Dissertations / Theses on the topic 'Insulin resistance'
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Walker, Adrian Bernard. "The effect of insulin on resistance artery function in insulin-resistant states." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312450.
Full textMaffeis, Laura <1981>. "Correlation between insulin resistance and treatment-resistant acne." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5654/1/maffeis_laura_tesi.pdf.
Full textMaffeis, Laura <1981>. "Correlation between insulin resistance and treatment-resistant acne." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5654/.
Full textCollison, Mary Williamson. "Insulin signalling in insulin resistance and cardiovascular disease syndromes." Thesis, University of Glasgow, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366184.
Full textSvanfeldt, Monika. "Perioperative nutrition and insulin resistance /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-637-9/.
Full textIsaksson, Bengt. "Insulin resistance in pancreatic cancer /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-493-3/.
Full textBerends, Lindsey Matara. "Developmental programming of insulin resistance." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648433.
Full textAli, Salmin. "GLUT 4 and Insulin Resistance." Wright State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=wright1409746939.
Full textEndre, Tomas. "The hypertension-prone man a study on the pathogenesis of hypertension with regard to insulin sensitivity /." Lund : Dept. of Medicine, Lund University, University Hospital MAS, 1997. http://books.google.com/books?id=3UlsAAAAMAAJ.
Full textStuart, Charles A., Mary E. A. Howell, Brian M. Cartwright, Melanie P. McCurry, Michelle L. Lee, Michael W. Ramsey, and Michael H. Stone. "Insulin Resistance and Muscle Insulin Receptor Substrate-1 Serine Hyperphosphorylation." Digital Commons @ East Tennessee State University, 2014. https://dc.etsu.edu/etsu-works/4117.
Full textGuarilha, Alessandra Lia Gasparetti. "Transdução do sinal da insulina em animais expostos ao frio : o papel do cross-talk entre o receptor 'beta' 3 - adrenergico e o receptor de insulina em tecido adiposo marrom." [s.n.], 2004. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310365.
Full textTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-08-04T02:29:02Z (GMT). No. of bitstreams: 1 Guarilha_AlessandraLiaGasparetti_D.pdf: 7883483 bytes, checksum: cefd0ee77fd363b470280f9b8a380ff9 (MD5) Previous issue date: 2004
Resumo: A exposição de animais homeotérmicos ao mo é utilizada como um método reprodutível para se obter um modelo animal de hipoinsulinemiaacompanhada por elevada mobilização periférica de glicose. No presente estudo, avaliaram-se as etapas iniciais e intermediárias da via de sinalização da insulina em tecidos periféricos de ratos expostos ao mo. Avaliou-se ainda, a comunicação intracelular entre o receptor (33-adrenérgicoe as vias de sinalização da insulina em tecido adiposo marrom de ratos expostos ao mo e tratados, ou não, com compostos agonista ou antagonista (33-adrenérgicos.A exposição de ratos ao mo promoveu a redução da secreção de insulina, acompanhada de um elevado clearance de glicose e maior captação de glicose por tecido muscular esquelético, adiposo branco e adiposo marrom. Tais fenômenos foram acompanhados por inibição da ativação da maior parte dos componentes da via de sinalização da insulina em tecido muscular esquelético e adiposo branco; por estimulação da maior parte dos componentes da via de sinalização da insulina em tecido adiposo marrom; e por efeitos variados (estímulo, inibição e não-modulação) de componentes da via de sinalização da insulina em figado. Por fim, este estudo demonstrou que a exposição ao mo ativa a sinalização (33-adrenérgicaem tecido adiposo marrom. Tal ativação leva à modulação da atividade de vários componentes da via de sinalização da insulina neste tecido. Entretanto, fatores independentes da sinalização (33-adrenérgica parecem contribuir para a complexa regulação do sinal da insulina obseIVada em tecido adiposo marrom de ratos expostos ao mo. Em conclusão, o presente estudo revelou alguns dos intrincados mecanismos pelos quais a exposição ao mo controla a atividade da insulina em animais homeotérmicos, podendo favorecer a identificação de potenciais alvos para a ação terapêutica em doenças onde a resistência à insulina desempenha papel central
Abstract: Cold exposure provides a reproducible model of improved glucose turnover accompanied by reduced blood levels of insulin. In the present study, the initial and intermediate steps of the insulin-signaling pathway in peripheral tissues of rats exposed to cold environment were evaluated. Also, the intracellular connection between insulin and ~3-adrenergic signaling in brown adipose tissue of cold exposed rats treated, or not, with ~3-adrenergic agonist or antagonist compounds were evaluated. During cold exposure, insulin secretion was significantly impaired, while whole body glucose clearance rates were significantly improved. This was accompanied by an increased glucose uptake by skeletal muscle, white adipose tissue and brown adipose tissue. These phenomena were paralleled by an apparent molecular resistance to insulin in skeletal muscle and white adipose tissue; by improved molecular response to insulin in brown adipose tissue; and by ambiguous effects (stimulation, inhibition and not modulation) of regulation of the insulin-signaling pathway in liver. Finally, cold exposure activated the ~3-adrenergic signaling in brown adipose tissue. It leads to modulation of activity of several components of the insulin signal transduction pathway in this tissue. However, ~3-adrenergic receptor independent mechanisms seem to contribute to the complex regulation of the insulin signaling observed in brown adipose tissue of rats exposed to cold. In conclusion, the present study revealed some of the complex mechanisms that participate in the cold-exposure-induced control of the insulin action in homeothermic animals. These results may favour the identification of novel potential targets for therapeutics in diabetes and related disorders
Doutorado
Medicina Experimental
Doutor em Fisiopatologia Medica
Morin-Papunen, L. (Laure). "Insulin resistance in polycystic ovary syndrome." Doctoral thesis, University of Oulu, 2000. http://urn.fi/urn:isbn:9514257405.
