Tesis sobre el tema "Insulin receptor gene"
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Gletsu, Nana Adwoa. "Insulin receptor translocation to the hepatocyte nucleus, regulation of gene expression". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ29039.pdf.
Texto completoPatel, Dhaval Subhas. "Analysis of the daf-2 insulin/igf-1 receptor gene in Caenorhabditis elegans". Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445066/.
Texto completoGriffiths, Matthew Rhodri. "Analysis of signal transduction pathways involved in the activation of gene transcription by the insulin receptor". Thesis, University of Bristol, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265456.
Texto completoTsukumo, Daniela Miti Lemos 1976. "Mutação inativadora do TLR4 protege contra a obesidade e a restencia a insulina induzidas por dieta hiperlipidica". [s.n.], 2008. http://repositorio.unicamp.br/jspui/handle/REPOSIP/311220.
Texto completoTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: Estudos recentes demonstram que a obesidade está associada com a resistência à insulina e com um estado de inflamação crônica subclínica. Os ¿Toll-Like Receptors¿ (TLRs) têm um papel fundamental na ativação do sistema imune através do reconhecimento de antígenos de microorganismos. O TLR4 é um subtipo de TLRs que é ativado pelo lipopolissacarídeo de bactérias gram-negativas e por outros agonistas, como os ácidos graxos saturados. A ativação do TLR4 estimula vias inflamatórias relacionadas à indução de resistência à insulina, como a JNK e a IKKß. Neste estudo, demonstrou-se que camundongos C3H/HeJ, que apresentam uma mutação inativadora do TLR4, estão protegidos da obesidade e da resistência à insulina induzidas por dieta hiperlipídica. Além disso, músculos sóleos isolados de camundongos C3H/HeJ estão protegidos da resistência à insulina induzida por ácidos graxos. Camundongos C3H/HeJ tratados com dieta hiperlipídica (DH) apresentam um menor ganho de peso, maior tolerância à glicose e maior sensibilidade à insulina em relação aos controles em DH. A análise morfométrica do tecido adiposo evidenciou que os adipócitos dos camundongos C3H/HeJ em DH são 30% menores em relação aos adipócitos dos camundongos controle tratados com a mesma dieta. Foi evidenciada uma maior fosforilação em tirosina do IRS-1 e maior fosforilação da Akt, após estímulo com insulina, em músculo, tecido adiposo e fígado de camundongos C3H/HeJ tratados com DH em relação aos controles. Observou-se uma maior ativação da JNK, da IKKß e da iNOS em músculo, tecido adiposo e fígado de animais controle tratados com DH quando comparado com camundongos C3H/HeJ tratados com a mesma dieta. O tratamento com palmitato reduziu a captação de glicose e a síntese de glicogênio em 40-50% em músculo sóleo isolado de camundongos controle, mas este efeito não foi observado em músculo sóleo isolado de camundongos C3H/HeJ. Em resumo, o nosso estudo demonstra que a inativação do TLR4 previne a obesidade induzida por dieta, a ativação da IKKß, da JNK, a resistência à insulina em camundongos em DH, além da resistência à insulina induzida por palmitato em músculo isolado. O estudo sugere que o TLR4 tem um papel importante na interligação entre o sistema imune inato e a resistência à insulina, sendo um possível alvo terapêutico para a obesidade, resistência à insulina e diabetes mellitus tipo 2
Abstract: Obesity is associated with insulin resistance and a state of abnormal inflammatory response. The Toll-like receptor 4 (TLR4) has an important role in inflammation and immunity and its expression has been reported in most tissues of the body, including the insulin-sensitive ones. Since it is activated by lipopolysaccharide (LPS) and saturated fatty acids, which are inducers of insulin resistance, TLR4 may be a candidate for participation in the cross-talk between inflammatory and metabolic signals. Here, we show that C3H/HeJ mice, which have a loss-of-function mutation in TLR4, are protected against the development of diet-induced obesity. In addition, these mice demonstrate decreased adiposity, increased oxygen consumption, a decreased respiratory exchange ratio, improved insulin sensitivity and enhanced insulin signaling capacity in adipose tissue, muscle and liver, as compared to control mice during high fat feeding. Moreover, in these tissues, control mice fed on a high fat diet show an increase in IKKß and JNK activity, which is prevented in C3H/HeJ mice. In isolated muscles from C3H/HeJ a protection from saturated fatty acid-induced insulin resistance is observed. Thus, TLR4 appears to be an important mediator of obesity and insulin resistance and a potential target for the therapy of these highly prevalent medical conditions
Doutorado
Ciencia Basica
Doutor em Clínica Médica
Harne, Amanda Janel. "Influence of vitamin D receptor gene polymorphisms on changes in insulin sensitivity with aerobic exercise training". College Park, Md. : University of Maryland, 2005. http://hdl.handle.net/1903/2191.
Texto completoThesis research directed by: Dept. of Kinesiology. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
Mardilovich, Katerina. "Insulin Receptor Substrate-2 (IRS-2): A Novel Hypoxia-Responsive Gene in Breast Cancer: A Dissertation". eScholarship@UMMS, 2011. https://escholarship.umassmed.edu/gsbs_diss/533.
Texto completoJain, Reema. "When too much sun is never enough: Association of the VDR gene polymorphisms with insulin resistance". AUT University, 2010. http://hdl.handle.net/10292/990.
Texto completoIggström, Sofia. "Investigation of the role of insulin receptor genes in wing polyphenism using gene knockdown and differential gene expression analysis in the non-model organism Gerris buenoi". Thesis, Uppsala universitet, Institutionen för ekologi och genetik, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-394909.
Texto completoGautam, Dinesh Chandra. "Analysis of insulin receptor function in the central nervous system by conditional inactivation of its gene in mice". [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=96492353X.
Texto completoRamaswamy, Girish. "Mechanical and geometric characterization of mouse cortical bone with osteoblast-specific knockout of insulin-like growth factor receptor gene". Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2009r/ramaswamy.pdf.
Texto completoCamporez, João Paulo Gabriel. "Efeito in vitro do deidroepiandrosterona (DHEA) sobre a via IRS/PI3-K/Akt e secreção de insulina em ilhotas pancreáticas de ratos". Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-03062008-151016/.
