Relevant bibliographies by topics / Insulin receptor gene

Academic literature on the topic 'Insulin receptor gene'

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Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Insulin receptor gene"

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Seino, S., M. Seino, and G. I. Bell. "Human Insulin-Receptor Gene." Diabetes 39, no. 2 (February 1, 1990): 129–33. http://dx.doi.org/10.2337/diab.39.2.129.

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Seino, S., M. Seino, and G. I. Bell. "Human insulin-receptor gene." Diabetes 39, no. 2 (February 1, 1990): 129–33. http://dx.doi.org/10.2337/diabetes.39.2.129.

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Brunetti, Antonio, and I. D. Goldfine. "Insulin receptor gene expression and insulin resistance." Journal of Endocrinological Investigation 18, no. 5 (May 1995): 398–405. http://dx.doi.org/10.1007/bf03347847.

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Morris, Brian J. "Insulin Receptor Gene in Hypertension." Clinical and Experimental Hypertension 19, no. 5-6 (January 1997): 551–65. http://dx.doi.org/10.3109/10641969709083169.

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Greenhill, Claire. "Insulin and the insulin receptor regulate gene expression." Nature Reviews Endocrinology 15, no. 6 (April 11, 2019): 315. http://dx.doi.org/10.1038/s41574-019-0206-6.

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Soler, A. P., K. A. Thompson, R. M. Smith, and L. Jarett. "Immunological demonstration of the accumulation of insulin, but not insulin receptors, in nuclei of insulin-treated cells." Proceedings of the National Academy of Sciences 86, no. 17 (September 1989): 6640–44. http://dx.doi.org/10.1073/pnas.86.17.6640.

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Although insulin is known to regulate nuclear-related processes, such as cell growth and gene transcription, the mechanisms involved are poorly understood. Previous studies suggested that translocation of insulin or its receptor to cell nuclei might be involved in some of these processes. The present investigation demonstrated that intact insulin, but not the insulin receptor, accumulated in nuclei of insulin-treated cells. Cell fractionation studies demonstrated that the nuclear accumulation of 125I-labeled insulin was time-, temperature-, and insulin-concentration-dependent. Electron microscopic immunocytochemistry demonstrated that the insulin that accumulated in the nucleus was immunologically intact and associated with the heterochromatin. Only 1% of the 125I-labeled insulin extracted from isolated nuclei was eluted from a Sephadex G-50 column as 125I-labeled tyrosine. Plasma membrane insulin receptors were not detected in the nucleus by immuno electron microscopy or when wheat germ agglutinin-purified extracts of the nuclei were subjected to PAGE, electrotransfer, and immunoblotting with anti-insulin receptor antibodies. These results suggested that internalized insulin dissociated from its receptor and accumulated in the nucleus without its membrane receptor. We propose that some of insulin's effects on nuclear function may be caused by the translocation of the intact and biologically active hormone to the nucleus and its binding to nuclear components in the heterochromatin.
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Rojek, Aleksandra, and Marek Niedziela. "Insulin Receptor and its Relationship with Different Forms of Insulin Resistance." Advances in Cell Biology 2, no. 2 (February 1, 2010): 59–90. http://dx.doi.org/10.2478/v10052-010-0004-8.

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SummaryInsulin plays an important role in maintaining the whole organism’s homeostasis. The presence of insulin receptors in all vertebrates and invertebrates cells reflects the diversity of regulatory processes in which this hormone is involved. Furthermore, many different factors may influence the level of insulin receptor expression. These factors include e.g. the sole insulin or stage of development. Mutations in the receptor may lead to the development of insulin resistance. These mutations differ in the level of severity and are frequently associated with diabetes mellitus, hypertension, cardiovascular disorders, heart failure, metabolic syndrome and infertility in women. More than 50 mutations in insulin receptor gene have already been characterized. These mutations are associated with rare forms of insulin resistance like leprechaunism, insulin resistance type A or Rabson-Mendenhall syndrome. Molecular analysis of insulin receptor gene may lead to a better understanding of molecular mechanisms underlying various types of insulin resistance and help to develop more efficient treatment.
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TAYLOR, SIMEON I., ALESSANDRO CAMA, DOMENICO ACCILI, FABRIZIO BARBETTI, MICHAEL J. QUON, MARIA DE LA LUZ SIERRA, YOSHIFUMI SUZUKI, et al. "Mutations in the Insulin Receptor Gene." Endocrine Reviews 13, no. 3 (August 1992): 566–95. http://dx.doi.org/10.1210/edrv-13-3-566.

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Taylor, S. I., T. Kadowaki, H. Kadowaki, D. Accili, A. Cama, and C. McKeon. "Mutations in Insulin-Receptor Gene in Insulin-Resistant Patients." Diabetes Care 13, no. 3 (March 1, 1990): 257–79. http://dx.doi.org/10.2337/diacare.13.3.257.

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Kitamura, Tadahiro, Yoshiaki Kido, Serge Nef, Jussi Merenmies, Luis F. Parada, and Domenico Accili. "Preserved Pancreatic β-Cell Development and Function in Mice Lacking the Insulin Receptor-Related Receptor." Molecular and Cellular Biology 21, no. 16 (August 15, 2001): 5624–30. http://dx.doi.org/10.1128/mcb.21.16.5624-5630.2001.