Full textBorer, Katharine Elizabeth. "Laminitis and insulin resistance in ponies." Thesis, Royal Veterinary College (University of London), 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.572136.
Full textLo, Kin Yui Alice. "Transcriptional regulation of adipose insulin resistance." Thesis, Massachusetts Institute of Technology, 2012. http://hdl.handle.net/1721.1/71466.
Full textPage 168 blank. Cataloged from PDF version of thesis.
Includes bibliographical references (p. 155-167).
Insulin resistance is a condition that underlies type 2 diabetes and various cardiovascular diseases. It is highly associated with obesity, making it a pressing medical problem in face of the obesity epidemic. The obesity association also makes adipose tissue the target of interest for ongoing research. Previous work on adipose insulin resistance has largely been focused on deciphering the signaling defects and abnormal adipokine secretion profiles. There is increasing awareness that transcriptional control is a source of dysregulation as well as an avenue of therapeutic intervention for insulin resistance. However, knowledge of transcriptional regulation and dysregulation of adipose insulin resistance remains fragmentary. Here, we present a genome-wide perspective on transcriptional regulation of adipocyte biology and adipose insulin resistance. We made use of the latest high-throughput sequencing technology to interrogate different aspects of transcriptional regulation, namely, histone modifications, protein-DNA interactions, and chromatin accessibility in adipocytes. In combination with the transcriptional outcomes measured by microarray and RNA-sequencing, we (1) characterized a largely unknown histone modification, H3K56 acetylation, in human adipocytes, and (2) set up four diverse in vitro insulin resistance models in mouse adipocytes and analyzed them in parallel with mouse adipose tissues from diet-induced obese mice. In both cases, through computational analysis of the experimentally identified cis-regulatory regions, we identified existing and novel trans-regulators responsible for adipose transcriptional regulation. Furthermore, by comprehensive pathway analysis of the in vitro models and mouse models, we identified aspects of in vivo adipose insulin resistance that are captured by the different in vitro models. Taken together, our studies present a systems view on adipose transcriptional regulation, which provides a wealth of novel resources for gaining insights into adipose biology and insulin resistance.
by Kin Yui Alice Lo.
Ph.D.
Raab, R. Michael. "Genomic analysis of hepatic insulin resistance." Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/33762.
Full textIncludes bibliographical references (leaves 159-191).
Type II Diabetes mellitus is a genetically complex disease characterized by insulin resistance in peripheral tissues, which results in simultaneous hyperglycemia and hyperinsulinemia. Because of the prevalence of type II diabetes, many researchers are investigating the genetics of glucose homeostasis, however, traditional mapping techniques have not been successful in determining all of the genes that regulate glycemia. To complement these efforts, we used DNA microarrays to find differentially expressed genes and combinatorial siRNA screening to investigate the effects of hepatic gene transcription during periods of high and low glucose production. This strategy provides a new approach to studying the molecular mechanisms of disease pathogenesis. Our investigations focused on discovering new genes that influence hepatic metabolism and glucose production. Hepatocytes help maintain whole body glycemia by providing glucose and other substrates during non-feeding periods. DNA microarrays containing 17,000 unique gene probes were used to study hepatic gene transcription during normal, insulin resistant, and fasting states in C57/BL/6J mice. We analyzed this data set using a combination of statistical and multivariate techniques to determine 41 different, genes that are differentially expressed and highly discriminatory of the treatment groups.