Texto completoThe dehydroepiandrosterone (DHEA) administration has resulted in reduction of abdominal fat and protection against insulin resistance from experimental animals and humans. So, the purpose of this project is measure the in vitro effects from DHEA: on protein expression of insulin receptor, the proteins IRS-1, IRS-2, PI3-K, Akt, and ERK-1/2; on gene expression of transcriptional factors PDX-1 and PGC-1, insulin, glucose transport GLUT-2 and glicocinase; and to measure the static insulin secretion, on cultured pancreatic islets of the rat. The culture of pancreatic islet for 24 hours with DHEA, did not induce nothing alteration on protein expression of the IR, IRS-1, IRS-2, PI3-K, Akt-1 and ERK-1/2, and static insulin secretion induced by glucose. However, happened increase ERK-1/2 phosphorylation and PGC-1 gene expression. The RINm5F cells, cultured by 72 hours, showed increase of the IRS-1 and IRS-2 expression. We conclude that 24 hours of the pancreatic islets culture are not sufficient time to look any alteration induced by DHEA, on insulin secretion, and on protein expression involved on IRS/PI3-K/Akt pathway. RINm5F cells can be an alternative model to research the direct effects from DHEA.
Azuma, Nobuyuki. "The significance of the Trp64Arg mutation of the β3-adrenergic receptor gene in impaired glucose tolerance, non-insulin-dependent diabetes mellitus, and insulin resistance in Japanese subjects". Kyoto University, 2003. http://hdl.handle.net/2433/148495.
Texto completoFilippi, Renée Zon. "Estudo da expressão das proteínas TFE3 e receptor de insulina nos hepatoblastomas a partir dos achados de expressão gênica". Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/5/5144/tde-26012012-100515/.
Texto completoHepatoblastoma is a rare tumor, and little is known about its pathogenesis and genetic alterations. Using a laser capture microdissection microscope we sampled areas of epithelial component of hepatoblastoma prior chemotherapy and their normal liver counterpart in order to perform the comparative gene expression analysis followed by the validation of selected genes by immunohistochemistry. Comparing tumor and non-diseased liver in two frozen samples, 70 differentially expressed genes were found, 19 overexpressed and 51 underexpressed in the tumor. Most of the genes were located at chromosomes 1 and 2. Of the genes selected for validation by immunohistochemistry, the most interesting findings came from Insulin receptor and TFE3 (both underexpressed genes). Insulin receptor was positive in non diseased liver and in the fetal component of the Hepatoblastoma but was consistently negative in the embryonal component (9/9 cases). The TFE3 staining was positive in the normal liver and fetal and embryonal components of the tumor in variable proportion of the cells, more marked in the embryonal component. The higher proportion of genes located at chromosomes 1 and 2 corroborates the cytogenetics findings reported in the literature related to Hepatoblastoma . The immunohistochemistry findings of different expression of insulin receptor in the fetal and embryonal components of Hepatoblastoma and the positivity of TFE3 in normal liver and in the tumors epithelial components deserves further investigation regarding the role of these genes to the pathogenesis of Hepatoblastoma
Curtain, Robert y n/a. "Candidate Gene Analysis of Migraine Susceptibility Regions on Chromosome 1q and 19p". Griffith University. School of Medical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20070810.132610.
Texto completoCurtain, Robert. "Candidate Gene Analysis of Migraine Susceptibility Regions on Chromosome 1q and 19p". Thesis, Griffith University, 2006. http://hdl.handle.net/10072/365960.
Texto completoThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Full Text
Zhang, Han. "An Optimized Polymerase Chain Reaction to Verify the Presence or Absence of the Growth Hormone Receptor Gene". Ohio University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1366378898.
Texto completoXu, Yongqin. "Studies on parental genomic imprinting of insulin-like growth factor-IImannose 6-phosphate receptor gene in humans : phenomenon, mechanism, and relevance to disease". Thesis, McGill University, 1997. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=37552.
Texto completoXu, Yongqin. "Studies on parental genomic imprinting of insulin-like growth factor-II/mannose 6-phosphate receptor gene in humans, phenomenon, mechanism, and relevance to disease". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0019/NQ44633.pdf.
Texto completoRocha, ívina Elaine dos Santos. "Sensibilidade insulínica e função da célula beta em indivíduos heterozigóticos para uma mutação no gene do receptor do GHRH". Universidade Federal de Sergipe, 2011. https://ri.ufs.br/handle/riufs/3798.
Texto completoGH e o fator de crescimento semelhante à insulina tipo I (IGF-I) apresentam funções sinérgicas sobre a síntese protéica e massa muscular. No tecido adiposo, o GH estimula a lipólise e oxidação lípidica, enquanto o IGF-I estimula a diferenciação dos pré adipócitos em adipócitos. No metabolismo glicídico, GH e IGF-I têm ações opostas, sendo o GH antagônico e o IGF-I sinérgico à sensibilidade insulínica (SI). Indivíduos heterozigóticos adultos para a mutação c.104=1G>A gene do receptor do hormônio liberador do GH (MUT/N) no, apresentam discreta redução do GH e níveis normais de IGF-I acompanhada de redução significativa da massa magra (Kg), com tendência à redução da massa gorda (Kg), em relação aos indivíduos homozigóticos normais (N/N). A SI e a função das células beta são desconhecidas nos indivíduos MUT/N. Para avaliá-las, foi realizado o teste de tolerância oral à glicose com administração de 75g de glicose e dosagens de glicose e insulina nos tempos 0, 30, 60, 90, 120 e 180 minutos em 25 indivíduos MUT/N (12 M/ 13 F; 40,08 ± 10,87 anos) e 25 N/N (14 M/ 11 F; 39,96 ± 12,49 anos). Não houve diferença na altura, contudo o peso, o IMC, a cintura e o quadril foram menores nos indivíduos MUT/N. A sensibilidade à insulina (SI) foi avaliada pelo HOMAir, onde menores valores, indicam maior SI e pelos QUICKI, OGIS 2 e OGIS 3, onde maiores valores, indicam maior SI. A função da célula beta foi avaliada pelo HOMA-beta, índice insulinogênico e área sob a curva da razão insulina/ glicose (ASC I/G). ANOVA indicou que não houve diferença entre as respostas glicêmica e insulinêmica entre os grupos. As áreas sob a curva de glicose e insulina foram semelhantes como também entre o número de pacientes com pré diabetes e diabetes. Não foram verificadas variações no HOMAir, QUICK, OGIS 2 e OGIS 3, HOMA beta, índice insulinogênico e ASC I/G entre os dois grupos. Em conclusão, a sensibilidade insulínica e a função de célula beta nos indivíduos MUT/N são semelhantes a dos indivíduos N/N.
Coutinho, Debora Cabral. "Estudo do gene do fator de crescimento insulina-símile 1 (IGF1) e de receptor (IGF1R) em crianças nascidas pequenas para a idade gestacional". Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-31082009-150428/.