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ABSTRACT Receptors of the insulin/insulinlike growth factor (IGF) family have been implicated in the regulation of pancreatic β-cell growth and insulin secretion. The insulin receptor-related receptor (IRR) is an orphan receptor of the insulin receptor gene (Ir) subfamily. It is expressed at considerably higher levels in β cells than either insulin or IGF-1 receptors, and it has been shown to engage in heterodimer formation with insulin or IGF-1 receptors. To address whether IRR plays a physiologic role in β-cell development and regulation of insulin secretion, we have characterized mice lacking IRR and generated a combined knockout of Irand Irr. We report that islet morphology, β-cell mass, and secretory function are not affected in IRR-deficient mice. Moreover, lack of IRR does not impair compensatory β-cell hyperplasia in insulin-resistant Ir +/− mice, nor does it affect β-cell development and function inIr −/− mice. We conclude that glucose-stimulated insulin secretion and embryonic β-cell development occur normally in mice lacking Irr.
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Dissertations / Theses on the topic "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.

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Patel, 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/.

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The daf-2 gene is a key regulator of growth, metabolism and longevity in the nematode Caenorhabditis elegans. The DAF-2 receptor functions in a pathway that is analogous to mammalian insulin/insulin-like growth factor signalling and determines whether animals proceed with full reproductive development or arrest in a long-lived diapausal state known as the dauer larva. Temperature-sensitive hypomorphic mutants of daf-2 constitutively arrest as dauers when raised at non-permissive temperatures. At permissive temperatures the animals develop into adults that are long-lived compared to wild-type adults. These alleles of daf-2 can be separated into two distinct classes (1 and 2) based on their pleiotropic phenotypes. In addition to their phenotypic differences, the two classes also differ in their epistatic interactions with other genes involved in dauer formation, suggesting that the DAF-2 receptor has multiple signalling outputs. In this thesis I have investigated the nature of the daf-2 allele class difference using a range of methods, including sequence analysis and homology modelling of mutant receptors. This generated the prediction that signalling flux through the receptor is a determinant of the class difference, with class 2 alleles having an asymmetrical alteration in signal transduction through DAF-2. Experimental testing of these predictions suggest that some phenotypes such Eat and Unc may be associated with asymmetrical signalling, while others such as early larval arrest may be correlated with a reduction in receptor level at the plasma membrane. A comparative analysis of the DAF-2 receptor with its homologues from Caenorhabditis briggsae, Caenorhabditis remanei and the parasitic nematode Brugia malayi suggests the large C-terminal extension in the Caenorhabditis species, which shorter in Brugia and not present in vertebrates, is an adaptive trait that has evolved by exon duplication for rapid growth and development and may contribute to the shortevity of these species. In addition, I have also performed an analysis of ins-7 and ins-35, two putative ligands of DAF-2 that are differentially regulated by the transcription factor DAF-16, using RNAi. Knockdown of both these genes lead to slight lifespan extension (10-20%) at 20 °C in all genetic backgrounds and slight suppression (-10%) at 25 °C in long-lived daf-2 mutant backgrounds compared to controls. This suggests that INS peptides may function as agonists a 20 °C and antagonists at 25 °C, and that this behaviour may be independent of their transcriptional regulation.
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Griffiths, 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.

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Tsukumo, 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.

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Orientador: Mario Jose Abdalla Saad
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-08-11T03:34:45Z (GMT). No. of bitstreams: 1 Tsukumo_DanielaMitiLemos_D.pdf: 7330041 bytes, checksum: 384133bd9ed3dd468d57225845733901 (MD5) Previous issue date: 2008
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
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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.

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Thesis (M.A.) -- University of Maryland, College Park, 2005.
Thesis 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.
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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.

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Breast cancer is the most common malignancy among women in the U.S. While many successful treatments exist for primary breast cancer, very few are available for patients with metastatic disease. The purpose of this study was to understand the role of Insulin Receptor Subtrate-2 (IRS-2) in breast cancer metastasis. IRS-2 belongs to the IRS family of cytoplasmic adaptor proteins that mediate signaling from cell surface receptors, many of which have been implicated in cancer. Although the IRS proteins are highly homologous in structure and have some complementary functions, growing evidence supports that the IRS proteins have unique roles in cancer. IRS-1 has been shown to promote tumor cell proliferation, while IRS-2 has been positively associated with cancer cell invasion, glycolysis and tumor metastasis. In the current work, we identified IRS-2 as a novel hypoxia-responsive gene in breast carcinoma cells. In contrast, IRS-1 expression does not increase in response to hypoxia, supporting the notion of their non-overlapping functions. Hypoxia promotes the adaptation and resistance of cancer cells to chemo- and radiation therapy, and also promotes tumor cell survival, invasion and metastasis by selecting for aggressive tumor cells that can survive under stressful low oxygen conditions. We have shown that IRS-2 upregulation in response to hypoxia promotes Akt signaling and tumor cell viability and invasion. We identified a cell context-dependent role for Hypoxia Inducible Factor (HIF) in the regulation of IRS-2 expression in hypoxia, with HIF-2 playing a more dominant role than HIF-1. We also demonstrate that binding of Snail, a regulator of the EMT, to the IRS-2 promoter keeps the chromatin in an open conformation that is permissive for HIF-dependent transcription of IRS-2 in hypoxia. IRS-2 is not upregulated by hypoxia in well-differentiated epithelial-like carcinoma cells that do not express Snail, implicating IRS-2 gene expression as part of the EMT programming. In summary, we have identified an endogenous mechanism by which cancer cells can shift the balance of IRS-1 and IRS-2 to favor IRS-2 expression and function, which promotes survival, invasion, and ultimately metastasis. Understanding the mechanism of IRS-2 regulation by hypoxia may reveal new therapeutic targets for metastatic breast cancer.
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Jain, 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.

