Islets最新文献_第4页

Impacts of the COVID-19 pandemic on a human research islet program. COVID-19大流行对人类研究岛计划的影响

IF 1.9 4区医学

Islets Pub Date : 2022-12-31 DOI: 10.1080/19382014.2022.2047571

Tina J Dafoe, Theodore Dos Santos, Aliya F Spigelman, James Lyon, Nancy Smith, Austin Bautista, Patrick E MacDonald, Jocelyn E Manning Fox

{"title":"Impacts of the COVID-19 pandemic on a human research islet program.","authors":"Tina J Dafoe, Theodore Dos Santos, Aliya F Spigelman, James Lyon, Nancy Smith, Austin Bautista, Patrick E MacDonald, Jocelyn E Manning Fox","doi":"10.1080/19382014.2022.2047571","DOIUrl":"10.1080/19382014.2022.2047571","url":null,"abstract":"Designated a pandemic in March 2020, the spread of severe acute respiratory syndrome virus 2 (SARS-CoV2), the virus responsible for coronavirus disease 2019 (COVID-19), led to new guidelines and restrictions being implemented for individuals, businesses, and societies in efforts to limit the impacts of COVID-19 on personal health and healthcare systems. Here we report the impacts of the COVID-19 pandemic on pancreas processing and islet isolation/distribution outcomes at the Alberta Diabetes Institute IsletCore, a facility specializing in the processing and distribution of human pancreatic islets for research. While the number of organs processed was significantly reduced, organ quality and the function of cellular outputs were minimally impacted during the pandemic when compared to an equivalent period immediately prior. Despite the maintained quality of isolated islets, feedback from recipient groups was more negative. Our findings suggest this is likely due to disrupted distribution which led to increased transit times to recipient labs, particularly those overseas. Thus, to improve overall outcomes in a climate of limited research islet supply, prioritization of tissue recipients based on likely tissue transit times may be needed.","PeriodicalId":14671,"journal":{"name":"Islets","volume":"14 1","pages":"101-113"},"PeriodicalIF":1.9,"publicationDate":"2022-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8928860/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41757250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

LDB1-mediated transcriptional complexes are sensitive to islet stress. ldb1介导的转录复合物对胰岛应激敏感。

IF 2.2 4区医学

Islets Pub Date : 2022-12-31 DOI: 10.1080/19382014.2021.2016028

Yanping Liu, Jessica D Kepple, Anath Shalev, Chad S Hunter

{"title":"LDB1-mediated transcriptional complexes are sensitive to islet stress.","authors":"Yanping Liu, Jessica D Kepple, Anath Shalev, Chad S Hunter","doi":"10.1080/19382014.2021.2016028","DOIUrl":"https://doi.org/10.1080/19382014.2021.2016028","url":null,"abstract":"Excess nutrients and proinflammatory cytokines impart stresses on pancreatic islet β-cells that, if unchecked, can lead to cellular dysfunction and/or death. Among these stress-induced effects is loss of key β-cell transcriptional regulator mRNA and protein levels required for β-cell function. Previously, our lab and others reported that LIM-domain complexes comprised the LDB1 transcriptional co-regulator and Islet-1 (ISL1) transcription factor are required for islet β-cell development, maturation, and function. The LDB1:ISL1 complex directly occupies and regulates key β-cell genes, including MafA, Pdx1, and Slc2a2, to maintain β-cell identity and function. Given the importance of LDB1:ISL1 complexes, we hypothesized that LDB1 and/or ISL1 levels, like other transcriptional regulators, are sensitive to β-cell nutrient and cytokine stresses, likely contributing to β-cell (dys)function under various stimuli. We tested this by treating β-cell lines or primary mouse islets with elevating glucose concentrations, palmitate, or a cytokine cocktail of IL-1β, TNFα, and IFNγ. We indeed observed that LDB1 mRNA and/or protein levels were reduced upon palmitate and cytokine (cocktail or singly) incubation. Conversely, acute high glucose treatment of β-cells did not impair LDB1 or ISL1 levels, but increased LDB1:ISL1 interactions. These observations suggest that LDB1:ISL1 complex formation is sensitive to β-cell stresses and that targeting and/or stabilizing this complex may rescue lost β-cell gene expression to preserve cellular function.","PeriodicalId":14671,"journal":{"name":"Islets","volume":" ","pages":"58-68"},"PeriodicalIF":2.2,"publicationDate":"2022-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8726731/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39772829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Dual regulation of miR-375 and CREM genes in pancreatic beta cells 胰腺β细胞中miR-375和CREM基因的双重调控