Texto completoChildren born small for gestational age (SGA) have a higher risk of remaining short in adulthood. The insulin-like growth factors 1 and 2 (IGF-1 and IGF-2) are the main factors determining endocrine fetal growth. GH is the main promoter of linear growth in the postnatal life, exerting its effects mostly through the IGF-1. The vast majority of known actions of IGF-1 and IGF-2 are mediated by the insulin-like growth factor type 1 receptor (IGF-1R), a member of the tyrosine kinase receptors family. The aim of this study was to investigate IGF1 and IGF1R genes mutations in children born small for gestational age without catch up growth in postnatal life. We selected 145 patients born SGA, 72 without catch-up and 73 with catch up. The whole coding region of the IGF1 gene was sequenced in 54 patients without catchup. In the other SGA children without catch-up and in 73 SGA with catch-up, only the exon 6 of IGF1 was sequenced to assess the influence of allelic variants present in this region. In patients with normal IGF1 sequence and IGF-1 and IGFBP-3 serum levels above the mean for age and sex (n = 23) total RNA was extracted from peripheral blood lymphocytes followed by cDNA synthesis with random primers. The IGF1R cDNA was amplified using specific primers followed by direct sequencing. IGF1R expression was analyzed by real-time PCR. No mutations were found in the IGF1 gene. However a highly polymorphic sequence was identified in the upstream core polyadenylation signal (UCPAS) located in IGF1 3\' UTR at exon 6. The frequency of the identified allelic variants was similar in SGA children with and without catch-up and in controls. Furthermore, children homozygous for the wild-type allele and those carrying the allelic variants in homozygous or heterozygous state presented similar weight and length at birth, as well as serum IGF-1 levels and postnatal growth features. Two novel nonconservative allelic variants were identified in IGF1R in 23 SGA children (8.7%) in the heterozygous state. The first variant (c.16G>A) was located in the exon one, leading to a substitution of glicine by arginine in the pro-IGF-1R signaling peptide (p.G6R). The second variant was located in exon 7 (c.1531 C>T), leading to a substitution of arginine by tryptophan in the amino acid 511 of the IGF1-R (p.R511W). Moreover, a decreased IGF1R expression was observed in 5 of the 23 patients with elevated serum IGF-1 concentrations. We conclude that the UCPAS allelic variants did not significantly influence the birth and postnatal characteristics of children born SGA, neither the adult height of normal individuals born adequate for gestational age. The IGF1R study identified two novel allelic variants in two patients and a reduced expression of the IGF1R was observed in five patients. Patients with alterations in IGF1R did not have a distinctive phenotype when compared with other children born SGA without changes in this gene, indicating the importance of molecular studies.
Rodrigues, Danitsa Marcos. "Efeito do polimorfismo A3669G do gene do receptor de glicocorticoide sobre o controle metabólico, comportamento alimentar e neuroimagem funcional em uma amostra de adolescentes". reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2015. http://hdl.handle.net/10183/139572.
Texto completoIntroduction: Glucocorticoids are involved in regulation and adaptation of the stress response, exerting effects through its receptors. Variations on the glucocorticoid receptors genes have been characterized functionally. The A3669G polymorphism of the glucocorticoid receptor gene is related to a change in the tissue sensitivity to glucocorticoids and altered metabolic profile. Physiological concentrations of glucocorticoids stimulate food intake and in the presence of insulin affect food preferences. The G variant of the A3669G polymorphism appears to lead to a lower risk for diabetes, in patients with Cushing's syndrome, and smoking, when associated with a polymorphism of the mineralocorticoid receptor gene, suggesting a modulation in reward pathways. The objective of this study is to evaluate the association of A3669G polymorphism variants with feeding behavior and metabolic parameters in a sample of students correlating with functional neuroimaging data. Methods: The sample includes students of 6 schools in Porto Alegre, evaluated at two occasions 2008 and in 2013. In 2008, 131 individuals had complete protocol assessment and, from these, 74 returned in for re- evaluation in 2013. The evaluation included genotyping, anthropometry, laboratory tests, feeding behavior and a functional MRI paradigm to verify brain activation in response to the visualization of palatable, non- palatable foods and neutral items. The association with phenotypes was performed using Student's t test and Chi-square; longitudinal study data were evaluated using Generalized Estimating Equations. Results: The variant of the A3669G polymorphism was found in 17.6% of the students in 2008 and 14.9% of the sample in 2013. There was no difference between groups in the sample composition; the comparison between groups of the mean caloric intake originating from proteins, carbohydrates and fats in 2008 revealed no significant differences; at this time, analysis showed lower consumption of sugars and total calories in the G carrier group. In 2013, these individuals showed a reduction in insulin level and resistance, with no differences in food intake. The fMRI data indicated that viewing a food palatable image by the wild-type allele carrier group activated a region involved in visual processing (middle occipital gyrus) and deactivated an area related to motor planning and sensitivity to taste (pre central gyrus). Conclusion: The results showed that G carriers of the A3669G polymorphism of glucocorticoid receptor gene had lower insulin resistance levels, preceded by modulation of their food preference. The findings in functional neuroimaging showed increased incentive salience on viewing palatable food images and a predisposition for impulsivity in noncarriers. Data suggest that reduction in glucocorticoids sensitivity at a cellular level affects food intake, by reducing consumption of palatable foods, possibly decreasing the risk for metabolic diseases.
Tomita, Tsutomu. "Expression of the gene for a membrane-bound fatty acid receptor in the pancreas and islet cell tumours in humans : evidence for GPR40 expression in pancreatic beta cells and implications for insulin secretion". Kyoto University, 2006. http://hdl.handle.net/2433/135624.
Texto completoKashyap, Abhishek S. "In vitro functional characterisation of IGF-I : VN-induced breast cancer progression". Thesis, Queensland University of Technology, 2012. https://eprints.qut.edu.au/62165/1/Abhishek_Kashyap_Thesis.pdf.
Texto completoAlmeida, Madson Queiroz de. "Expressão dos genes IGF-II, IGF-IR, SF-1 e DAX-1 em tumores adrenocorticais de crianças e adultos". Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-31102008-153148/.
