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insulin

insulin的相关文献在1992年到2023年内共计453篇,主要集中在内科学、肿瘤学、基础医学 等领域,其中期刊论文441篇、会议论文2篇、专利文献10篇;相关期刊104种,包括世界胃肠病学杂志:英文版、健康(英文)、临床医学国际期刊(英文)等; 相关会议2种,包括中华医学会北京分会2010年北京市病理技术年会暨北京市病理技术第三次学术研讨会、中国畜牧兽医学会2008年学术年会暨第一届中国兽医临床大会等;insulin的相关文献由1678位作者贡献,包括Ikuo Yokoyama、Christian Carpéné、Jean Marie Ntaganda等。

insulin—发文量

期刊论文>

论文:441 占比:97.35%

会议论文>

论文:2 占比:0.44%

专利文献>

论文:10 占比:2.21%

总计:453篇

insulin—发文趋势图

insulin

-研究学者

  • Ikuo Yokoyama
  • Christian Carpéné
  • Jean Marie Ntaganda
  • Toshiyuki Moritan
  • Yusuke Inoue
  • Alberto Krayyem Arbex
  • Guo-Xun Chen
  • Henk JG Bilo
  • Mario Ciampolini
  • Moses S Elisaf
  • 期刊论文
  • 会议论文
  • 专利文献