IF 2.2 4区医学

Islets Pub Date : 2022-04-04 DOI: 10.1080/19382014.2022.2060688

D. Keller, Isis G. Perez

引用次数: 0

Modeling type 2 diabetes in rats by administering tacrolimus 他克莫司对大鼠2型糖尿病的影响

IF 2.2 4区医学

Islets Pub Date : 2022-03-29 DOI: 10.1080/19382014.2022.2051991

J. C. Quintana-Pérez, F. García-Dolores, A. S. Valdez-Guerrero, Diana Alemán-González-Duhart, M. Arellano-Mendoza, S. Rojas Hernández, I. Olivares-Corichi, J. R. García Sánchez, J. T. Trujillo Ferrara, F. Tamay-Cach

{"title":"Modeling type 2 diabetes in rats by administering tacrolimus","authors":"J. C. Quintana-Pérez, F. García-Dolores, A. S. Valdez-Guerrero, Diana Alemán-González-Duhart, M. Arellano-Mendoza, S. Rojas Hernández, I. Olivares-Corichi, J. R. García Sánchez, J. T. Trujillo Ferrara, F. Tamay-Cach","doi":"10.1080/19382014.2022.2051991","DOIUrl":"https://doi.org/10.1080/19382014.2022.2051991","url":null,"abstract":"ABSTRACT The prevalence of diabetes is rapidly increasing. The current number of diagnosed cases is ~422 million, expected to reach ~640 million by 2040. Type 2 diabetes, which constitutes ~95% of the cases, is characterized by insulin resistance and a progressive loss of β-cell function. Despite intense research efforts, no treatments are yet able to cure the disease or halt its progression. Since all existing animal models of type 2 diabetes have serious drawbacks, one is needed that represents the complete pathogenesis, is low cost and non-obese, and can be developed relatively quickly. The aim of this study was to evaluate a low-cost, non-obese model of type 2 diabetes engendered by administering a daily high dose of tacrolimus (an immunosuppressant) to Wistar rats for 4 weeks. The biochemical and antioxidant markers were measured at basal and after the 4-week tacrolimus treatment. At week 4, the values of these parameters closely resembled those observed in human type 2 diabetes, including fasting blood glucose at 141.5 mg/dL, blood glucose greater than 200 mg/dL at 120 min of the glucose tolerance test, blood glucose at varied levels in the insulin tolerance test, and elevated levels of cholesterol and triglyceride. The tacrolimus treatment produced hypoinsulinemia and sustained hyperglycemia, probably explained by the alteration found in pancreatic β-cell function and morphology. This model should certainly be instrumental for evaluating possible type 2 diabetes treatments, and for designing new immunosuppressants that do not cause pancreatic damage, type 2 diabetes, or new-onset diabetes after transplantation (NODAT).","PeriodicalId":14671,"journal":{"name":"Islets","volume":"14 1","pages":"114 - 127"},"PeriodicalIF":2.2,"publicationDate":"2022-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45875558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Determinants and dynamics of pancreatic islet architecture 胰岛结构的决定因素和动力学

IF 2.2 4区医学

Islets Pub Date : 2022-03-08 DOI: 10.1080/19382014.2022.2030649

Melissa T. Adams, B. Blum

引用次数: 15

Comparative analysis of reconstructed architectures from mice and human islets. 小鼠与人胰岛重构结构的比较分析。

IF 2.2 4区医学

Islets Pub Date : 2022-01-01 DOI: 10.1080/19382014.2021.1987827

Gerardo J Félix-Martínez, J R Godínez-Fernández

引用次数: 4

Identification of protease serine S1 family member 53 as a mitochondrial protein in murine islet beta cells. 小鼠胰岛β细胞中蛋白酶丝氨酸S1家族成员53作为线粒体蛋白的鉴定。

IF 2.2 4区医学

Islets Pub Date : 2022-01-01 Epub Date: 2021-10-12 DOI: 10.1080/19382014.2021.1982325

Noriko Mizusawa, Nagakatsu Harada, Takeo Iwata, Izumi Ohigashi, Mitsuo Itakura, Katsuhiko Yoshimoto