Texto completoIntroduction: The molecular pathogenesis of adrenocortical tumors is heterogeneous and incompletely understood. Insulin-like growth factor II (IGF-II) overexpression has been demonstrated in adult adrenocortical carcinomas. IGF-II exerts its mitogenic effects through interaction with IGF-I receptor (IGF-IR). In addition, steroidogenic factor 1 gene (SF-1) and dosage-sensitive sex reversal-adrenal hypoplasia congenita critical region on the X chromosome gene (DAX-1), which regulate adrenal development and steroidogenesis, have been also involved in adrenocortical tumorigenesis. Objectives: To analyze gene and protein expression of IGF-II, IGF-IR, SF-1 and DAX-1 in pediatric and adult adrenocortical tumors. We also evaluated the effects of a selective IGF-IR kinase inhibitor (NVP-AEW541) on adrenocortical tumor cell lines. Methods: Gene expression was determined by quantitative real-time PCR in 57 adrenocortical tumors (37 adenomas and 20 carcinomas) from 23 children and 34 adults. Twenty and three patients were younger than 15 years. A tissue microarray analysis was performed on a large cohort of 109 ACT (71 adenomas and 38 carcinomas; 39 children and 70 adults) In addition, the effects of NVP-AEW541 treatment (0.3 to 30M) on proliferation and apoptosis were investigated in the NCI H295 cell line and in a new cell line established from a pediatric adrenocortical adenoma of our cohort. Results: IGF-II transcripts were overexpressed in pediatric adrenocortical carcinomas and adenomas (mean ± SE, 50.8 ± 18.5 vs. 31.2 ± 3.7, respectively; p= 0.23). IGF-II gene expression was significantly higher in adult adrenocortical carcinomas than in adenomas (270.5 ± 130.2 vs. 16.1 ± 13.3; p= 0.0001). The percentual of neoplastic cells immunostaining for IGF-II was not statistically different between pediatric adrenocortical adenomas and carcinomas (14.1 ± 2.8% vs. 31.1 ± 13.1%, respectively; p= 0.32). Otherwise, the percentual of positive neoplastic cells for IGF-II was significantly higher in adult adrenocortical carcinomas than in adenomas (34.4 ± 5.8% vs. 14.2 ± 3.2, respectively; p= 0.03). IGF-IR mRNA levels were significantly higher in pediatric adrenocortical carcinomas than in adenomas (9.1 ± 1.2 vs. 2.6 ± 0.3; p= 0.0001), whereas similar IGF-IR expression levels were identified in adult adrenocortical carcinomas and adenomas (1.6 ± 0.3 vs. 1.8 ± 0.5, respectively; p= 0.75). In a Cox multivariate analysis, IGF-IR gene expression [hazard ratio (HR) 2.0, 95% confidence interval (CI) 1.2 to 3.1; p= 0.004] and Weiss score (HR 1.7, 95% CI 1.2 to 2.7; p= 0.003) were independent biomarkers of metastasis in pediatric and adult adrenocortical tumors, respectively. Furthermore, NVP-AEW541 blocked cell proliferation in a dose- and time-dependent manner in both NCI H295 and pediatric adrenocortical cell lines through a significant increase of apoptosis. Additionally, SF-1 gene overexpression was identified in 13% and 15% of pediatric and adult adrenocortical tumors, respectively. The percentual of neoplastic cells with nuclear immunoreactivity for SF-1 was significantly higher in pediatric than in adult adrenocortical tumors (29.1 ± 5.4% vs. 8.3 ± 2.3%, respectively; p= 0.0001). These findings suggest that SF-1 overexpression occurs at the translational level in pediatric adrenocortical tumors. DAX-1 gene overexpression was identified in 39% of adrenocortical tumors with a similar frequency in children and adults. Similarly, DAX-1 protein overexpression was identified in 36% and 27% of pediatric and adult adrenocortical tumors, respectively. DAX-1 immunostaining on nuclei was not statistically different in benign and malignant adrenocortical tumors (29.2 ± 3.8% vs. 21.4 ± 5.8% of neoplastic cells, respectively; p= 0.12). Conclusion: IGF-II overexpression has a pivotal role to adrenocortical tumorigenesis. IGFIR overexpression was a potential biomarker of metastases in children with adrenocortical carcinoma. We demonstrated that a selective IGF-IR kinase inhibitor had anti-tumor effects in adult and pediatric ACT cell lines, suggesting that IGF-IR inhibitors represent a promising therapy for human adrenocortical carcinoma. In addition, SF-1 overexpression might be mainly involved in pediatric adrenocortical tumorigenesis. DAX-1 overexpression has an important role to molecular pathogenesis of benign and malignant adrenocortical tumors
Liu, Ying. "Partial characterization of rat and pufferfish insulin receptor genes and identification of sequences regulating the alterative splicing of insulin receptor pre-mRNA /". Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21979522.
Texto completoLegrand, Alain. "Liposomes cibles et vecteurs retroviraux pour le transfert et l'expression du gene de la preproinsuline i de rat dans des cellules eucaryotes". Orléans, 1987. http://www.theses.fr/1987ORLE2011.
Texto completoLiu, Ying y 劉穎. "Partial characterization of rat and pufferfish insulin receptor genes and identification of sequences regulating the alterative splicing ofinsulin receptor pre-mRNA". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31240641.
Texto completoGao, Hui. "Estrogen signaling in metabolic disease : a functional genomics approach /". Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-974-2/.
Texto completoAcharya, Deepak. "Creating chimeras of human G-protein coupled receptors (HGPR40/43) for diabetic drug development". Muncie, Ind. : Ball State University, 2009. http://cardinalscholar.bsu.edu/398.
Texto completoClayton, Simon James. "Regulation of oestrogen receptor and oestrogen responsive genes by insulin, IGF-I, oestrogen and antioestrogens in breast cancer cells". Thesis, University of Newcastle Upon Tyne, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283743.
Texto completoTOZZO, PETREA STEPHANIE. "Regulation de l'expression du recepteur de l'insuline et de son gene chez le rat : effets du developpement postnatal, du jeune et du diabete insulinopenique". Paris 11, 1992. http://www.theses.fr/1992PA11T015.
Texto completoRouard, Mathias. "Déterminants génétiques du diabète sucré : détection de mutations dans le gène du récepteur de l'insuline et du facteur nucléaire hépatocytaire (HNF-1[alpha]) comme bases moléculaires du syndrome d'insulinorésistance extrême de type A et du diabète MODY3". Montpellier 1, 1997. http://www.theses.fr/1997MON1T038.
Texto completoStefano, José Tadeu. "Efeito do interferon-alfa sobre a expressão de genes do sistema IGF em pacientes portadores de hepatite C". Universidade de São Paulo, 2005. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-08102014-142922/.