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    • Stuti Pandey; Pawan Kumar Pandey; Alakh Niranjan Sahu; Himanshu Verma; Manmath Kumar Nandi
    • 摘要: Background:The prime objective of the current research was to evaluate the whole plant hydroalcoholic extract of Ludwigia octovalvis(HLO)against hyperglycemia,and oxidative stress biomarkers in rats induced with diabetes comorbid depression,diabetes comorbid depression(streptozotocin-nicotinamide+electric footshocks).Methods:2,2-Diphenyl-1-picrylhydrazyl assay of HLO versus ascorbic acid was done.Effects of 200 and 400 mg/kg body weight/day HLO doses versus 25 mg/kg body weight/day metformin was studied through insulin,glucose,superoxide dismutase,lipid peroxidation,catalase,and behavioral assessment(forced swim and open field tests).Results:IC50 values of HLO and ascorbic acid were 33.52 and 27.86μg/mL respectively.Both the HLO doses showed intended results with respect to oxidative stress biomarkers in diabetes comorbid depression rats in comparison to metformin.Open field test showed better results for HLO in diabetes comorbid depression rats.However,hypoglycemic effects,and forced swim test performance of metformin was slightly higher than the 400 mg dose,followed by the 200 mg dose of HLO.Ethyl gallate,gallic acid,β-sitosterol,and quercetin in HLO might resulted in attenuating diabetic as well as depression biomarkers.Conclusion:Inhibition of glucosidase and lipase activity,and AMP-activated protein kinase phosphorylation might be the possible biochemical changes occurred in HLO treated rats.
    • Pamela K Xaverius; Steven W Howard; Deborah Kiel; Jerry E Thurman; Ethan Wankum; Catherine Carter; Clairy Fang; Romi Carriere
    • 摘要: BACKGROUND Diabetes rates among pregnant women in the United States have been increasing and are associated with adverse pregnancy outcomes.AIM To investigate differences in birth outcomes(preterm birth,macrosomia,and neonatal death)by diabetes status.METHODS Cross-sectional design,using linked Missouri birth and death certificates(singleton births only),2010 to 2012(n=204057).Exposure was diabetes non-diabetic,pre-pregnancy diabetes-insulin dependent(PD-I),pre-pregnancy diabetes-non-insulin dependent(PD-NI),gestational diabetes-insulin dependent(GD-I),and gestational diabetes-non-insulin dependent(GD-NI).Outcomes included preterm birth,macrosomia,and infant mortality.Confounders included demographic characteristics,adequacy of prenatal care,body mass index,smoking,hypertension,and previous preterm birth.Bivariate and multivariate logistic regression assessed differences in outcomes by diabetes status.RESULTS Women with PD-I,PD-NI,and GD-I remained at a significantly increased odds for preterm birth(aOR 2.87,aOR 1.77,and aOR 1.73,respectively)and having a very large baby[macrosomia](aOR 3.01,aOR 2.12,and aOR 1.96,respectively);in reference to non-diabetic women.Women with GDNI were at a significantly increased risk for macrosomia(aOR1.53),decreased risk for their baby to die before their first birthday(aOR 0.41)and no difference in risk for preterm birth in reference to non-diabetic women.CONCLUSION Diabetes is associated with the poor birth outcomes.Clinical management of diabetes during pregnancy and healthy lifestyle behaviors before pregnancy can reduce the risk for diabetes and poor birth outcomes.
    • Chi B.Ahn; Ji-Hyun Lee; Joo H.Kim; Tae H.Kim; Hee-Sook Jun; Kuk H.Son; Jin W.Lee
    • 摘要: Type 1 diabetes is caused by insulin deficiency due to the loss of beta cells in the islets of Langerhans.In severe cases,islet transplantation into the portal vein is performed.However,due to the loss of transplanted islets and the failure of islet function,the 5-year insulin independence rate of these patients is<50%.In this study,we developed a long-term,insulin-secreting,3 Dbioprinted construct implanted subcutaneously with the aim of preventing islet loss.The bioprinted construct was fabricated by the multi-layer bioprinting of beta-cell(mouse insulinoma-6:MIN-6)-encapsulated alginate bioink and poly(caprolactone)biodegradable polymer.A glucose response assay revealed that the bioprinted constructs proliferated and released insulin normally during the 4-week in vitro period.Bioprinted MIN-6 generated clusters with a diameter of 100-200μm,similar to the original pancreatic islets in the construct.In an in vivo study using type 1 diabetes mice,animals implanted with bioprinted constructs showed three times higher insulin secretion and controlled glucose levels at 8 weeks after implantation.Because the implanted,bioprinted constructs had a positive effect on insulin secretion in the experimental animals,the survival rate of the implanted group(75%)was three times higher than that of the non-implanted group(25%).The results suggest that the proposed,3 D-bioprinted,subcutaneous construct can be a better alternative to portal vein islet transplantation.
    • Christian Carpéné; Nathalie Boulet; Jean-Louis Grolleau; Nathalie Morin
