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Paraneoplastic syndromes associated with lung cancer

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World Journal of Clinical Oncology 2014年第3期5卷 197-223页

作者： Nobuhiro Kanaji Naoki Watanabe Nobuyuki Kita Shuji Bandoh Akira Tadokoro Tomoya Ishii Hiroaki Dobashi Takuya Matsunaga Department of Internal Medicine Division of Endocrinology and Metabolism Hematology Rheumatology and Respiratory MedicineFaculty of MedicineKagawa University

Paraneoplastic syndromes are signs or symptoms that occur as a result of organ or tissue damage at locations remote from the site of the primary tumor or metastases. Paraneoplastic syndromes associated with lung cancer can impair various organ functions and include neurologic, endocrine, dermatologic, rheumatologic, hematologic, and ophthalmological syndromes, as well as glomerulopathy and coagulopathy(Trousseau's syndrome). The histological type of lung cancer is generally dependent on the associated syndrome, the two most common of which are humoral hypercalcemia of malignancy in squamous cell carcinoma and the syndrome of inappropriate antidiuretic hormone secretion in small cell lung cancer. The symptoms often precede the diagnosis of the associated lung cancer, especially when the symptoms are neurologic or dermatologic. The proposed mechanisms of paraneoplastic processes include the aberrant release of humoral mediators, such as hormones and hormone-like peptides, cyto-kines, and antibodies. Treating the underlying cancer is generally the most effective therapy for paraneoplastic syndromes, and treatment soon after symptom onset appears to offer the best potential for symptom improvement. In this article, we review the diagnosis, potential mechanisms, and treatments of a wide variety of paraneoplastic syndromes associated with lung cancer.

关键词： Paraneoplastic syndrome Small cell lung cancer Non-small cell lung cancer Symptom Diagnosis Treatment Endocrine Neurologic Hematologic Trousseau’s syndrome

Nuclear factor-Y mediates pancreatic β-cell compensation by repressing reactive oxygen species-induced apoptosis under metabolic stress

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Chinese Medical Journal 2023年第8期136卷 922-932页

作者： Siyuan He Xiaoqian Yu Daxin Cui Yin Liu Shanshan Yang Hongmei Zhang Wanxin Hu Zhiguang Su Molecular Medicine Research Center and National Clinical Research Center for Geriatrics West China Hospitaland State Key Laboratory of BiotherapySichuan UniversityChengduSichuan 610041China Clinical Translational Innovation Center West China HospitalSichuan UniversityChengduSichuan 610041China division of endocrinology and Metabolism West China HospitalSichuan UniversityChengduSichuan 610041China

Background:Pancreaticβ-cells elevate insulin production and secretion through a compensatory mechanism to override insulin resistance under metabolic stress conditions.Deficits inβ-cell compensatory capacity result in hyperglycemia and type 2 diabetes(T2D).However,the mechanism in the regulation ofβ-cell compensative capacity remains elusive.Nuclear factor-Y(NF-Y)is critical for pancreatic islets’homeostasis under physiological conditions,but its role inβ-cell compensatory response to insulin resistance in obesity is unclear.Methods:In this study,using obese(ob/ob)mice with an absence of NF-Y subunit A(NF-YA)inβ-cells(ob,Nf-yaβKO)as well as rat insulinoma cell line(INS1)-based models,we determined whether NF-Y-mediated apoptosis makes an essential contribution toβ-cell compensation upon metabolic stress.Results:Obese animals had markedly augmented NF-Y expression in pancreatic islets.Deletion ofβ-cell Nf-ya in obese mice worsened glucose intolerance and resulted inβ-cell dysfunction,which was attributable to augmentedβ-cell apoptosis and reactive oxygen species(ROS).Furthermore,primary pancreatic islets from Nf-yaβKO mice were sensitive to palmitate-inducedβ-cell apoptosis due to mitochondrial impairment and the attenuated antioxidant response,which resulted in the aggravation of phosphorylated c-Jun N-terminal kinase(JNK)and cleaved caspase-3.These detrimental effects were completely relieved by ROS scavenger.Ultimately,forced overexpression of NF-Y in INS1β-cell line could rescue palmitate-inducedβ-cell apoptosis,dysfunction,and mitochondrial impairment.Conclusion:Pancreatic NF-Y might be an essential regulator ofβ-cell compensation under metabolic stress.