Texto completoThe current investigation aimed to study the role of the GH-IGF-IGFBP axis in liver tissue and in T and B lymphocytes in patients with hepatitis C virus (HCV) before and after therapeutic regimen based on interferon alfa-2a or alfa-2b (3 million U SC 3x/wk) and ribavirin (1000-1200 mg qid). It has been shown that IGF-I plays an important role in the modulation of the immune response, besides its role as a growth factor for the immunologic cells. It also presents a predictive value in the evaluation of the hepatic reserve of these patients. Among 80 patients enrolled for this investigation, 39 began treatment with interferon-? and ribavirin, according to an established protocol. Two patients were excluded during treatment due to severe depressive disorders accompanied by suicidal thoughts and 2 patients died. Of the 35 patients who concluded the treatment, 18 eventually presented virological response. Of these, 15 (43%) maintained sustained virological response (SVR). The levels of AST and ALT enzymes in both pre and post-treatment periods were statistically different for both patients with SVR and those who did not present such response. In the group with SVR, aminotransferases basal levels were statistically lower when compared to the group of patients without SVR. In the group of non-responsive patients, the average of the scores of parenchyma activity was statistically lower in post-treatment period when compared to pre-treatment period. Furthermore, comparing post-treatment periods in both groups with and without SVR, the average of the scores of parenchyma activity was statistically lower in the group without SVR when compared to the group with SVR. Mean plasma concentrations of free IGF-I before treatment in patients who eventually achieved SVR was statistically higher in comparison to the group of non-responsive patients. Mean plasma concentrations of IGFBP3 were statistically higher in the group with RVS when compared to the group of patients without SVR. An increase of IGF-IR mRNA content was observed in hepatic tissue from all patients with CHC in comparison to normal liver. These results were confirmed by immunohistochemical analysis for the IGF-IR. IGF-IR mRNA content in liver tissue samples from patients who achieved SVR after treatment was statistically lower than that observed before treatment There was not statistical difference between IGF-I mRNA content in hepatic tissues from both groups of patients with and without SVR, in pre and post-treatment periods. IGF-I mRNA expression in T lymphocytes from patients with SVR was statistically higher in comparison to the non-responsive group of patients, considering both pre and post-treatment periods altogether. No statistical difference was observed in IGF-IR mRNA expression in both groups of patients with and without SVR, in pre and post-treatment periods. The statistical analysis did not disclose any statistically significant differences in IGF-I or IGF-IR mRNA expressions in B lymphocytes from patients with or without SVR, in pre and post-treatment periods. A decrease in hepatic IGF-IR mRNA content observed in patients who achieved SVR after therapy, suggested an improvement in hepatic damage. The hypothesis that the INF-? affects components of the IGF system contributing to these findings could not be discarded. However, it is unlike that these effects would play relevant role because any differences were observed in the hepatic IGF-IR mRNA expression in non-responsive patients. It remains to be elucidated whether IGF-IR up-regulation would be involved in hepatocyte regeneration or CHC would result from direct activation of IGF-IR gene by HCV and/or as a consequence of chronic aggression to hepatic parenchyma. Plasma concentration of free IGF-I >1.35 ng/ml was considered to be a predictive response to the treatment of hepatitis C with a probability ratio (odds ratio) of 17.33±1.02 (confidence interval: 2.26 -127.34)
GERARD, PIERRE-EMMANUEL. "Les syndromes d'insulinoresistance extreme : recherche de mutations sur les genes des recepteurs de l'insuline et les transporteurs de glucose glut-4". Nice, 1993. http://www.theses.fr/1993NICE6546.
Texto completoSantana, Laura Ferreira. "Expressão gênica do receptor de IGF-1 em células da granulosa luteinizadas de mulheres com síndrome dos ovários policísticos (SOP), não obesas, com sensibilidade à insulina normal, tratadas e não tratadas com metformina". Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/17/17145/tde-26092013-155217/.
Texto completoOBJECTIVE: evaluation of the gene expression of the IGF-I receptor in luteinized cumulus granulosa cells from non-obese women with normal insulin sensitivity and with polycystic ovarian syndrome (PCOS)treated or nor with metformin. STUDY MODEL: prospective,longitudinal, randomized. PATIENTS AND METHODS: we evaluated 12 women withovulatory cycles and 9 women with PCOS who had been treated for at least 8 weeks with a metformin dose of 1700 mg/day. All groups were similar interms of weight, body mass index (BMI), and waist circumference and all had normal insulin sensitivity. All women were submitted to controlled ovarian stimulation with a GnRH agonist in a long protocol and with gonadotropins for IVF/ICSI cycles. Cumulus granulosa cells were obtained by microdissection of the five largest pre-ovulatory follicles. Gene expression of the IGF-1 receptor was determined by semiquantitative RT-PCR. Serum and follicular concentrations of estradiol, progesterone, testosterone, FSH, LH, insulin, SHBG, and IGF-1 were determined. Data were analyzed statistically by ANOVA and by the Newman-Keuls test and the Pearson coefficient and linear multiple regression were calculated, with the level of significance set at 5%. RESULTS: no difference in geneexpression of the IGF-I receptor were observed between the three groups studied (P>0.05). The number of oocytes (20.4 vs. 13.1 vs. 11.5, P= 0.009) and the serum levels of estradiol (1,896.00 pcg/mL vs. 985.20 pcg/mL vs.908.10 pcg/mL,P = 0.03) and testosterone (1.43 ng/mL vs.0.89 ng/mL vs. 0.82 ng/mL pcg/mL,P = 0.02) were higher in the group of women with PCOS not treated with metformin than in women with ovulatory cycles and in women treated with metformin, respectively. The women with ovulatory cycles (50.710±42.520 ng/mL) presented higher follicular concentrations of progesterone compared with women with PCOS treated (13.660±5.212 ng/mL) or not with metformin (17.680±6.644 ng/mL) (P=0.01). Multiple regression revealed that serum testosterone was not affected by the gene expression of the IGF-1 receptor or by BMI. CONCLUSIONS: the high serum concentrations of estradiol and testosterone and the larger number of oocytes in the group ofwomen with PCOS not treated with metformin lead us to conclude that women with PCOS probably have greater sensitivity to stimulation ofovarian steroidogenesis than women without the disease, although no difference was detected in the expression of the IGF-I receptor between the three groups studied. The similarity ofthe present results for the women with PCOS treated with metformin and for the women with ovulatory cycles leads us to hypothesize that one of the possible mechanisms of action of metformin on the IGF-1 system in cumulus granulosa cells may be of the post-receptor type.
Voropanov, Anca-Maria. "Development of new molecular genetic epidemiological approaches with application to the human growth hormone, insulin-like growth factor I, and leptin receptor genes". Thesis, University of Southampton, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271624.
Texto completoKannisto, Katja. "The metabolic syndrome : studies on thrifty genes /". Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-051-6/.
Texto completoPaz, Ana Helena da Rosa. "Superexpressão de betacelulina em células-tronco mesenquimais induz secreção de insulina in vitro e melhora quadro de hiperglicemia em modelo experimental de diabetes". reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2009. http://hdl.handle.net/10183/26898.