(cont.) Hepatocytes perform many physiological roles, thus to investigate which genes from the microarray analysis affected hepatic metabolism, we developed combinatorial RNA-interference (RNAi) based gene silencing techniques. Using combinatorial siRNA screening, we silenced genes that were over-expressed within the microarray data set to study loss of function effects on hepatic metabolism, which was quantified by measuring intracellular metabolite concentrations in relevant metabolic pathways. Based upon the metabolite dependent clustering of experimental and control samples using Fisher Discriminant Analysis, four of the silenced genes had a significant effect on key metabolites involved in hepatic glucose output. Of these four genes, three were shown to influence hepatic glucose output in our primary cell model.
by R. Michael Raab.
Ph.D.
Aksentijević, Dunja. "Myocardial insulin resistance in experimental uraemia." Thesis, University of Hull, 2008. http://hydra.hull.ac.uk/resources/hull:5757.
Full textTewari, Nilanjana. "Mechanisms underlying obesity-related insulin resistance." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/34081/.
Full textMalik, Muhammad Omar. "Insulin resistance, ethnicity and cardiovascular risk." Thesis, University of Glasgow, 2015. http://theses.gla.ac.uk/6517/.
Full textNowak, Christoph. "Insulin Resistance : Causes, biomarkers and consequences." Doctoral thesis, Uppsala universitet, Molekylär epidemiologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-316891.
Full textBarber, Collin. "SIRT3: Molecular Signaling in Insulin Resistance." Thesis, The University of Arizona, 2014. http://hdl.handle.net/10150/315823.
Full textPost-translational modification of intracellular proteins through acetylation is recognized as an important regulatory mechanism of cellular energy homeostasis. Specific proteins called sirtuins deacetylate other mitochondrial proteins involved in glucose and lipid metabolism, activating them in metabolic processes. SIRT3 is a sirtuin of particular interest as it is found exclusively in mitochondria and has been shown to affect a variety of cellular metabolic processes. The activity of this enzyme is related to cellular insulin sensitivity. This study attempted to identify the relationship between insulin sensitivity and change in amount of SIRT3 following a bout of exercise in non-diabetic individuals. We find a moderate inverse correlation between insulin sensitivity and increase in SIRT3 abundance following exercise. This suggests that this protein may not be involved directly in cells’ ability to regulate energy homeostasis or that it may act through another mechanism not investigated in this study.
Campbell, Ian William. "Insulin resistance, hypertension and the insulin-responsive glucose transporter, GLUT-4." Thesis, University of Glasgow, 1997. http://theses.gla.ac.uk/8472/.
Full textKershner, David. "Oral Glucose Insulin Secretion Test for Identifying Patients with Insulin Resistance." ScholarWorks, 2018. https://scholarworks.waldenu.edu/dissertations/5634.
Full textFrangioudakis, Georgia St Vincent's Clinical School UNSW. "Insulin signal transduction in vivo in states of lipid-induced insulin resistance." Awarded by:University of New South Wales. St Vincent's Clinical School, 2004. http://handle.unsw.edu.au/1959.4/27419.
Full textWiggam, Malcolm Ivan. "Aspects of insulin resistance in essential hypertension and insulin-dependent diabetes mellitus." Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387971.
Full textVerchere, Cameron Bruce. "Control of insulin secretion from the perfused rat pancreas : effects of acetylcholine and a somatostatin analog, SMS 201-995." Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/26657.
Full textMedicine, Faculty of
Cellular and Physiological Sciences, Department of
Graduate
Bikman, Benjamin Thomas Dohm G. Lynis. "Modulation of IKK[beta] with AMPK improves insulin sensitivity in skeletal muscle." [Greenville, N.C.] : East Carolina University, 2008. http://hdl.handle.net/10342/1081.
Full textPresented to the faculty of the Department of Exercise and Sport Science. Advisor: G. Lynis Dohm. Title from PDF t.p. (viewed Apr. 23, 2010). Includes bibliographical references.
Mohteshamzadeh, Mobin. "Hypertension, insulin resistance and vitric oxide bioavailability." Thesis, University of Newcastle upon Tyne, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270768.
Full textHale, P. J. "Insulin resistance in diabetes mellitus and obesity." Thesis, University of Oxford, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.371516.
Full textPang, Shengru [Verfasser], and Marco [Akademischer Betreuer] Prinz. "Microglial activation during obesity-induced insulin resistance." Freiburg : Universität, 2017. http://d-nb.info/1187132764/34.
Full textWinter, Stephen A. "Dietary sucrose, insulin resistance and the heart." Thesis, University of Bath, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260222.
Full textPickavance, Lucy Cecilia. "Thiazolidinedione treatment in models of insulin resistance." Thesis, University of Liverpool, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367553.