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The metabolism of vitamin D commences with exposure of the skin to sunlight. The growing recognition of its role in insulin resistance, autoimmune disorders, infections, cancer, as well as the health of cells that influence physical and mental function have profound implications on how we define vitamin D requirements and why we should care whether they are met or not. Most of the actions of vitamin D are mediated by the vitamin D receptor (VDR), a protein whose gene sequence can vary, giving rise to polymorphic forms which are potent enough to affect the binding capacity of this protein to vitamin D. Some of these polymorphic forms of VDR gene may be associated with reduced effectiveness of vitamin D and hence predispose individuals to diseases such as type 2 diabetes and insulin resistance. An earlier study, the Surya Study, looked at the responsiveness of the South-Asian women living in Auckland to vitamin D. The research described here is an extension of this study and its focus was to identify the associations/linkages between certain polymorphic forms of the VDR gene and the disease conditions and intervention responsiveness in the same women. The first objective was to compare two well known techniques for genotyping single nucleotide polymorphisms (SNPs) of the VDR gene at the 3’ end, namely BsmI, ApaI and TaqI: the newer real-time polymerase chain reaction (qPCR) and the traditional restriction fragment length polymorphism polymerase chain reaction (RFLP-PCR) techniques. This comparison was performed to evaluate alternative methods for genotyping which consumed less time than RFLP-PCR. When the presence of each polymorphism by both the techniques was compared in this cohort of South-Asian women, it was found that RFLP-PCR proved to be a more reliable technique than qPCR for genotyping the VDR gene. Another objective of this project was to investigate the prevalence of the above three polymorphisms along with Cdx-2 and FokI SNPs which are present at the 5’ end of the VDR gene, in the population under study and their possible association with phenotypes such as vitamin D responsiveness and insulin resistance. These women were screened and biochemical data was collected during the earlier Surya Study. Of these, eighty-one women were then selected for intervention based on them having high insulin resistance (HOMA-IR>1.93) and serum 25(OH)D<50 nmol/L. Out of these eighty-one women, forty-two were given vitamin D supplement and thirty-nine were given a placebo for six months. Baseline and endpoint measurements included insulin resistance (HOMA-IR), insulin sensitivity (HOMA2%S) etc. How each individual responded to treatment in the intervention group was analysed in the context of the polymorphisms that they had. An association of insulin resistance with BsmI, ApaI and TaqI SNPs was observed in this cohort of 239 women. The response to insulin resistance in the vitamin D supplemented group significantly differed for FokI genotype compared to other genotypes. This explained why certain women responded to treatment better than the others. When the frequencies of the genotypes of these five SNPs of the VDR gene were compared to other studies of different ethnicities, the results of this study were consistent with few studies but contradictory to others. The possible reasons for these differences could be because of small sample size and different ethnicities under study due to which the frequency of alleles and hence the genotypes differed.
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Iggström, 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.

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Wing polyphenism is a type of phenotypic plasticity present in several insect species whereby a genotype have the ability to develop alternative wing morphs when exposed to different environmental cues. One organism demonstrating a clear case of wing polyphenism is the water strider species, Gerris buenoi, which develop long- or short wings depending on exposure to different photoperiods (the time the organism is exposed to light during a 24 h period). The molecular mechanism behind wing polyphenism in insects in general, and in water striders in particular, is largely unknown. From a study on wing polyphenism in the Brown planthopper (Nilaparvata lugens), some candidate genes have been identified and include two insulin receptor genes and the Forkhead transcription factor (FOXO). Since these genes have been demonstrated to affect wing polyphenism in Brown planthopper (BPH) and since G. buenoi contains an additional insulin receptor homolog, the potential role of these genes in regulating wing polyphenism in G. buenoi have in this project been investigated. The functional genetic technique RNA interference (RNAi) was used to evaluate the function of the genes. This method knock down gene expression in the genes mentioned above, one at a time, to investigate if they have a function in wing polyphenism in G. buenoi. DsRNA with specific homology to each target gene was successfully produced. However, when attempting to inject the dsRNA through micro injection all injected liquid leaked out from the body cavity, and the RNAi was therefore not successful. Further optimisation of the injection protocol has to be done to be able to perform RNAi properly in the future. Thereafter, RT-qPCR was used to evaluate whether the insulin receptor genes and FOXO are differentially expressed between the two photoperiods giving rise to the different wing morphs. The differential gene expression experiment showed differences between the mRNA levels of all target genes between G. buenoi being reared in the two different photoperiods. More specific upregulation of the genes FOXO and insulin receptor 2 in short winged G. buenoi were demonstrated. Further, insulin receptor 1-like, was also demonstrated to be upregulated in the short winged morph. Results presented in this project are in line with the previously identified regulation pattern in BPH, still the results need further evaluation. Since gene expression differences were present for all candidate genes between G. buenoi reared in the different photoperiods, theses genes could still be seen as potential candidate genes in wing polyphenism in water striders.
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Gautam, 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.

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Ramaswamy, 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.

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Books on the topic "Insulin receptor gene"

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Petrisor, Bradley Allan. Analysis of the insulin receptor-related gene promoter. Ottawa: National Library of Canada, 1994.

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Jørn, Nerup, Mandrup-Poulsen Thomas, and Hökfelt Bernt, eds. Genes and gene products in the development of diabetes mellitus: Basic and clinical aspects : proceedings of the 3rd Nordisk Insulin Symposium "Genes and Gene Products in the Development of Diabetes Mellitus", Oslo, Norway, 3-5 July 1989. Amsterdam: Excerpta Medica, 1989.

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C, Baxter R., Gluckman Peter D, and Rosenfeld Ron G, eds. The insulin-like growth factors and their regulatory proteins: Proceedings of the Third International Symposium on Insulin-Like Growth Factors, Sydney, 6-10 February 1994. Amsterdam: Excerpta Medica, 1994.

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Shier, Peter. Characterization of the gene encoding the insulin receptor-related receptor, IRR : a putative receptor for a member of the insulin family. 1992.