Texto completoBetacellulin (BTC), a ligand of the epidermal growth factor receptor, has been shown to promote growth and differentiation of pancreatic β-cells and to improve glucose metabolism in experimental diabetic rodent models. Mesenchymal stem cells (MSCs) have already been proved to be multipotent. Recent work has attributed to rat and human MSCs the potential to differentiate into insulin secreting cells. Our goal was to evaluate the effects of betacellulin overexpression in rat MSCs. MSCs were characterized by flow cytometry and mesoderm differentiation markers. MSCs were electroporated with a plasmid containing BTC cDNA. Transfected cells were cultivated in H-DMEM with 10mM Nicotinamide. Radioimmunoassay analysis showed that 104 MSC-BTC cells produced up to 0,4ng/mL of insulin, in contrast, MSCs transfected with the empty vector produced insignificant levels of insulin. Also MSC-BTC cells were positive for insulin in immunohistochemistry. RT-PCR showed expression of pancreatic marker genes. When transplanted to streptozotocin diabetic rats, MSC-BTC cells could revert hyperglycemia. Our results demonstrate that BTC overabundance enhances glucose-induced insulin secretion in mesenchymal stem cells in vitro as well as in vivo.
Karjalainen, M. (Minna). "Genetic predisposition to spontaneous preterm birth:approaches to identify susceptibility genes". Doctoral thesis, Oulun yliopisto, 2011. http://urn.fi/urn:isbn:9789514296956.
Texto completoTiivistelmä Suomessa syntyy noin 5,5 % lapsista ennenaikaisina eli raskauden kestettyä vähemmän kuin 37 täyttä viikkoa. Näillä lapsilla on alttius hengenvaarallisiin sairauksiin, ja osalle heistä jää pysyvä kehitysvamma. Noin 70 % ennenaikaisista syntymistä käynnistyy spontaanisti. Tärkein ennenaikaisen syntymän riskitekijä on kohdunsisäinen tulehdusreaktio. Myös perinnöllisten tekijöiden tiedetään vaikuttavan spontaanin ennenaikaisen syntymän (SEAS) käynnistymiseen, mutta alttiusgeenejä tunnetaan huonosti. Työssä pyrittiin tunnistamaan SEAS:lle altistavia perinnöllisiä tekijöitä. Perimänlaajuista kytkentäanalyysiä käyttäen etsittiin SEAS:ään liittyviä perimän kohtia tutkimalla toistuvasti ennenaikaisia syntymiä kokeneita isoja pohjoissuomalaisia perheitä. Kytkentäsignaalien lähellä olevia geenejä tutkittiin tutkimusaineistossa, joka koostui suomalaisista äideistä ja lapsista. Surfaktanttiproteiini A:ta (SP-A), SP-C:tä, SP-D:tä ja mannoosia sitovaa lektiiniä (MBL) koodaavia geenejä tutkittiin ehdokasgeeneinä SEAS:lle tässä populaatiossa, koska nämä proteiinit osallistuvat elimistön puolustukseen ja voivat siten vaikuttaa SEAS:ään liittyvään tulehdusreaktioon. Lisäksi tutkittiin SP-C:n ilmentymistä ihmisen ja hiiren sikiökalvoilla, istukassa ja kohdussa. Kytkentäsignaaleja havaittiin kromosomikohdissa 15q26.3, Xq13.1 ja Xq21.1, kun tutkittavana ilmiasuna oli ennenaikaisena syntyminen. Lisätutkimukset osoittivat, että sikiön insuliininkaltaisen kasvutekijän 1 reseptoria koodaava IGF1R-geeni (kohta 15q26.3) ja androgeenireseptorigeeni AR (lähellä kohtaa Xq13.1) ovat mahdollisia uusia SEAS:n alttiusgeenejä. Nämä geenit eivät selittäneet SEAS:ää äideissä. Sikiön SP-D:tä koodaavan geenin Met31Thr-polymorfismi tunnistettiin mahdolliseksi riskitekijäksi, mutta tämä polymorfismi ei selittänyt SEAS:ää äideissä. SP-A:ta ja MBL:ää koodaavat geenit eivät liittyneet SEAS:ään. SP-C:tä koodaavan geenin Thr138Asn-polymorfismi ei ollut yhteydessä SEAS:ään. Sikiön Thr138Asn-polymorfismi liittyi kuitenkin vahvasti sikiökalvojen puhkeamisen ja SEAS:n väliseen kestoon. SP-C:n havaittiin ilmentyvän ihmisen ja hiiren sikiökalvoilla ja istukassa sekä raskaana olevan hiiren kohdussa. Tulokset antavat uutta tietoa SEAS:n perinnöllisestä taustasta. Tämä tieto voi auttaa selvittämään sen käynnistymiseen johtavia biologisia mekanismeja ja johtaa lopulta uusiin hoitokeinoihin, joilla pystytään estämään spontaaneja ennenaikaisia syntymiä
Yaseen, Mohamed A. [Verfasser]. "A molecular biological study of the preimplantation of insulin like growth factor genes and their receptors in in vitro produced bovine embryos to improve in vitro culture systems and embryo quality / Mohamed A. Yaseen". Braunschweig : Bundesforschungsanst. für Landwirtschaft, 2002. http://d-nb.info/996825843/34.
Texto completoKinoshita, Asako [Verfasser]. "Chronic effects of Fusarium-mycotoxins in rations with different concentrate proportions on gene expression of muscular and hepatic glucose transporters and insulin receptors as well as of hepatic enzymes relevant for energy metabolism in lactating dairy cows / Asako Kinoshita". Hannover : Bibliothek der Tierärztlichen Hochschule Hannover, 2011. http://d-nb.info/1018968431/34.
Texto completoColli, Máikel Luís. "Papel do PTPN2 e MDA5, dois genes candidatos para diabete melito tipo 1, nas respostas das células beta pancreáticas a citocinas pró-‐inflamatórias e ao RNA de fita dupla intracelular". reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2010. http://hdl.handle.net/10183/26121.