Full textShmueli, Ehoud. "Glucose metabolism and insulin resistance in cirrhosis." Thesis, University of Newcastle Upon Tyne, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308777.
Full textEason, Robert C. "Treating type 2 diabetes through insulin resistance." Thesis, Aston University, 2002. http://publications.aston.ac.uk/10953/.
Full textAl-Naser, Al Zekri Huda M. "Oligo/amenorrhoea : endocrine profiles, ovarian ultrasound, insulin resistan and anthropometric factors; relationships between insulin resistance and ovarian function." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360284.
Full textBlond, Emilie. "Mécanisme de l'insulino-résistance lors de la modulation in vivo et in vitro par l'acide nicotinique et les polyphénols." Thesis, Lyon 1, 2012. http://www.theses.fr/2012LYO10169.
Full textSong, Xiao Mei. "Insulin signal transduction in skeletal muscle : special consideration for insulin resistance and diabetes /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4502-0/.
Full textDanielsson, Anna. "Insulin signalling in human adipocytes : mechanisms of insulin resistance in type 2 diabetes." Doctoral thesis, Linköping : Univ, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-10327.
Full textSlevin, Karen Aoife. "Dietary fat and insulin sensitivity." Thesis, University of Surrey, 2000. http://epubs.surrey.ac.uk/843068/.
Full textSundström, Johan. "Left ventricular hypertrophy and the insulin resistance syndrome." Doctoral thesis, Uppsala University, Department of Public Health and Caring Sciences, 2001. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-580.
Full textLeft ventricular hypertrophy (LVH) and the insulin resistance syndrome are common conditions associated with a markedly increased cardiovascular risk. In a fairly large prospective longitudinal study of men from the general population, we found that an unfavorable serum fatty acid profile and components of the insulin resistance syndrome such as dyslipidemia, obesity and hypertension at age 50 predicted the prevalence of LVH at age 70. In cross-sectional analyses at age 70, several components of the insulin resistance syndrome were significantly related to left ventricular relative wall thickness and concentric remodeling, but less to LVH. Left ventricular relative wall thickness was inversely related to insulin sensitivity in skeletal muscle and borderline significantly directly related to insulin sensitivity in the myocardium in a healthy, normotensive sample of the cohort investigated with positron emission tomography, whereas left ventricular mass index was not related to myocardial or skeletal muscle insulin sensitivity. At age 70, echocardiographic LVH was related to a variety of common electrocardiographic diagnoses. In a prospective mortality analysis with baseline at age 70 and a median follow-up time of five years, echocardiographic and electrocardiographic LVH predicted mortality independently of each other and of other cardiovascular risk factors, implying that echocardiographic and electrocardiographic LVH in part carry different prognostic information.
In summary, components of the insulin resistance syndrome predicted LVH twenty years later, but were cross-sectionally more related to increased left ventricular relative wall thickness and concentric remodeling. Echocardiographic and electrocardiographic LVH predicted mortality independently of each other and of components of the insulin resistance syndrome.
Baba, Reizo, Masaaki Koketsu, Masami Nagashima, Akiko Tamakoshi, and Hiroshi Inasaka. "Role of Insulin Resistance in Non-Obese Adolescents." Nagoya University School of Medicine, 2010. http://hdl.handle.net/2237/14178.
Full textSpence, M. "Dietary effects on insulin resistance and vascular risk." Thesis, Queen's University Belfast, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492315.
Full textNygren, Jonas. "The sites and mechanisms of postoperative insulin resistance /." Stockholm, 1997. http://diss.kib.ki.se/1997/91-628-2695-6.
Full textSundström, Johan. "Left ventricular hypertrophy and the insulin resistance syndrome /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-4919-0/.
Full textField, Polly Ann. "The effects of insulin resistance on chylomicron metabolism." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302120.
Full textBradley, Una Marie. "Insulin resistance : the effect of diet and autoimmunity." Thesis, Queen's University Belfast, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534638.
Full textKhoo, Eric Yin Hao. "Studies in body composition, insulin resistance and exercise." Thesis, University of Nottingham, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.546233.
Full textAlzadjali, Matlooba A. "Insulin Resistance : A New Target in Heart Failure." Thesis, University of Dundee, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.505652.
Full textHumphreys, P. "Biochemical and genetic studies of human insulin resistance." Thesis, University of Cambridge, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604777.
Full textHunter, Steven J. "Insulin resistance : underlying mechanisms and influence of treatment." Thesis, Queen's University Belfast, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337044.
Full textPickersgill, Laura. "Lipid-induced insulin resistance in human skeletal muscle." Thesis, University of Newcastle Upon Tyne, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413955.
Full text