and the 10-year atherosclerotic cardiovascular disease(ASCVD) risk score. Results Among the 549 participants, 267(48.6%) had no coronary plaques, 201(36.6%) had noncalcified coronary plaques, and 81(14.8%) had calcified or mixed coronary plaques. The measures of CVD risk including FRS and ASCVD risk score and the likelihood of having elevated FRS significantly increased across the groups of participants without coronary plaques, with noncalcified coronary plaques, and with calcified or mixed coronary plaques. However, only calcified or mixed coronary plaques were significantly associated with an elevated ASCVD risk score [odds ratio(OR) 2.41; 95% confidence interval(CI) 1.09-5.32] compared with no coronary plaques, whereas no significant association was found for noncalcified coronary plaques and elevated ASCVD risk score(OR 1.25; 95% CI 0.71-2.21) after multivariable adjustment. Conclusion Calcified or mixed coronary plaques might be more associated with an elevated likelihood of having CVD than noncalcified coronary plaques.

关键词： Coronary plaque composition Framingham risk score 10-year atherosclerotic cardiovascular disease risk score

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Association between Selenium in Soil and Diabetes in Chinese Residents Aged 35–74 Years:Results from the 2010 National Survey of Chronic diseases and Behavioral Risk Factors Surveillance

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Biomedical and Environmental Sciences 2020年第4期33卷 260-268页

作者： WANG Qi Qi YU Shi Cheng XU Cheng Dong LIU Jian Jun LI Yuan Qiu ZHANG Man Hui LONG Xiao Juan LIU Yun Ning BI Yu Fang ZHAO Wen Hua YAO Hong Yan Chinese Center for disease Control and Prevention Beijing 102206China State Key Laboratory of Resources and Environmental Information System Institute of Geographic Sciences and Natural Resources ResearchChinese Academy of SciencesBeijing 100101China Peking University Third Hospital Beijing 100191China National Center for Chronic and Non communicable disease Control and Prevention Chinese Center for Disease Control and PreventionBeijing 100050China Shanghai National Clinical Research Center for Endocrine and metabolic diseases Shanghai Institute of Endocrine and Metabolic DiseasesRuijin HospitalShanghai Jiao Tong University School of MedicineShanghai 200025China National institute for Nutrition and Health Chinese Center for Disease Control and PreventionBeijing 100050China

Objective To explore the association between soil selenium levels and the risk of diabetes in Chinese adults aged 35–74 years.Methods Data for this study were derived from the China Chronic diseases and Behavioral Risk Factors Surveillance 2010 survey.Selenium concentrations in soil were obtained from the Atlas of Soil Environmental Background Values in China.A two-level binary logistic regression model was used to determine the association between soil selenium concentrations and the risk of diabetes,with participants nested within districts/counties.Results A total of 69,332 participants aged 35–74 years,from 158 districts/counties were included in the analysis.Concentrations of selenium in soil varied greatly across the 158 districts/counties,with a median concentration of 0.219 mg/kg(IQR:0.185–0.248).The results showed that both Quartile 1(0.119–0.185 mg/kg)and Quartile 4(0.249–0.344 mg/kg)groups were positively associated with diabetes compared to a soil selenium concentration of 0.186–0.219 mg/kg(Quartile 2),crude odds ratios(ORs)(95%CI)were 1.227(1.003–1.502)and 1.280(1.048–1.563).The P values were 0.045 and 0.013,for Quartile 1 and Quartile 4 groups,respectively.After adjusting for all confounding factors of interest,the Quartile 1 group became non-significant,and the Quartile 4 group had an adjusted OR(95%CI)of 1.203(1.018–1.421)relative to the reference group(Quartile 2),the P values was 0.030.No significant results were seen for the Quartile 3 group(0.220–0.248 mg/kg)compared to the reference group.Conclusion Excessive selenium concentrations in soil could increase the risk of diabetes among Chinese adults aged 35–74 years.

关键词： Selenium Diabetes Odds ratio Behavioral risk factors Survey

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metabolically healthy obesity:Is it really healthy for type 2 diabetes mellitus?

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World Journal of Diabetes 2022年第2期13卷 70-84页

作者： Qi Wu Ming-Feng Xia Xin Gao Department of Endocrinology and Metabolism Zhongshan HospitalFudan UniversityShanghai 200032China Fudan Institute for Metabolic Disease Fudan UniversityShanghai 200032China

metabolically healthy obese(MHO)individuals are reported to have a lower risk of developing cardiovascular diseases in comparison with individuals with metabolic syndrome.However,the association between MHO and type 2 diabetes(T2DM)is still controversial.Some studies indicated that MHO is a favorable phenotype for T2DM,but more studies showed that MHO individuals have an increased risk of developing T2DM compared with metabolically healthy normalweight individuals,especially among those who would acquire metabolically unhealthy obesity.This has been supported by finding insulin resistance and lowgrade inflammatory responses in MHO individuals with a tendency for impaired beta-cell dysfunction.Studies also showed that liver fat accumulation increased the risk of incidence of T2DM in MHO.Here,we reviewed current literature on the relationship between MHO and T2DM,discussed the determinants for the development of diabetes in MHO,and summarized the measures for the prevention of T2DM in MHO.

关键词： metabolically healthy obesity Type 2 diabetes Non-alcoholic fatty liver diseases Insulin resistance Low-grade inflammatory status Beta-cell dysfunction

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Growth inhibition and apoptosis induction by alternol in pancreatic carcinoma cells

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World Journal of Gastroenterology 2015年第15期21卷 4526-4535页

作者： Pei-Fang Cong Ying-Chun Qu Jie-Peng Chen Li-Li Duan Cheng-Jiang Lin Xiao-Lin Zhu Jesse Li-Ling Mei-Xia Zhang Laboratory of metabolic disease Research and Drug Development China Medical University Strand Biotechnology institute of Research Nanchuan institute of Biological Research Joint Key Laboratory for Bio-resource Research and Utilization of Sichuan and Chongqing

AIM: To investigate the effect of alternol on pancreatic cancer cells.METHODS: Pancreatic cancer cells PANC-1 and Bx PC3 were treated with various concentrations of alternol for 24, 48 and 72 h. Cell proliferation was measured by cell counting. Cell cycle distribution and mitochondrial membrane potential were determined by flow cytometry. Apoptosis was determined by a Td T-mediated d UTP nick end labeling assay and Hoechst staining. Expression of caspase 3, Bcl-2, p53 and p21 was measured by western blotting.RESULTS: Alternol showed dose- and time-dependent inhibition of the proliferation of PANC-1 and Bx PC3 cells in vitro. Alternol induced apoptosis and cell cycle arrest at S phase and decreased mitochondrial membrane potential. Alternol activated caspase 3, upregulated p53 and p21 expression, and downregulated Bcl-2 expression in a dose-dependent manner.CONCLUSION: Our results suggested that alternol is a candidate for treatment of pancreatic cancer.

关键词： Pancreatic cancer Alternol Chemotherapy Cell cycle Apoptosis

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