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Genes and Gene Products in the Development of Diabetes Mellitus (Nordisk insulin symposia). Elsevier, 1989.

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Baxter, R. C., and Peter D. Gluckman. The Insulin-Like Growth Factors and Their Regulatory Proteins: Proceedings of the Third International Symposium on Insulin-Like Growth Factors, Sydn (International Congress Series). Elsevier Science Pub Co, 1994.

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Book chapters on the topic "Insulin receptor gene"

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McKeon, Catherine. "Transcriptional Regulation of the Insulin Receptor Gene Promoter." In Advances in Experimental Medicine and Biology, 79–89. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2988-0_9.

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Granner, D., D. Chu, C. Davis, and N. Chrapkiewicz. "Recriprocal Regulation of Pepck Gene and Gene 33 Transcription by Insulin." In The Steroid/Thyroid Hormone Receptor Family and Gene Regulation, 195–206. Basel: Birkhäuser Basel, 1989. http://dx.doi.org/10.1007/978-3-0348-5466-5_14.

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Trembath, R. C., S. Li, and D. J. Galton. "DNA Polymorphisms of the Insulin Receptor Gene and Non-Insulin-Dependent Diabetes Mellitus." In Verhandlungen der Deutschen Gesellschaft für Innere Medizin, 495–98. Munich: J.F. Bergmann-Verlag, 1987. http://dx.doi.org/10.1007/978-3-642-85460-6_124.

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Taylor, Simeon I., Domenico Accili, Alessandro Cama, Hiroko Kadowaki, Takashi Kadowaki, Eiichi Imano, and Maria de la Luz Sierra. "Mutations in the Insulin Receptor Gene in Patients with Genetic Syndromes of Insulin Resistance." In Advances in Experimental Medicine and Biology, 197–213. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5949-4_19.

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Werner, Haim, Bethel Stannard, Mark A. Bach, Charles T. Roberts, and Derek LeRoith. "Regulation of Insulin-Like Growth Factor I Receptor Gene Expression in Normal and Pathological States." In Advances in Experimental Medicine and Biology, 263–72. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5949-4_24.

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Bauskin, A. R., M. Zion, J. Szpirer, C. Szpirer, M. Q. Islam, G. Levan, G. Klein, and Y. Ben-Neriah. "Expression and Chromosomal Assignment of a Novel Protein-Tyrosine Kinase Gene Related to the Insulin Receptor Family." In Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, 453–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74621-5_79.

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Lemamy, Guy Joseph, Majida Esslimani Sahla, Marie Laurence Berthe, and Pascal Roger. "Is the Mannose-6-Phosphate/Insulin-Like Growth Factor 2 Receptor Coded by a Breast Cancer Suppressor Gene?" In Hormonal Carcinogenesis V, 305–10. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-69080-3_28.

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Luthman, Holger, Ingrid Delin, Anna Glaser, Rolf Luft, Svante Norgren, and Anna Wedell. "Molecular Genetics of NIDDM and the Genes for Insulin and Insulin Receptor." In Advances in Experimental Medicine and Biology, 101–11. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2910-1_8.

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Rosen, Kenneth M., Bruce M. Wentworth, Edward D. Lamperti, Stanislaus Kinota, Richard O’Brien, Nadia Rosenthal, Bruce Yankner, and Lydia Villa-Komaroff. "Expression of the IGF-II Gene in Brain and Muscle." In Molecular and Cellular Biology of Insulin-like Growth Factors and Their Receptors, 219–29. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5685-1_19.

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Murphy, Liam J., and Henry G. Friesen. "Regulation of Insulin-Like Growth Factor-1 Gene Expression by Estrogen." In Molecular and Cellular Biology of Insulin-like Growth Factors and Their Receptors, 153–68. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5685-1_14.

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Conference papers on the topic "Insulin receptor gene"

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Ahmed, Sumaya, and Nasser Rizk. "The Expression of Bile Acid Receptor TGR5 in Adipose Tissue in Diet-Induced Obese Mice." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0212.

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Bile acids are significant physiological factors for digestion, solubilization, absorption, toxic metabolites and xenobiotics. In addition, bile acids are responsible of signal transduction as well as metabolic regulation that activate several receptors such as farnesoid X receptor (FXR) and the membrane G-protein receptor 5 (TGR5). Activation of TGR5 by bile acids is associated with prevention of obesity as well as ameliorating the resistance to insulin via increasing energy expenditure. The objective of this research is to investigate TGR5 gene expression level in different fat depots including visceral or epididymal adipose tissue (eWAT), brown adipose tissue and inguinal adipose tissue (iWAT) and to study the response of TGR5 gene expression to the antiobesity treatment (SFN). Three groups of male CD1 mice were used in this study; lean group fed with SCD, DIO mice on HFD and DIO obese mice treated with anti-obesity treatment. Body weight (BW) and phenotype data were evaluated by weekly including blood samples for analysis of glucose, insulin, leptin, triglycerides (TG). Total RNA was extracted from different fat depots and RT-PCR profiler array technology was used to in order to assess the mRNA expression of TGR5 and leptin. There was significant downregulation of TGR5 gene expression level in obese (DIO) mice and remarkable upregulation of TGR5 gene expression after successful weight loss in DIO mice treated with SFN in time dependent manner at 1 weeks and 4 weeks of ip applications. In conclusion, obesity is associated with decrease in expression of TGR5 in different fat depots and treatment with anti-obesity drug (Sulforaphane) causes stepwise upregulation of TGR5 gene expression in epididymal white adipose tissue parallel stepwise decrease in body weight. Increase of expression of TGR5 in DIO mice in eWAT is accompanied by improvement in glucose homeostasis and insulin action.
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Ihle, Kate E. "Insulin receptor substrate (IRS) gene knockdown impacts complex behavior and shortens lifespan in honey bee workers." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.115016.