关键词： Nuclear factor-Y β-cell compensation Apoptosis Mitochondria Oxidative stress Obesity Lipotoxicity

New approaches for patients with advanced radioiodine-refractory thyroid cancer

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World Journal of Clinical Oncology 2022年第1期13卷 9-27页

作者： Fabian Pitoia Fernando Jerkovich Pierpaolo Trimboli Anabella Smulever division of endocrinology Hospital de Clinicas Jose de San MartinUniversity of Buenos AiresBuenos Aires 1120Argentina Clinic for endocrinology and Diabetology Lugano Regional HospitalEnte Ospedaliero CantonaleLugano 1111Switzerland Faculty of Biomedical Sciences Universitàdella Svizzera ItalianaLugano 1111Switzerland

The cumulative evidence over the past decades has shown that the incidence of differentiated thyroid carcinoma(DTC)has exponentially increased.Approximately 10%of patients with DTC exhibit recurrent or metastatic disease,and about two-thirds of the latter will be defined as refractory to radioactive iodine(RAIR)treatment.Since this condition implies 10-year survival rates less than 10% after detection,using available treatments,such as systemic and targeted therapies,have become increasingly relevant.The initiation of these treatments aims to reach stabilization,tumor volume reduction,and/or symptom improvement and it should be decided by highly specialized endocrinologists/oncologists on the basis of patient’s features.Considering that despite enlarged progression-free survival was proven,multikinase inhibitors remain non-curative,their benefits last for a limited time and the side effects potentially cause harm and quality of life reduction.In this context,molecular testing of cancer cells provides a promising spectrum of targeted therapies that offer increased compatibility with individual patient needs by improving efficacy,progression free survival,overall survival and adverse events profile.This review article aims to provide a summary of the current therapeutic strategies in advanced RAIR-DTC,including approved target therapies as well as those for off-label use,RAI resensitization agents,and immunotherapy.

关键词： Advanced differentiated thyroid cancer Radioactive iodine refractory thyroid cancer Multikinase inhibitors Systemic therapy Target therapy

Insulin requirement profiles and related factors of insulin pump therapy in patients with type 2 diabetes

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Science China(Life Sciences) 2019年第11期62卷 1506-1513页

作者： Xubin Yang Hongrong Deng Xiuzhen Zhang Daizhi Yang Jinhua Yan Bin Yao Jianping Weng Wen Xu Department of endocrinology and Metabolism Guangdong Provincial Key Laboratory of Diabetologythe Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhou 510630China Department of endocrinology and Metabolism Shenzhen People s HospitalShenzhen 518020China Department of endocrinology of the First Affiliated Hospital Division of Life Sciences and Medicine of the University of Science and Technology of China(USTC)Hefei 230026China

Continuous subcutaneous insulin infusion(CSII)is an effective therapy to control hyperglycemia in both patients with type 1 diabetes and type 2 diabetes.However,there is little data investigating the insulin dose setting during CSII therapy in type 2 diabetes to achieve optimal glycemic control and avoid the risk of hypoglycemia.Thus,this study is aimed to assess the dose characteristics of insulin requirement and explore the related clinical factors in patients with type 2 diabetes who were treated with CSII.A total of 327 patients(195 males)aged 52.9±12.5 years old were included in this study.Patients were treated with CSII to achieve the target fasting capillary blood glucose(4.4-7.0 mmol L^(-1))and 2-h postprandial capillary blood glucose(4.4-10.0 mmol L^(-1))by adjusting insulin infusion according to the seven-point capillary blood glucose profiles.Total daily insulin dose(TDD),total daily insulin dose per kilogram(TDD kg-1)and the ratio of total basal insulin dose(TBD)to TDD(%TBa)were calculated after patients achieved the glucose targets for at least 3 days via 1-2 weeks of CSII treatment.And insulin dose,insulin dosing patterns and the relevant clinical factors were analyzed.The mean ratio of basal/bolus insulin distribution of all patients was 40%:60%.Patients with central obesity needed more TDD(51.3±17.1 U versus 43.5±14.0 U,P<0.05)and TDD kg^(-1)(0.8±0.3 U kg^(-1)versus 0.7±0.2 U kg^(-1),P<0.05)than those without central obesity.Pearson's correlation analysis demonstrated that TDD was positively correlated with body mass index(BMI),waist circumference(WC),baseline fasting plasma glucose(FPG),fasting C-peptide level,2 h-postprandial C-peptide level and time to achieve glycemic target(all P<0.05);TDD kg^(-1)was positively correlated with waist-to-hip ratio(WHR),baseline FPG,glycosylated hemoglobin Ale(HbAlc),fasting C-peptide level and time to achieve glycemic target,and negatively correlated with BMI(all P<0.05).Multiple linear regression analyses revealed that BMI(β=1.796,P<0.01),WC(β=0.109,P<0.01),ba

关键词： continuous subcutaneous insulin infusion insulin requirement profiles type 2 diabetes

miR-145 improves metabolic inflammatory disease through multiple pathways

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Journal of Molecular Cell Biology 2020年第2期12卷 152-162页