{"title":"Identification of protease serine S1 family member 53 as a mitochondrial protein in murine islet beta cells.","authors":"Noriko Mizusawa, Nagakatsu Harada, Takeo Iwata, Izumi Ohigashi, Mitsuo Itakura, Katsuhiko Yoshimoto","doi":"10.1080/19382014.2021.1982325","DOIUrl":"https://doi.org/10.1080/19382014.2021.1982325","url":null,"abstract":"The aim of this study was to identify genes that are specifically expressed in pancreatic islet β-cells (hereafter referred to as β-cells). Large-scale complementary DNA-sequencing analysis was performed for 3,429 expressed sequence tags derived from murine MIN6 β-cells, through homology comparisons using the GenBank database. Three individual ESTs were found to code for protease serine S1 family member 53 (Prss53). Prss53 mRNA is processed into both a short and long form, which encode 482 and 552 amino acids, respectively. Transient overexpression of myc-tagged Prss53 in COS-7 cells showed that Prss53 was strongly associated with the luminal surfaces of organellar membranes and that it underwent signal peptide cleavage and N-glycosylation. Immunoelectron microscopy and western blotting revealed that Prss53 localized to mitochondria in MIN6 cells. Short hairpin RNA-mediated Prss53 knockdown resulted in Ppargc1a downregulation and Ucp2 and Glut2 upregulation. JC-1 staining revealed that the mitochondria were depolarized in Prss53-knockdown MIN6 cells; however, no change was observed in glucose-stimulated insulin secretion. Our results suggest that mitochondrial Prss53 expression plays an important role in maintaining the health of β-cells.","PeriodicalId":14671,"journal":{"name":"Islets","volume":" ","pages":"1-13"},"PeriodicalIF":2.2,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a6/f0/KISL_14_1982325.PMC8812782.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39510073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

IsletLab: an application to reconstruct and analyze islet architectures. IsletLab:一个用于重建和分析岛屿结构的应用程序。

IF 2.2 4区医学

Islets Pub Date : 2022-01-01 DOI: 10.1080/19382014.2021.2008742

Gerardo J Félix-Martínez

引用次数: 2

Vesiculin derived from IGF-II drives increased islet cell mass in a mouse model of pre-diabetes. 来源于IGF-II的Vesiculin在糖尿病前期小鼠模型中驱动胰岛细胞质量增加。

IF 2.2 4区医学

Islets Pub Date : 2022-01-01 DOI: 10.1080/19382014.2021.1982326

Kate L Lee, Jacqueline F Aitken, Xun Li, Kirsten Montgomery, Huai-L Hsu, Geoffrey M Williams, Margaret A Brimble, Garth J S Cooper

{"title":"Vesiculin derived from IGF-II drives increased islet cell mass in a mouse model of pre-diabetes.","authors":"Kate L Lee, Jacqueline F Aitken, Xun Li, Kirsten Montgomery, Huai-L Hsu, Geoffrey M Williams, Margaret A Brimble, Garth J S Cooper","doi":"10.1080/19382014.2021.1982326","DOIUrl":"https://doi.org/10.1080/19382014.2021.1982326","url":null,"abstract":"Pancreatic islet-cell function and volume are both key determinants of the maintenance of metabolic health. Insulin resistance and islet-cell dysfunction often occur in the earlier stages of type 2 diabetes (T2D) progression. The ability of the islet cells to respond to insulin resistance by increasing hormone output accompanied by increased islet-cell volume is key to maintaining blood glucose control and preventing further disease progression. Eventual β-cell loss is the main driver of full-blown T2D and insulin-dependency. Researchers are targeting T2D with approaches that include those aimed at enhancing the function of the patient's existing β-cell population, or replacing islet β-cells. Another approach is to look for agents that enhance the natural capacity of the β-cell population to expand. Here we aimed to study the effects of a new putative β-cell growth factor on a mouse model of pre-diabetes. We asked whether: 1) 4-week's treatment with vesiculin, a two-chain peptide derived by processing from IGF-II, had any measurable effect on pre-diabetic mice vs vehicle; and 2) whether the effects were the same in non-diabetic littermate controls. Although treatment with vesiculin did not alter blood glucose levels over this time period, there was a doubling of the Proliferating Cell Nuclear Antigen (PCNA) detectable in the islets of treated pre-diabetic but not control mice and this was accompanied by increased insulin- and glucagon-positive stained areas in the pancreatic islets.","PeriodicalId":14671,"journal":{"name":"Islets","volume":"14 1","pages":"14-22"},"PeriodicalIF":2.2,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/33/83/KISL_14_1982326.PMC8632304.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10379915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

An overview of current advancements in pancreatic islet transplantation into the omentum. 胰岛移植到网膜的最新进展概述。

IF 2.2 4区医学

Islets Pub Date : 2021-09-03 Epub Date: 2021-08-17 DOI: 10.1080/19382014.2021.1954459

Kimia Damyar, Vesta Farahmand, David Whaley, Michael Alexander, Jonathan R T Lakey

引用次数: 0