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Zhao, Ronghua, Ron Geyer, John Decoteau, and Alan Casson. "Abstract A9: Expression of insulin-like growth factor II and of the type 1 receptor gene in esophageal adenocarcinoma." In Abstracts: Frontiers in Cancer Prevention Research 2008. American Association for Cancer Research, 2008. http://dx.doi.org/10.1158/1940-6207.prev-08-a9.

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Potter, A., A. Potter, A. Casa, A. Casa, A. Lee, and A. Lee. "Gene Targets of Insulin-Like Growth Factor-I Receptor (IGF-IR) Signaling and Their Potential Role in Breast Cancer." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-4167.

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Sparano, J., R. Gray, L. Goldstein, B. Childs, D. Brassard, R. Bugarini, S. Rowley, et al. "Gene Expression Profiling of Phenotypically-Defined Hormone-Receptor Positive Breast Cancer: Evidence for Increased Transcriptional Activity of the Insulin Growth Factor Receptor Pathway and Other Pathways." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-5165.

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Kim, Mi Kyung, Han-Sung Kang, Sei Hyun Ahn, Kyeong-Man Hong, Siddhartha Kumar Mishra, Kyung Hwan Shin, Jungsil Ro, Keun Seok Lee, and Seok Won Kim. "Abstract 2610: Association of polymorphisms and haplotypes in the insulin-like growth factor 1 receptor (IGF1R) gene with breast cancer in Korean women." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2610.

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Diniz, Ornella Moreira. "NUTRIGENÔMICA NA OBESIDADE E NO DIABETES MELLITUS TIPO (DM) II." In I SIMPÓSIO MARANHENSE DE GENÉTICA E GENÔMICA EM SAÚDE. Doity - Plataforma de Eventos, 2022. http://dx.doi.org/10.55664/simaggens2022.018.

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Introdução: A dieta equilibrada exerce papel fundamental no controle pois é um fator que também exerce influência sobre os genes no desenvolvimento e evolução da diabetes mellitus tipo II e obesidade. (SANTOS, AMBROSIO-ALBUQUERQUE, 2019). A nutrigenômica, identifica e caracteriza as “assinaturas dietéticas” que denotam a ação dos nutrientes na natureza e expressão do genoma e posteriormente os seus efeitos sobre a saúde (FISCHER, et al., 2020) e vem buscado desvendar o impacto que os fatores nutricionais têm sobre a mediação e expressão de genes específicos, veiculando o potencial destes compostos no controle de doenças e os seus efeitos (SANTOS, AMBROSIO-ALBUQUERQUE, 2019). Objetivo: O objetivo dessa pesquisa foi identificar os dados da literatura e a interação da nutrigenômica, entre obesidade e diabetes mellitus tipo II. Métodos: Para o desenvolvimento desse estudo, foi realizada uma pesquisa literária, no banco de dados eletrônicos científicos PubMed, Scielo e artigos sobre o tema. Resultados e Discussão: As diferenças genéticas nos indivíduos decorrem das distintas respostas que temos com o meio em que habitamos em especial a alimentação. Com frequência pesquisas moleculares afirmam que determinados fatores ambientais não interferem na expressão gênica. Então, surge a nutrigenômica para ligar esses dois conceitos (SANTOS, AMBROSIO-ALBUQUERQUE, 2019). Foram descobertos 65 genes envolvidos no Diabetes Mellitus tipo II, que participam de metabolismos bioquímicos, regulatórios e sinais de transdução do DNA, capazes de produzir fenótipos associados com essas doenças (SALES, PELEGRINI, GOERSCH, 2014). As proteínas fabricadas por um determinado gene agem ligadas com outras proteínas. Por exemplo, o polimorfismo (IVS6+G82A) da guanina para tirosina (G-T) na interação genética da tirosina fosfatase 1B (PTP 1B) com um polimorfismo (Gln223Arg) no gene receptor da leptina (LEPR) (FUJII, MEDEIROS, YAMADA, 2010). A tirosina fosfatase 1B estabelece relação com a resistência à insulina e a obesidade (FUJII, MEDEIROS, YAMADA, 2010). A obesidade é um processo inflamatório. Alguns alimentos contêm bioativos anti-inflamatórios, como o ácido cafeico, a quercetina, o tirosol, e o licopeno inibindo a expressão dos genes COX2 e iNOS por meio da diminuição da translocação do fator nuclear Kappa-B do citoplasma para o núcleo (FUJII, MEDEIROS, YAMADA, 2010). A modulação da expressão gênica ocorre durante a transcrição, da síntese de mediadores inflamatórios tendo papel fundamental na obesidade. Assim, a interleucina-1 é um desses mediadores que, após a ativação, estimula a produção de muitas outras moléculas durante a cascata de inflamação (SALES, PELEGRINI, GOERSCH, 2014). O composto bioativo -tocoferol, atua reduzindo o nível desse processo inflamatório crônico que acontece em pessoas obesos. Estudos indicam que esse componente pode ajudar no tratamento da obesidade (FUJII, MEDEIROS, YAMADA, 2010). Conclusão: Apesar de mais estudos que evidenciem a interação de fatores ambientais com o genes, serem necessários, os estudos disponíveis já demonstram mecanismos que elucidam que essa interação existe e que é possível modular os genes através de fatores ambientais, auxiliando no tratamento das pessoas acometidas por obesidade e diabetes mellitus tipo II.
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Cruz, Ana Caroline Mesquita, and Mayana Aguiar Vasconcelos. "ACOMPANHAMENTO NUTRICIONAL EM MULHERES COM SÍNDROME DOS OVÁRIOS POLICÍSTICOS - UMA REVISÃO BIBLIOGRÁFICA." In I Congresso Brasileiro de Saúde Pública On-line: Uma abordagem Multiprofissional. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/2817.