    • 摘要: BACKGROUND When combined with vanadium salts,catecholamines strongly activate glucose uptake in rat and mouse adipocytes.AIM To test whether catecholamines activate glucose transport in human adipocytes.METHODS The uptake of 2-deoxyglucose(2-DG)was measured in adipocytes isolated from pieces of abdominal subcutaneous tissue removed from women undergoing reconstructive surgery.Pharmacological approaches with amine oxidase inhibitors,adrenoreceptor agonists and antioxidants were performed to unravel the mechanisms of action of noradrenaline or adrenaline(also named epinephrine).RESULTS In human adipocytes,45-min incubation with 100μmol/L adrenaline or noradrenaline activated 2-DG uptake up to more than one-third of the maximal response to insulin.This stimulation was not reproduced with millimolar doses of dopamine or serotonin and was not enhanced by addition of vanadate to the incubation medium.Among various natural amines and adrenergic agonists tested,no other molecule was more efficient than adrenaline and noradrenaline in stimulating 2-DG uptake.The effect of the catecholamines was not impaired by pargyline and semicarbazide,contrarily to that of benzylamine or methylamine,which are recognized substrates of semicarbazide-sensitive amine oxidase.Hydrogen peroxide at 1 mmol/L activated hexose uptake but not pyrocatechol or benzoquinone,and only the former was potentiated by vanadate.Catalase and the phosphoinositide 3-kinase inhibitor wortmannin inhibited adrenaline-induced activation of 2-DG uptake.CONCLUSION High doses of catecholamines exert insulin-like actions on glucose transport in human adipocytes.At submillimolar doses,vanadium did not enhance this catecholamine activation of glucose transport.Consequently,this dismantles our previous suggestion to combine the metal ion with catecholamines to improve the benefit/risk ratio of vanadium-based antidiabetic approaches.
    • Genaro G Ortiz; Miguel Huerta; Héctor A González-Usigli; Erandis D Torres-Sánchez; Daniela LC Delgado-Lara; Fermín P Pacheco-Moisés; Mario A Mireles-Ramírez; Blanca MG Torres-Mendoza; Roxana I Moreno-Cih; Irma E Velázquez-Brizuela
    • 摘要: Insulin,a key pleiotropic hormone,regulates metabolism through several signaling pathways in target tissues including skeletal muscle,liver,and brain.In the brain,insulin modulates learning and memory,and impaired insulin signaling is associated with metabolic dysregulation and neurodegenerative diseases.At the receptor level,in aging and Alzheimer’s disease(AD)models,the amount of insulin receptors and their functions are decreased.Clinical and animal model studies suggest that memory improvements are due to changes in insulin levels.Furthermore,diabetes mellitus(DM)and insulin resistance are associated with age-related cognitive decline,increased levels ofβ-amyloid peptide,phosphorylation of tau protein;oxidative stress,pro-inflammatory cytokine production and dyslipidemia. Recent evidence shows that deleting brain insulin receptors leads to mildobesity and insulin resistance without influencing brain size and apoptosis development.Conversely, deleting insulin-like growth factor 1 receptor (IGF-1R) affects brain size anddevelopment, and contributes to behavior changes. Insulin is synthesized locally in the brain andis released from the neurons. Here, we reviewed proposed pathophysiological hypotheses toexplain increased risk of dementia in the presence of DM. Regardless of the exact sequence ofevents leading to neurodegeneration, there is strong evidence that mitochondrial dysfunctionplays a key role in AD and DM. A triple transgenic mouse model of AD showed mitochondrialdysfunction, oxidative stress, and loss of synaptic integrity. These alterations are comparable tothose induced in wild-type mice treated with sucrose, which is consistent with the proposal thatmitochondrial alterations are associated with DM and contribute to AD development. Alterationsin insulin/IGF-1 signaling in DM could lead to mitochondrial dysfunction and low antioxidantcapacity of the cell. Thus, insulin/IGF-1 signaling is important for increased neural processing andsystemic metabolism, and could be a specific target for therapeutic strategies to decreasealterations associated with age-related cognitive decline.
    • Tian-Nan Wang; Xin-Ge Hu; Guo-Xun Chen