作者： Min He Nan Wu Man Cheong Leong Weiwei Zhang Zi Ye Rumei Li Jinyang Huang Zhaoyun Zhang Lianxi Li Xiao Yao Wenbai Zhou Naijia Liu Zhihong Yang Xuehong Dong Yintao Li Lili Chen Qin Li Xuanchun Wang Jie Wen Xiaolong Zhao Bin Lu Yehong Yang Qinghua Wang Renming Hu Department of endocrinology and Metabolism Huashan HospitalShanghai Medical CollegeInstitute of Endocrinology and DiabetologyFudan UniversityShanghaiChina Department of Geriatrics Zhongshan HospitalShanghai Medical CollegeFudan UniversityShanghaiChina division of endocrinology and Metabolism the Keenan Research Centre in the Li Ka Shing Knowledge InstituteSt.Michaers HospitalUniversity of TorontoOntarioCanada

Chronic inflammation plays a pivotal role in insulin resistance and type 2 diabetes,yet the mechanisms are not completely understood.Here,we demonstrated that serum LPS levels were significantly higher in newly diagnosed diabetic patients than in normal control.miR-145 level in peripheral blood mononuclear cells decreased in type 2 diabetics.LPS repressed the transcription of miR-143/145 cluster and decreased miR-145 levels.Attenuation of miR-145 activity by anti-miR-145 triggered liver inflammation and increased serum chemokines in C57BL/6 J mice.Conversely,lentivirus-mediated miR-145 overexpression inhibited macrophage infiltration,reduced body weight,and improved glucose metabolism in db/db mice.And miR-145 overexpression markedly reduced plaque size in the aorta in ApoE−/−mice.Both OPG and KLF5 were targets of miR-145.miR-145 repressed cell proliferation and induced apoptosis partially by targeting OPG and KLF5.miR-145 also suppressed NF-κB activation by targeting OPG and KLF5.Our findings provide an association of the environment with the progress of metabolic disorders.Increasing miR-145 may be a new potential therapeutic strategy in preventing and treating metabolic diseases such as type 2 diabetes and atherosclerosis.

关键词： type 2 diabetes osteoprotegerin Kruppel-like factor 5 monocyte NF-κB

肝细胞NLRP3与PKCε互作驱动肝脏胰岛素抵抗和脂肪变性

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Science Bulletin 2023年第13期68卷 1413-1429,M0004页

作者：秦伟伟翁建平 Department of endocrinology Institute of Endocrine and Metabolic DiseasesThe First Affiliated Hospital of USTCDivision of Life Sciences and MedicineClinical Research Hospital of Chinese Academy of Sciences(Hefei)University of Science and Technology of ChinaHefei 230027China

肝脏胰岛素抵抗(IR)是非酒精性脂肪性肝病(NAFLD)的重要特征之一,与肝脏脂肪变性密切相关.肝脏IR发病机制仍不清楚,本研究通过转录组学筛选鉴定到肝细胞NLRP3是肝脏IR的重要诱导因子,进一步证实其在人和小鼠NAFLD模型肝脏组织中表达增加... 详细信息

肝脏胰岛素抵抗(IR)是非酒精性脂肪性肝病(NAFLD)的重要特征之一,与肝脏脂肪变性密切相关.肝脏IR发病机制仍不清楚,本研究通过转录组学筛选鉴定到肝细胞NLRP3是肝脏IR的重要诱导因子,进一步证实其在人和小鼠NAFLD模型肝脏组织中表达增加.功能方面,肝细胞特异性NLRP3功能丧失或获得分别改善或加重高脂饮食(HFD)诱导的肝脏IR及脂肪变性.机制方面,NLRP3直接结合并促进蛋白激酶C蛋白(PKCs)的激活,从而损害胰岛素信号通路和增加肝脏脂肪变性;相反,抑制PKCe明显阻断HFD诱导的NLRP3缺陷小鼠的有益作用.此外,研究筛选发现转录因子阴阳1(YY1)调控NLRP3启动子.治疗方面,腺相关病毒血清型8介导的肝脏NLRP3敲低减轻瘦素受体缺陷(db/db)小鼠的肝脏IR和脂肪变性.同时,药理抑制NLRP3显著减轻饮食诱导的代谢紊乱.综上,本研究揭示了肝细胞NLRP3是肝脏IR和脂肪变性的直接驱动因素,并提示YY1-NLRP3-PKCε轴为NAFLD的潜在治疗靶点.