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Introdução: Síndrome dos Ovários Policísticos (SOP) é uma doença crônica caracterizada como um distúrbio hormonal que pode afetar de 5 a 10% das mulheres em idade reprodutiva. Tal patologia está relacionada a altos índices de obesidade, resistência à insulina, diabetes mellitus 2 e problemas cardiovasculares causando repercussões à saúde ao longo da vida das portadoras. A SOP pode apresentar sintomas clínicos como hirsutismo, irregularidade menstrual, acne e infertilidade o que pode afetar diretamente a questão psicossocial nas portadoras. Os profissionais da nutrição precisam ter conhecimento frente a essa síndrome, pois a alteração do estilo de vida tem se instituído como tratamento de primeira linha em mulheres com SOP e obesidade. Objetivo: Compreender a fisiopatologia e a importância da abordagem dietoterápica em mulheres com SOP. Metodologia: coleta disponibilizada a partir de artigos científicos encontrados em sites de base de dados Pubmed, Scielo e Lilac, publicados nos últimos 10 anos. Foram utilizados os descritores "síndrome dos ovários policísticos", "síndrome metabólica", "obesidade" e "auxilio nutricional". Resultados: A fisiopatologia da SOP envolve o descontrole na esteroidogênese ovariana por um defeito intrínseco nas células da teca, redução da sensibilidade à insulina (atribuída a um defeito pós-receptor nas vias de sinalização da insulina), excesso de estresse oxidativo, além dos fatores genéticos e ambientais, porém o (s) gene (s) responsáveis pela SOP permanecem indefinidos. Dietas sem sido estudadas como método não medicamentoso e estudos mostram os benefícios da alteração do estilo de vida com a prática de atividade física e uma abordagem dietoterápica tem auxiliado na redução de peso em pacientes obesas com SOP o que afeta diretamente em uma melhora no ambiente hormonal e na composição corporal. No entanto, vale ressaltar que essas anormalidades metabólicas também podem estar presentes em pacientes não obesas. Alimentos in natura ou minimamente processados tem sido estudados principalmente por auxiliarem na prevenção de síndrome metabólica, diabetes mellitus tipo 2, doenças cardiometabólicas além de contribuir para a diminuição do estresse oxidativo nessa síndrome. Conclusão: Pode-se concluir que a orientação nutricional tem se constituído um modulador positivo mediante a sintomatologia e a nível metabólico na SOP.
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Resende, Ana Flávia Morais, Guilherme Rabelo Nasuk, Bruna Calixto de Jesus, Allan Luis Barboza Atum, and José Antônio Silva Júnior. "EXPRESSÃO MIOCÁRDICA RELACIONADA À CINÉTICA DO CÁLCIO EM ANIMAIS COM EXPOSIÇÃO PRÉ-NATAL AO ÁLCOOL." In Congresso Médico Acadêmico da Universidade Nove de Julho. Universidade Nove de Julho, 2022. http://dx.doi.org/10.5585/comamedvg.2022.16.

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Introdução: A exposição alcoólica pré-natal (E.P.A.) é considerada uma das principais responsáveis pelas alterações congênitas humanas. No sistema cardiovascular, a E.P.A. pode levar a alterações na expressão de genes relacionados à homeostase cardiovascular. Estudos têm mostrado que miócitos cardíacos expostos ao etanol durante a embriogênese não amadurecem morfológica ou funcionalmente, bem como apresentam alterações no transporte e captação/ligação de Ca2+ pelo retículo sarcoplasmático (SR). Uma diminuição da concentração citosólica de Ca2+ resultante do um efeito inibitório do álcool nas proteínas reguladoras desse íon pode resultar em diminuição do volume sistólico e alterações na frequência cardíaca. Objetivo: Analisar o impacto da E.P.A. na ativação da via de transdução de sinal da cinética do cálcio pela análise da expressão de RNA mensageiro de componentes desta via. Materiais e Métodos: O estudo foi aprovado pelo Comitê de Ética no Uso de Animais (CEUA = 9355120319 ID 000115). Foram utilizados camundongos isogênicos da linhagem C57Bl/6. As fêmeas progenitoras foram separadas e randomizadas no grupo controle (n=4) e no grupo de exposição ao álcool (n=11). O protocolo do grupo E.P.A. durante a gestação, foi a exposição do álcool na proporção de 10% (v/v) diluídos em água de consumo. Após 45 dias, 10 filhotes de cada grupo (n=20) foram anestesiados com isoflurano (<20 seg.) e decapitados. O ventrículo esquerdo (VE) foi coletado e tratado. A expressão relativa foi obtida por técnica RT-qPCR utilizando placas customizadas TaqMan®, sendo utilizado como controle endógeno o gene rRNA 18S. A estatística foi calculada com a aplicação IBM SPSS Statistics for Windows, Version 25.0. (Armonk, NY: IBM Corp., 2017); A normalidade foi testada através do teste de Shapiro-Wilk e os dados representados por média ± EPM. Comparação entre grupos: Teste T para amostras independentes sendo considerado o valor de significância p ≤0,05. Resultados: No grupo E.P.A, houve redução de 65,51% (p<0,001) e 60,17% (p<0,001) na expressão dos genes Calsequestrina 2 (Casq2) e Família de trocadores de soluto (Na-Ca) 8, membro A1 (Slc8a1), respectivamente, quando comparados ao grupo Controle. Por sua vez, o grupo E.P.A. apresentou aumento de 254,86% (p<0,001), 231,70% (p<0,001) e 183,37% (p<0,001) na expressão dos genes ATPase, transporte de Ca ++, músculo cardíaco, contração lenta 2 (Atp2a2), Receptor 2 de Rianodina, Cardíaco (RyR-2) e Fosfolamban (Pln) nessa ordem, quando comparado ao grupo Controle. Conclusão: Concluímos que a agressão mediada pelo álcool no miocárdio pode modular a via de cinética de cálcio. Estes resultados indicam que o insulto gerado pelo álcool, por meio de EPA e dependendo da concentração e/ou duração do estímulo, pode comprometer a expressão proteica de componentes da cinética do cálcio em favor de uma disfunção cardíaca. Palavras-chave: Álcool; cálcio; genes.
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Reports on the topic "Insulin receptor gene"