Texto completoIn type 1 diabetes (T1D) several genes and environmental factors, such as viral infections, interact to trigger a chronic autoimmune assault against the insulin-producing pancreatic beta cells. During this process beta cells have an important role in maintenance/amplification of this autoimmune response via a cross-talk with the immune system. In recent years the development of high-throughput techniques for searching new genetic variants significantly increased the number of known genes potentially contributing for T1D. To clarify how these new candidate genes modify pancreatic beta responses to proinflammatory mediators and viruses, we used data from our previous array studies and an online beta cell database (www.t1dbase.org) to select candidate genes that are expressed in beta cells and modified by cytokines or the viral by-product double-stranded RNA (dsRNA). Two genes were identified, PTPN2 and MDA5, and further studied in this thesis. PTPN2 is a protein tyrosine phosphatase with several targets including STAT1, a key transcription factor involved in beta cell death. We confirmed at mRNA and protein levels the expression of PTPN2 in a beta cell linage (INS-1E), primary FACS-purified rat beta cells and human islets. Exposure to cytokines or to intracellular dsRNA increased PTPN2 expression. Knockdown of PTPN2, by using specific small interference (si)RNAs, exacerbated beta cell apoptosis after treatment with a combination of cytokines (interleukin-1! (IL-1!) + interferon-" (IFN-")) or intracellular dsRNA, and converted IFN-" alone in a pro-apoptotic stimulus. Importantly, PTPN2 silencing amplified STAT1 phosphorylation. The double knockdown of PTPN2 and STAT1 protected beta cells against cytokine-induced apoptosis, suggesting that PTPN2 acts as a negative regulator of the pro-apoptotic transcription factor STAT1. Knocking-down PTPN2, however, did not affect to any major extent the expression of cytokines and chemokines. The second candidate gene, MDA5, is an helicase involved in recognition of intracellular viral nucleic acids. Since MDA5 works as a receptor for detection of viral infection, this gene was only evaluated in the context of the viral mimetic dsRNA. Transfection of INS-1E cells and FACSpurified rat beta cells with dsRNA significantly upregulated the mRNA expression of MDA5. The silencing of MDA5 and RIG-I (another helicase involved in recognition of intracellular dsRNA) did not modify dsRNA-induced apoptosis. On the other hand, the knockdown of MDA5, but not of RIG-I, decreased the expression of several cytokines/chemokines in beta cells exposed to intracellular dsRNA. In conclusion, our data suggest that these two candidate genes may have important roles in the development of T1D via their actions at the beta cell level. PTPN2 seems to prevent beta cells apoptosis by controlling STAT1 activation, while MDA5 might regulate the local autoimmune assault via decreasing recruitment and activation of immune cells.
Freire, Bruna Lucheze. "Sequenciamento paralelo em larga escala de genes alvo é uma ferramenta útil no diagnótico etiológico de crianças nascidas pequenas para idade gestacional". Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-15082018-104927/.
Texto completoDiseases affecting human growth are most likely caused by genetic factors. The main goal of this project is to apply the technology of massive parallel sequencing to comprehend growth disturbs in children born small for gestational age (SGA), known as the children with Z-score of height and/or weight at birth less or equal -2. SGA is a heterogeneous condition, and as its causes we can find maternal, placental and fetal factors, of which, the most important are the genetic alterations. Children born SGA that do not have catch-up growth spontaneously up to the second year of life may remain with short stature when adults and they usually present other clinical features, such as dimorphisms, congenital anomalies and neuropsychomotor developmental delay. We used the Sure Select technology (Agilent Technologies, CA, USA) to study approximately 390 genes chosen by participate of the IGFs/IGF1R system, or genes already associated with growth disorders, or candidate genes found in previous studies of aCGH (Array Comparative Genomic Hybridization) or exome sequencing. We sequenced 80 patients, and had a mean coverage of 354x, with more than 99% of the target region with > 10 reads. We found 58 variants, 18 classified as pathogenic or probably pathogenic in 19 patients, 32 variants of unknown significance and 7 probably benign and 1 probably pathogenic for a condition non associated to short stature (``incidental finding``) Among the probably pathogenic and pathogenic we found a great heterogeneity in genes, with variants identified in 10 different genes PTPN11 (x3), BLM (x3), NPR2 (x2), ANKRD11 (x2), SRCAP (x2), FGFR3 (x2), IGF1R, SHOC2, SHOX, NIPBL and a 22q11 deletion. In conclusion, the technique of targeted gene panel sequencing is a useful tool to establish the molecular diagnose in children SGA. We could identify the molecular cause in 23.75% of the casuistic, mostly patients with clinically recognized syndromes. However, variants at IGFs/IGF1R system are not frequently associated with the studied condition
Giabicani, Eloïse. "Croissance et système des IGFs (insulin-like growth factors) : l’apport physiopathologique des maladies soumises à empreinte parentale New clinical and molecular insights into Silver–Russell syndrome Roles of Type 1 Insulin-Like Growth Factor (IGF) Receptor and IGF-II in Growth Regulation: Evidence From a Patient Carrying Both an 11p Paternal Duplication and 15q Deletion Diagnosis and Management of Postnatal Fetal Growth Restriction Chromosome 14q32.2 imprinted region disruption as an alternative molecular diagnosis of Silver-Russell Syndrome". Thesis, Sorbonne université, 2019. https://accesdistant.sorbonne-universite.fr/login?url=http://theses-intra.upmc.fr/modules/resources/download/theses/2019SORUS304.pdf.
Texto completoFetal growth is dependant of environemental, genetic and hormonal factors which interact to ensure a proper development. Insulin-like growth factors (IGF) system plays a key role in fetal growth by interactions with these differents systems. In this work, we studied the roles of the IGF system in fetal growth restriction diseases. We used both clinical and experimental approaches to enhance knowledge on functional consequences of genetic ou epigenetic defects of IGF system actors. We set-up a functional test to assess IGF1R activity in vitro in patients with restricted fetal and postnatal growth. We also documented the IGF-I bioavailability in patients with Silver-Russell syndrome, which is an imprinting disorder responsible for fetal and postnatal growth restriction. We characterized the clinical and molecular overlap of Silver-Russell and Temple syndrome (another imprinting disease affecting growth and metabolism) and confirmed the central role of IGF2 in the physiopathology of these disorders. These results confirmed the integration of imprinted genes in a large co-regulation network and the major role of IGF system actors in fetal growth which is usually impaired when these imprinted genes are affected
LIN, SU-JUN y 林姝君. "Protein kinase activity of the insulin receptor is essential for insulin regulated gene expression". Thesis, 1989. http://ndltd.ncl.edu.tw/handle/73610856507480219086.
Texto completoChen, Mark Hung-Chih y 陳泓志. "The insulin-like growth factor 1 gene, insulin-like growth factor 2 gene and their receptor involve in zebrafish(danio rerio) development". Thesis, 2002. http://ndltd.ncl.edu.tw/handle/35705257532260604357.
