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1
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.
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Maffeis, 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.
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Physiologically during puberty and adolescence, when juvenile acne usually appears, the response to a glucose load is increased if compared to the one observed in adult and at pre-pubertal age, while insulin sensitivity is reduced. Insulin is a hormone that acts at different levels along the axis which controls the sex hormones. It increases the release of LH and FSH by pituitary gland, stimulates the synthesis of androgens in the gonads and stimulates the synthesis of androgenic precursors in adrenal glands. Finally, it acts in the liver by inhibiting the synthesis of Sex Hormone Binding Globulin (SHBG). Insulin is also able to act directly on the production of sebum and amplify the effects of Iinsulin Growth Factor-1 in the skin, inhibiting the synthesis of its binding protein (IGF Binding Protein-1).
In female subjects with acne and Polycystic Ovary Syndrome (PCOS) insulin resistance is a well known pathogenetic factor, while the relationship between acne and insulin resistance has been poorly investigated in males so far.
The purpose of this study is to investigate the correlation between insulin resistance and acne in young males who do not respond to common therapies. Clinical and biochemical parameters of glucose, lipid metabolism, androgens and IGF-1 were evaluated. Insulin resistance was estimated by Homeostasis Model assessment (HOMA-IR) and Oral Glucose Tolerance Test was also performed. We found that subjects with acne had higher Sistolic and Diastolic Blood Pressure, Waist/Hip Ratio, Waist Circumference, 120' OGTT serum insulin and serum IGF-1 and lower HDL-cholesterol than subjects of comparable age and gender without acne.
The results thus obtained confirmed what other authors have recently reported about a metabolic imbalance in young males with acne. Furthermore, these results support the hypothesis that insulin resistance might play an important role in the pathogenesis of treatment-resistant acne in males.
3
Maffeis, 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 textAbstract:
Physiologically during puberty and adolescence, when juvenile acne usually appears, the response to a glucose load is increased if compared to the one observed in adult and at pre-pubertal age, while insulin sensitivity is reduced. Insulin is a hormone that acts at different levels along the axis which controls the sex hormones. It increases the release of LH and FSH by pituitary gland, stimulates the synthesis of androgens in the gonads and stimulates the synthesis of androgenic precursors in adrenal glands. Finally, it acts in the liver by inhibiting the synthesis of Sex Hormone Binding Globulin (SHBG). Insulin is also able to act directly on the production of sebum and amplify the effects of Iinsulin Growth Factor-1 in the skin, inhibiting the synthesis of its binding protein (IGF Binding Protein-1).
In female subjects with acne and Polycystic Ovary Syndrome (PCOS) insulin resistance is a well known pathogenetic factor, while the relationship between acne and insulin resistance has been poorly investigated in males so far.
The purpose of this study is to investigate the correlation between insulin resistance and acne in young males who do not respond to common therapies. Clinical and biochemical parameters of glucose, lipid metabolism, androgens and IGF-1 were evaluated. Insulin resistance was estimated by Homeostasis Model assessment (HOMA-IR) and Oral Glucose Tolerance Test was also performed. We found that subjects with acne had higher Sistolic and Diastolic Blood Pressure, Waist/Hip Ratio, Waist Circumference, 120' OGTT serum insulin and serum IGF-1 and lower HDL-cholesterol than subjects of comparable age and gender without acne.
The results thus obtained confirmed what other authors have recently reported about a metabolic imbalance in young males with acne. Furthermore, these results support the hypothesis that insulin resistance might play an important role in the pathogenesis of treatment-resistant acne in males.
4
Collison, 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.
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5
Svanfeldt, Monika. "Perioperative nutrition and insulin resistance /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-637-9/.
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Isaksson, Bengt. "Insulin resistance in pancreatic cancer /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-493-3/.
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Berends, Lindsey Matara. "Developmental programming of insulin resistance." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648433.
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Ali, Salmin. "GLUT 4 and Insulin Resistance." Wright State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=wright1409746939.
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9
Endre, 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.
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10
Stuart, 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.