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Barash, Itamar, and Robert Rhoads. Translational Mechanisms Governing Milk Protein Levels and Composition. United States Department of Agriculture, 2006. http://dx.doi.org/10.32747/2006.7696526.bard.

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Original objectives: The long-term goal of the research is to achieve higher protein content in the milk of ruminants by modulating the translational apparatus of the mammary gland genetically, nutritionally, or pharmacologically. The short-term objectives are to obtain a better understanding of 1) the role of amino acids (AA) as regulators of translation in bovine and mouse mammary epithelial cells and 2) the mechanism responsible for the synergistic enhancement of milk-protein mRNA polyadenylation by insulin and prolactin. Background of the topic: In many cell types and tissues, individual AA affect a signaling pathway which parallels the insulin pathway to modulate rates and levels of protein synthesis. Diverse nutritional and hormonal conditions are funneled to mTOR, a multidomain serine/threonine kinase that regulates a number of components in the initiation and elongation stages of translation. The mechanism by which AA signal mTOR is largely unknown. During the current grant period, we have studied the effect of essential AA on mechanisms involved in protein synthesis in differentiated mammary epithelial cells cultured under lactogenic conditions. We also studied lactogenic hormone regulation of milk protein synthesis in differentiated mammary epithelial cells. In the first BARD grant (2000-03), we discovered a novel mechanism for mRNA-specific hormone-regulated translation, namely, that the combination of insulin plus prolactin causes cytoplasmic polyadenylation of milk protein mRNAs, which leads to their efficient translation. In the current BARD grant, we have pursued the signaling pathways of this novel hormone action. Major conclusions/solutions/achievements: The positive and negative signaling from AA to the mTOR pathway, combined with modulation of insulin sensitization, mediates the synthesis rates of total and specific milk proteins in mammary epithelial cells. The current in vitro study revealed cryptic negative effects of Lys, His, and Thr on cellular mechanisms regulating translation initiation and protein synthesis in mammary epithelial cells that could not be detected by conventional in vivo analyses. We also showed that a signaling pathway involving Jak2 and Stat5, previously shown to lead from the prolactin receptor to transcription of milk protein genes, is also used for cytoplasmic polyadenylation of milk protein mRNAs, thereby stabilizing these mRNAs and activating them for translation. Implications: In vivo, plasma AA levels are affected by nutritional and hormonal effects as well as by conditions of exercise and stress. The amplitude in plasma AA levels resembles that applied in the current in vitro study. Thus, by changing plasma AA levels in the epithelial cell microenvironment or by sensitizing the mTOR pathway to their presence, it should be possible to modulate the rate of milk protein synthesis. Furthermore, knowledge that phosphorylation of Stat5 is required for enhanced milk protein synthesis in response to lactogenic opens the possibility for pharmacologic approaches to increase the phosphorylation of Stat5 and, thereby, milk protein production.
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Hansen, Peter J., and Amir Arav. Embryo transfer as a tool for improving fertility of heat-stressed dairy cattle. United States Department of Agriculture, September 2007. http://dx.doi.org/10.32747/2007.7587730.bard.

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The overall objective of the current proposal is to develop procedures to improve the pregnancy rate achieved following transfer of fresh or cryopreserved embryos produced in the laboratory into heat-stress recipients. The overall hypothesis is that pregnancy rate in heat-stressed lactating cows can be improved by use of embryo transfer and that additional gains in pregnancy rate can be achieved through development of procedures to cryopreserve embryos, select embryos most likely to establish and maintain pregnancy after transfer, and to enhance embryo competence for post-transfer survival through manipulation of culture conditions. The original specific objectives were to 1) optimize procedures for cryopreservation (Israel/US), 2) develop procedures for identifying embryos with the greatest potential for development and survival using the remote monitoring system called EmbryoGuard (Israel), 3) perform field trials to test the efficacy of cryopreservation and the EmbryoGuard selection system for improving pregnancy rates in heat-stressed, lactating cows (US/Israel), 4) test whether selection of fresh or frozen-thawed blastocysts based on measurement of group II caspase activity is an effective means of increasing survival after cryopreservation and post-transfer pregnancy rate (US), and 5) identify genes in blastocysts induced by insulin-like growth factor-1 (IGF-1) (US). In addition to these objectives, additional work was carried out to determine additional cellular determinants of embryonic resistance to heat shock. There were several major achievements. Results of one experiment indicated that survival of embryos to freezing could be improved by treating embryos with cytochalasin B to disrupt the cytoskeleton. An additional improvement in the efficacy of embryo transfer for achieving pregnancy in heat-stressed cows follows from the finding that IGF-1 can improve post-transfer survival of in vitro produced embryos in the summer but not winter. Expression of several genes in the blastocyst was regulated by IGF-1 including IGF binding protein-3, desmocollin II, Na/K ATPase, Bax, heat shock protein 70 and IGF-1 receptor. These genes are likely candidates 1) for developing assays for selection of embryos for transfer and 2) as marker genes for improving culture conditions for embryo production. The fact that IGF-1 improved survival of embryos in heat-stressed recipients only is consistent with the hypothesis that IGF-1 confers cellular thermotolerance to bovine embryos. Other experiments confirmed this action of IGF-1. One action of IGF-1, the ability to block heat-shock induced apoptosis, was shown to be mediated through activation of the phosphatidylinositol 3-kinase pathway. Other cellular determinants of resistance of embryos to elevated temperature were identified including redox status of the embryo and the ceramide signaling pathway. Developmental changes in embryonic apoptosis responses in response to heat shock were described and found to include alterations in the capacity of the embryo to undergo caspase-9 and caspase-3 activation as well as events downstream from caspase-3 activation. With the exception of IGF-1, other possible treatments to improve pregnancy rate to embryo transfer were not effective including selection of embryos for caspase activity, treatment of recipients with GnRH.and bilateral transfer of twin embryos. In conclusion, accomplishments achieved during the grant period have resulted in methods for improving post-transfer survival of in vitro produced embryos transferred into heat-stressed cows and have lead to additional avenues for research to increase embryo resistance to elevated temperature and improve survival to cryopreservation. In addition, embryo transfer of vitrified IVF embryos increased significantly the pregnancy rate in repeated breeder cows.
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Meidan, Rina, and Robert Milvae. Regulation of Bovine Corpus Luteum Function. United States Department of Agriculture, March 1995. http://dx.doi.org/10.32747/1995.7604935.bard.