Texto completo國防醫學院
生命科學研究所
90
The characteristics of high growth rate, easy breeding and maintenance have made the zebrafish (Danrio rerio) as world-wide recognized species and important embryo model for functional genomics and proteomics research in the post-genomics era. This dissertation focused on the zebrafish growth related genes and its function, especially IGF-1, IGF-2 and IGF-1R. In this study, we plan to dissect the mechanisms of paracrine/autocrine modes of IGF action in the thorax development. We cloned zebrafish (Danio rerio) IGF-1 cDNA and its genomic sequence from zebrafish brain cDNA library and an adult zebrafish genomic library, respectively. These two cDNA sequences differ from with each other in different length of 5- and 3-untranslated region (5UTR and 3UTR) and one nucleotide difference at glutamine (A9, CAG/IGF-1a and CAA/IGF-1b) of the A domain. The results of IGF-1 mRNA expression and genomic Southern blotting, RPA, 5悐ACE suggested that the zebrafish have more than two IGF-1 genes. All these findings suggest that the expression of pro-IGF-1 Ea-2 is not controlled by alternative splicing but alternative gene usage in the zebrafish. Results of RT-PCR and Southern blot analysis showed that, only one form of IGF-1 Ea-2 mRNA was expressed in all tested adult tissues of zebrafish, even under condition of growth hormone, prolactin or insulin administration and fasting. The encoding proIGF-1a Ea-2 protein is 100% identity to proIGF-1b Ea-2. So, we tested the hypothesis whether E domain can mimic IGF-1 function. In this research, a synthetic peptide of the predicted zebrafish Ea-2 polypeptide (designated as zfEa-2) was not only increased 3 fold of branchial cartilage specific sulfate uptake in vitro compared with control group but also increased the [3H]thymidine incorporation into DNA on the mouse spleen cell. For further understanding the zfEa-2 polypeptide action mechanism, the aIR-3 was used to block the IGF-1 signal transduction. We demonstrated that aIR-3 couldn掐 inhibit the zfEa-2 signal but inhibit the IGF-1 sulfate uptake capability. These findings strongly suggest that the zfEa-2 can mimic IGF-1 function as a local mediator in zebrafish. These findings strongly suggest that the zfEa-2 polypeptide has another receptor to trigger the sulfation signal in zebrafish. Finally, The IGFs system exhibits an important role on the zebrafish development. So, we are further cloning the IGF-2a cDNA and IGF-2b gene from library. Meantime, we are search one zebrafish IGF-1Ra EST clone and get the 5UTR sequence for morpholino gene knock-down functional assay. In conclusion, this dissertation hopes to provide a new vision on the IGF gene family (IGF-1, IGF-2, IGF-1R) to distribute onto the growth regulation mechanism. Based on these researches, it can provide some information to construct the growth gene-chip network in the future.
Wang, Jhih-Hao y 王志浩. "Study of Human TR4 Nuclear Receptor in Insulin-like Growth Factor-I Gene Regulation". Thesis, 2008. http://ndltd.ncl.edu.tw/handle/876u9p.
Texto completo國立東華大學
生物技術研究所
96
Nuclear receptors are a family of transcription factors. They can bind to hormone response elements of target genes, control their expression, and many important physiology processes. The ligands of many nuclear receptors have not been identified, so they are called orphan receptors. TR4 is an orphan receptor. TR4 can control gene expression, animal growth and development, and the function of the liver. Collins and associates observed insulin-like growth factor-I (IGF-I) decreases in the blood and the liver of TR4 gene knockout mice in 2003. IGF-I regulated the body growth of human and mice. Therefore, we hypothesized TR4 was an potential activator of IGF-I gene expression. To demonstrate our hypothesis, we selected four sequence, IGF-DR2,IGF-DR4,IGF-DR6 and IGF-rDR4, to perform electrophoresis mobility assay (EMSA) and dual-luciferase assay. The result of EMSA suggested TR4 could bind to IGF-DR6 and IGF-rDR4. The result of dual-luciferase assay suggested TR4 interacted with IGF-DR6 and GF-rDR4 in HeLa cell line acted a repressor. However, the result was opposite our original hypothesis. The reason was that HeLa cell line wasn’t derived from the liver tissue. Our study showed TR4 might participate to regulate IGF-I gene expression. Furthermore, we will detect the effect of TR4 on IGF-I gene expression to demonstrate whether TR4 can regulate IGF-I gene expression in cells.
WU, SHEUE-MEI y 吳雪美. "Identification of the subtype gene of 2 adrenergic receptor expressed in clonal hamster insulin secreting cells". Thesis, 1992. http://ndltd.ncl.edu.tw/handle/98957332742613639344.
Texto completoWu, Xue-Mei y 吳雪美. "Identification of the subtype gene of 2 adrenergic receptor expressed in clonal hamster insulin secreting cells". Thesis, 1992. http://ndltd.ncl.edu.tw/handle/34332968404715354944.
Texto completoFan, Tzu-Wei y 范子威. "Arsenic Methylation Capability, Gene Polymorphisms of Insulin receptor substrate-1 and Phosphatidylinositol 3-kinase, and Metabolic Syndrome". Thesis, 2008. http://ndltd.ncl.edu.tw/handle/54533934955062823767.
Texto completo臺北醫學大學
公共衛生學研究所
96
The cross-sectional study was conducted to explore the relationships among arsenic methylation capability, genetic polymorphisms of insulin receptor substrate-1 (IRS-1) codon 972 and phosphatidylinositol 3-kinase (PI3-K) codon 326, cigarette smoking, betel nut chewing and metabolic syndrome. The study subjects were recruited from commuity health examination of Puzih, Taibao and Budai Township of Chayi County in southwestern Taiwan. A standardized personal interview based on structural questionnaire was carried out by well-trained interviewers. Information obtained from interview included demographic characteristics, environmental exposure, personal and familial disease history and lifestyle. There were 900 study subjects who gave their consent were recruited for questionnaire interview and collectd their blood and urine samples. Random selected 560 subjects to carry out the gene polymorphism experiment. DNA was extracted from buffy coat to analyze the gene polymorphism of the IRS-1 codon 972 and PI3-K codon 326 utilizing the polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) assay. Urine samples of these subjects were examined by high performance liquid chromatography (HPLC) to separate arsenite (AsIII), dimethyarsinic acid (DMAV) monomethylarsonic acid (MMAV) and arsenate (AsV), and then quantified by hydride generator combined with atomic absorption spectrometry (HGAAS). It was found that metabolic syndrome prevalence was 28.89%. After adjusted potential confounders, subjects had cumulative betel nut exposure >7.49 × 104 year-quids compared to those who had cumulative betel nut exposure 0 year-quids, the metabolic syndrome risk was significantly increased, the odds ratio was 1.97, 95% confidence interval was 1.05 - 3.70. Subjects had cigarette smoking, alcohol drinking and betel nut chewing compared to non smoker, non drinking and non chewer, the metabolic syndrome risk was borderline significantly increased, the odds ratio was 1.86, and 95% confidence interval was 0.99 - 3.51. Total arsenic concentration, MMA%, DMA% and SMI were divided into three groups using their tertile of controls, respectively. The odds ratio of metabolic syndrome was significantly increased for those second tertile versus first tertile group. There were no associations among IRS-1 codon 972 or PI3-K codon 326 polymorphisms and the metabolic syndrome risk. The metabolic syndrome risk was significantly higher in the study subjects had cigarette smoking, alcohol drinking, betel nut chewing, worse arsenic methylation capability, and PI3-K codon 326 Met/Ile or Ile/Ile genotype than those with non smoker, non drinker, non betel nut chewer, better arsenic methylation capability, and PI3-K codon 326 Met/Met genotype.