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Insulin resistance in metabolic syndrome subjects is profound in spite of muscle insulin receptor and insulin-responsive glucose transporter (GLUT4) expression being nearly normal. Insulin receptor tyrosine kinase phosphorylation of insulin receptor substrate-1 (IRS-1) at Tyr896 is a necessary step in insulin stimulation of translocation of GLUT4 to the cell surface. Serine phosphorylation of IRS-1 by some kinases diminishes insulin action in mice. We evaluated the phosphorylation status of muscle IRS-1 in 33 subjects with the metabolic syndrome and seventeen lean controls. Each underwent euglycemic insulin clamps and a thigh muscle biopsy before and after 8 weeks of either strength or endurance training. Muscle IRS-1 phosphorylation at six sites was quantified by immunoblots. Metabolic syndrome muscle IRS-1 had excess phosphorylation at Ser337 and Ser636 but not at Ser307, Ser789, or Ser1101. Ser337 is a target for phosphorylation by glycogen synthase kinase 3 (GSK3) and Ser636 is phosphorylated by c-Jun N-terminal kinase 1 (JNK1). Exercise training without weight loss did not change the IRS-1 serine phosphorylation. These data suggest that baseline hyperphosphorylation of at least two key serines within muscle IRS-1 diminishes the transmission of the insulin signal and thereby decreases the insulin-stimulated translocation of GLUT4. Excess fasting phosphorylation of muscle IRS-1 at Ser636 may be a major cause of the insulin resistance seen in obesity and might prevent improvement in insulin responsiveness when exercise training is not accompanied by weight loss.
11
Guarilha, 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.
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Orientador: Licio Augusto Velloso<br>Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas<br>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<br>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<br>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<br>Doutorado<br>Medicina Experimental<br>Doutor em Fisiopatologia Medica
12
Morin-Papunen, L. (Laure). "Insulin resistance in polycystic ovary syndrome." Doctoral thesis, University of Oulu, 2000. http://urn.fi/urn:isbn:9514257405.
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Abstract
The polycystic ovary syndrome, described first as the association
of bilateral polycystic ovaries and amenorrhoea, oligomenorrhoea,
hirsutism and obesity, was later shown to be a complex metabolic syndrome.
The first purpose of this study was to investigate the occurrence
of hyperinsulinaemia and the severity of insulin resistance and
glucose tolerance disorders in polycystic ovary syndrome by means of
the oral glucose tolerance test and the euglycaemic hyperinsulinaemic
clamp. The next goal was to investigate whether women with polycystic
ovary syndrome would benefit from insulin-sensitising drugs, and
in particular to compare the effects of metformin and a contraceptive
pill containing ethinyl oestradiol and cyproterone acetate. Altogether,
81 women with polycystic ovary syndrome and 34 healthy control subjects
were involved in the study.
Marked impairment of insulin sensitivity in obese subjects
with polycystic ovary syndrome, including a decrease of both cellular
oxidative and non-oxidative utilisation of glucose, and a slight non-significant
decrease of insulin sensitivity in non-obese subjects was observed.
Both non-obese and obese subjects with polycystic ovary syndrome
exhibited increased abdominal obesity compared with the controls,
confirming the fact that obesity, in particular abdominal obesity,
is an important contributor in the development of insulin resistance
in this syndrome.
Metformin alleviated hyperandrogenism by essentially decreasing
ovarian, but not adrenal androgen secretion. The improvement of
hyperandrogenism and ovarian function seemed to be mediated by the
improvement of hyperinsulinaemia, which resulted itself from subtle
improvements in both hepatic insulin extraction and insulin sensitivity.
Metformin decreased abdominal obesity and the release of free fatty
acids from adipose tissue, and improved ovarian cyclicity and fertility.
The transient decrease in serum leptin levels observed may have
some role in the improvement of ovarian function. The contraceptive
pill significantly improved hyperandrogenism and hirsutism, and
it slightly affected glucose metabolism. Thus, it could be the treatment
of choice in women with hirsutism problems and no fertility hopes.
Metformin could be the drug of choice for women with polycystic
ovary syndrome who wish to conceive. Because of its beneficial metabolic
effects, the value of metformin in reducing the risk of cardiovascular
diseases in polycystic ovary syndrome needs to be further studied.