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The main goal of this research plan was to elucidate regulatory mechanisms controlling the development, function of the bovine corpus luteum (CL). The CL contains two different sterodigenic cell types and therefore it was necessary to obtain pure cell population. A system was developed in which granulosa and theca interna cells, isolated from a preovulatory follicle, acquired characteristics typical of large (LL) and small (SL) luteal cells, respectively, as judged by several biochemical and morphological criteria. Experiments were conducted to determine the effects of granulosa cells removal on subsequent CL function, the results obtained support the concept that granulosa cells make a substaintial contribution to the output of progesterone by the cyclic CL but may have a limited role in determining the functional lifespan of the CL. This experimental model was also used to better understand the contribution of follicular granulosa cells to subsequent luteal SCC mRNA expression. The mitochondrial cytochrome side-chain cleavage enzyme (SCC), which converts cholesterol to pregnenolone, is the first and rate-limiting enzyme of the steroidogenic pathway. Experiments were conducted to characterize the gene expression of P450scc in bovine CL. Levels of P450scc mRNA were higher during mid-luteal phase than in either the early or late luteal phases. PGF 2a injection decreased luteal P450scc mRNA in a time-dependent manner; levels were significantly reduced by 2h after treatment. CLs obtained from heifers on day 8 of the estrous cycle which had granulosa cells removed had a 45% reduction in the levels of mRNA for SCC enzymes as well as a 78% reduction in the numbers of LL cells. To characterize SCC expression in each steroidogenic cell type we utilized pure cell populations. Upon luteinization, LL expressed 2-3 fold higher amounts of both SCC enzymes mRNAs than SL. Moreover, eight days after stimulant removal, LL retained their P4 production capacity, expressed P450scc mRNA and contained this protein. In our attempts to establish the in vitro luteinization model, we had to select the prevulatory and pre-gonadotropin surge follicles. The ratio of estradiol:P4 which is often used was unreliable since P4 levels are high in atretic follicles and also in preovulatory post-gonadotropin follicles. We have therefore examined whether oxytocin (OT) levels in follicular fluids could enhance our ability to correctly and easily define follicular status. Based on E2 and OT concentrations in follicular fluids we could more accurately identify follicles that are preovulatory and post gonadotropin surge. Next we studied OT biosynthesis in granulosa cells, cells which were incubated with forskolin contained stores of the precursor indicating that forskolin (which mimics gonadotropin action) is an effective stimulator of OT biosynthesis and release. While studying in vitro luteinization, we noticed that IGF-I induced effects were not identical to those induced by insulin despite the fact that megadoses of insulin were used. This was the first indication that the cells may secrete IGF binding protein(s) which regonize IGFs and not insulin. In a detailed study involving several techniques, we characterized the species of IGF binding proteins secreted by luteal cells. The effects of exogenous polyunsaturated fatty acids and arachidonic acid on the production of P4 and prostanoids by dispersed bovine luteal cells was examined. The addition of eicosapentaenoic acid and arachidonic acid resulted in a dose-dependent reduction in basal and LH-stimulated biosynthesis of P4 and PGI2 and an increase in production of PGF 2a and 5-HETE production. Indomethacin, an inhibitor of arachidonic acid metabolism via the production of 5-HETE was unaffected. Results of these experiments suggest that the inhibitory effect of arachidonic acid on the biosynthesis of luteal P4 is due to either a direct action of arachidonic acid, or its conversion to 5-HETE via the lipoxgenase pathway of metabolism. The detailed and important information gained by the two labs elucidated the mode of action of factors crucially important to the function of the bovine CL. The data indicate that follicular granulosa cells make a major contribution to numbers of large luteal cells, OT and basal P4 production, as well as the content of cytochrome P450 scc. Granulosa-derived large luteal cells have distinct features: when luteinized, the cell no longer possesses LH receptors, its cAMP response is diminished yet P4 synthesis is sustained. This may imply that maintenance of P4 (even in the absence of a Luteotropic signal) during critical periods such as pregnancy recognition, is dependent on the proper luteinization and function of the large luteal cell.
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