关键词： NLRP3 Hepatic IR NAFLD PKCε

Pharmacologic adjunctive to insulin therapies in type 1 diabetes:The journey has just begun

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World Journal of Diabetes 2019年第4期10卷 234-240页

作者： Spyridon N Karras Theocharis Koufakis Pantelis Zebekakis Kalliopi Kotsa division of endocrinology and Metabolism and Diabetes Center First Department of Internal MedicineMedical School Aristotle University of Thessaloniki AHEPA University Hospital

Treatment of type 1 diabetes(T1 D) is currently based exclusively on insulin replacement therapy. However, there is a need for better glycemic control, lower hypoglycemia rates, more effective weight management, and further reduction of cardiovascular risk in people with T1 D. In this context, agents from the pharmaceutical quiver of type 2 diabetes are being tested in clinical trials, as adjunctive to insulin therapies for T1 D patients. Despite the limited amount of relevant evidence and the inter-class variability, it can be said that these agents have a role in optimizing metabolic control, assisting weight management and reducing glycemic variability in people with T1 D. Specific safety issues, including the increased risk of hypoglycemia and diabetic ketoacidosis, as well as the effects of these treatments on major cardiovascular outcomes should be further assessed by future studies, before these therapeutic choices become widely available for T1 D management.

关键词： Type 1 diabetes Insulin Adjunctive therapies Cardiovascular risk

Newly discovered endocrine functions of the liver

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World Journal of Hepatology 2021年第11期13卷 1611-1628页

作者： Jane Rhyu Run Yu division of endocrinology Diabetesand MetabolismUCLA David Geffen School of MedicineLos AngelesCA 90095United States

The liver,the largest solid visceral organ of the body,has numerous endocrine functions,such as direct hormone and hepatokine production,hormone metabolism,synthesis of binding proteins,and processing and redistribution of metabolic fuels.In the last 10 years,many new endocrine functions of the liver have been discovered.Advances in the classical endocrine functions include delineation of mechanisms of liver production of endocrine hormones[including 25-hydroxyvitamin D,insulin-like growth factor 1(IGF-1),and angiotensinogen],hepatic metabolism of hormones(including thyroid hormones,glucagon-like peptide-1,and steroid hormones),and actions of specific binding proteins to glucocorticoids,sex steroids,and thyroid hormones.These studies have furthered insight into cirrhosis-associated endocrinopathies,such as hypogonadism,osteoporosis,IGF-1 deficiency,vitamin D deficiency,alterations in glucose and lipid homeostasis,and controversially relative adrenal insufficiency.Several novel endocrine functions of the liver have also been unraveled,elucidating the liver’s key negative feedback regulatory role in the pancreaticαcell-liver axis,which regulates pancreaticαcell mass,glucagon secretion,and circulating amino acid levels.Betatrophin and other hepatokines,such as fetuin-A and fibroblast growth factor 21,have also been discovered to play important endocrine roles in modulating insulin sensitivity,lipid metabolism,and body weight.It is expected that more endocrine functions of the liver will be revealed in the near future.

关键词： Liver Endocrine function Hormone Amino acids Hepatokine Fibroblast growth factor 21

Improving Cardiovascular Risk Assessment to Optimize Therapy

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World Journal of Cardiovascular Diseases 2023年第1期13卷 7-20页

作者： Allen Adolphe Shane Wilder Teodor Duro Robert Philip Eaton David S. Schade division of General Internal Medicine University of New Mexico School of Medicine Albuquerque USA division of endocrinology University of New Mexico School of Medicine Albuquerque USA

Background: Quantifying ten-year cardiovascular risk can be challenging. Different online risk calculators provide different risk estimates and online risk calculators use only one point in time. However, risk factors occur over the lifetime of the individual. Purpose: This manuscript provides three solutions to improving ten-year cardiovascular risk assessment in individuals at intermediate risk. Methods: Measuring Lipoprotein(a)—Lp(a) is recommended for assessing cardiovascular risk in all individuals who are in the intermediate risk category by standard online risk calculators. Lp(a) is primarily determined by genetic inheritance. It has the undesirable properties of being proatherosclerotic, proinflammatory, and prothrombotic. Measuring apolipoprotein B (apo B) provides a good index of the number of atherosclerotic particles present. Studies have demonstrated that small, dense LDL cholesterol particles are more atherogenic than larger, less dense LDL cholesterol particles. Measuring high sensitivity C-reactive protein (hsCRP) provides a good estimation of the degree of inflammation in the vascular system. Inflammation is a critical component of heart attacks and strokes. It is increased in diabetes and obesity. Treatment to reduce inflammation results in a reduction of cardiovascular events, independent of lipid values. Results: The above three risk factors should be measured in all patients with an intermediate risk score. Routine assays are readily available at a reasonable cost. They are independent risk factors for cardiovascular disease. Their recommendation is based on the pathophysiology of atherosclerotic cardiovascular disease. Successful therapy will result in the decrease of each of these risk factors. Conclusion: The recommended approach will improve the assessment of cardiovascular risk and guide the physician and patient to the correct treatment recommendations.

关键词： Cardiovascular Disease Atherosclerosis Risk Equations Apolipoprotein B Lipoprotein(a) High Sensitivity C-Reactive Protein