    • 摘要: Currently,glucose transporter 4(GLUT4)has been considered as the key player for the insulin-stimulated glucose transport in the muscle and adipose tissues.The development of recombinant DNA techniques allows the creations of genetically knockout,knockdown and transgenic animals and cells for the study of GLUT4’s physiological functions.Here,we have used key words to search the PubMed and summarized the methods used in Slc2a4 gene knockout,GLUT4 knockdown and overexpression in the whole body and tissue specific manner.The whole body GLUT4-null mice have growth retardation,but normal glucose tolerance and basal glucose turnover rates.Compared with whole body Slc2a4 knockout mice,adipose and muscle double knockout mice have impaired insulin tolerance and glucose intolerance.The results of GLUT4 knockdown in 3T3-L1 adipocytes have shown that its expression is needed for lipogenesis after,but not during,differentiation.Transgenic mice with the whole body GLUT4 overexpression have normal body weight and lowered blood glucose level.The adipose tissue specific overexpression of GLUT4 leads to increases in mouse body weight and adipose tissue weight.The insulin-stimulated GLUT4 translocation in the skeletal muscle contributes to the regulation of glucose homeostasis.Data from both transgenic overexpression and tissue specific Slc2a4 knockout indicate that GLUT4 probably plays a role in the glucose uptake in the fasting state.More studies are warranted to use advanced molecular biology tools to decipher the roles of GLUT4 in the control of glucose homeostasis.
    • Ching-Chung Liang; Steven W Shaw; Yung-Hsin Huang; Tsong-Hai Lee
    • 摘要: BACKGROUND Diabetes mellitus(DM)is a serious and growing global health burden.It is estimated that 80%of diabetic patients have micturition problems such as poor emptying,urinary incontinence,urgency,and urgency incontinence.Patients with diabetic bladder dysfunction are often resistant to currently available therapies.It is necessary to develop new and effective treatment methods.AIM To examine the therapeutic effect of human amniotic fluid stem cells(hAFSCs)therapy on bladder dysfunction in a type 2 diabetic rat model.METHODS Sixty female Sprague-Dawley rats were divided into five groups:Group 1,normal-diet control(control);group 2,high-fat diet(HFD);group 3,HFD plus streptozotocin-induced DM(DM);group 4,DM plus insulin treatment(DM+insulin);group 5,DM plus hAFSCs injection via tail vein(DM+hAFSCs).Conscious cystometric studies were done at 4 and 12 wk after insulin or hAFSCs treatment to measure peak voiding pressure,voided volume,intercontraction interval,bladder capacity,and residual volume.Immunoreactivities and/or mRNA expression of muscarinic receptors,nerve growth factor(NGF),and sensory nerve markers in the bladder and insulin,MafA,and pancreatic-duodenal homeobox-1(PDX-1)in pancreatic beta cells were studied.RESULTS Compared with DM rats,insulin but not hAFSCs treatment could reduce the bladder weight and improve the voided volume,intercontraction interval,bladder capacity,and residual volume(P0.05).The immunoreactivities and mRNA expression of M2-and M3-muscarinic receptors(M2 and M3)were increased mainly at 4 wk(P0.05).CONCLUSION Insulin but not hAFSCs therapy can recover the bladder dysfunction caused by DM;however,hAFSCs and insulin therapy can help to regain bladder function to near the levels of control.
    • Fidan Huseynova; Alamdar Mammadov; Irada Huseynova; Frédéric Cuisinier; Véronique Barragan-Montero
    • 摘要: Insulin, an old but still actual molecule, has many roles in various cellular processes including bone formation and also angiogenesis. Insulin effects on different cell types were investigated, and we intended to check its effect on dental pulp cells (DPC) during osteoblast differentiation. First, bone differentiation ability of isolated dental pulp cells was assessed by alizarin red (AR) staining. Insulin increased dental pulp cell proliferation after 25 hours of culture. It increased mRNA expression of osteogenic markers such as Col1, RunX2, ALP, Osc, Mef2C and expression of genes involved in TGF b pathway such as Smad3, TSP1, VEGF at different time points.
    • Efterpi Mougakou; Maria Kyziroglou; Alexandra Tsankof; Evangelos Cholongitas; Konstantinos Tziomalos
    • 摘要: Diabetes mellitus(DM)is an independent risk factor for admission to intensive care unit and death in patients with coronavirus disease 2019(COVID-19).On the other hand,medications used in the management of COVID-19 are potentially associated with increases in blood glucose levels and a higher incidence of infections.Accordingly,care of patients with DM and acute COVID-19 requires careful consideration of both diseases.Hyperglycemia and hypoglycemia are associated with adverse outcomes and therefore frequent measurement of blood glucose levels and a basal-bolus insulin regimen are required in most patients.Regarding the management of COVID-19,dexamethasone increases blood glucose levels and might also increase the risk for infections.On the other hand,limited data suggest that antiviral and immunomodulatory agents used in COVID-19 are not strongly associated with higher incidence of infections in this population.As knowledge evolves in this field,optimization of the management of both DM and COVID-19 will hopefully improve the outcome of these patients。
    • 夏训明(编译)
    • 摘要: 美国FDA于2021年7月28日批准了一种胰岛素生物仿制药(biosimilar)Semglee(insulin glargine-yfgn,甘精胰岛素-yfgn),可用于成人和儿童治疗1型糖尿病,也可用于成人治疗2型糖尿病。Semglee的仿制对象是Lantus(insulin glargine,甘精胰岛素,一种长效胰岛素类似物),并且可以与Lantus相互替代。Semglee也是FDA批准的第一种可与仿制对象相互替代的胰岛素类生物仿制药产品。
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