13
Borer, 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.
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14
Lo, Kin Yui Alice. "Transcriptional regulation of adipose insulin resistance." Thesis, Massachusetts Institute of Technology, 2012. http://hdl.handle.net/1721.1/71466.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biological Engineering, 2012.<br>Page 168 blank. Cataloged from PDF version of thesis.<br>Includes bibliographical references (p. 155-167).<br>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.<br>by Kin Yui Alice Lo.<br>Ph.D.
15
Raab, R. Michael. "Genomic analysis of hepatic insulin resistance." Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/33762.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Chemical Engineering, February 2006.<br>Includes bibliographical references (leaves 159-191).<br>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.<br>(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.<br>by R. Michael Raab.<br>Ph.D.
16
Aksentijević, Dunja. "Myocardial insulin resistance in experimental uraemia." Thesis, University of Hull, 2008. http://hydra.hull.ac.uk/resources/hull:5757.
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Cardiac complications are a major cause of death in patients with chronic kidney disease (CKD). Left ventricular hypertrophy (LVH) is a significant contributing factor to uraemic cardiomyopathy and results in significant molecular, cellular and metabolic remodelling. Progression of LVH leads to the development of insulin resistance, a feature common to CKD and heart failure, further jeopardising survival of the uraemic heart. The aim of this thesis was to investigate the effect of uraemia on cardiac physiology, function and metabolism. Specifically, the aim of the study was to examine the cellular mechanisms underlying the development of myocardial insulin resistance in uraemia. The experimental model was induced surgically via a two-stage 5/6 nephrectomy in adult male Sprague-Dawley rats over three, six weeks or nine weeks. An integrated experimental approach combining in vivo and ex vivo methods was used to characterize the morphology and physiology of the experimental model, examine myocardial function and energy provision; assess alterations in myocardial protein expression and determine potential mechanism involved in the development of insulin resistance. Uraemic animals exhibited impaired renal function (creatinine 69±2 vs. 40±2 uM n=41; p<0.05), cardiac hypertrophy (dry heart weight: tibia length 0.5±0.01 vs. 0.4±0.01 g/cm; n=30; p<0.05), impaired glucose tolerance, hyperinsulinaemia, anaemia and hypertension. In perfused hearts, uraemia caused a limited response of the uraemic heart to an increase in workload, demonstrated by cardiac dysfunction and metabolic adaptation. This profile was exacerbated in the presence of insulin. In vivo studies highlighted that insulin sensitivity was reduced in uraemic animals (HOMA-IR 1.27±0.3 vs. 0.58±0.1; n=8 p<0.02) and declined progressively with renal dysfunction. LV tissue from the uraemic model showed an increase in myocardial GLUT4 and normal insulin mediated translocation mechanism. In conclusion, uraemic animals exhibited a reduction in insulin sensitivity, glucose intolerance and hyperinsulinaemia, indicating onset of insulin resistance after 6 weeks of uraemia. Profile of myocardial GLUT4 expression and response to insulin stimulation suggested that insulin resistance is not a consequence of impaired translocation. The lack of overt metabolic remodelling suggests a compensatory phase of left ventricular hypertrophy.
17
Tewari, Nilanjana. "Mechanisms underlying obesity-related insulin resistance." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/34081/.
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This thesis investigates the effect of body composition on insulin resistance and the impact of supplementation with nutritional support or carbohydrate treatment. Insulin resistance occurs as a response to a number of stressors, including surgery. However, the mechanism underlying the development of insulin resistance is as yet unclear. Adipose tissue distribution appears to play a role in the development of insulin resistance and obesity-related complications. In obese and non-obese patients undergoing open abdominal surgery who received preoperative carbohydrate or placebo, there was a significant fall in perioperative insulin sensitivity and changes in the expression of genes relating to carbohydrate and fat oxidation. There was no influence of perioperative carbohydrate or obesity on change in insulin sensitivity. Patients undergoing neoadjuvant chemotherapy for oesophageal cancer underwent pre and post chemotherapy assessment of insulin sensitivity and body composition. There was a significant reduction in insulin sensitivity despite minimal change in body composition and adequate nutritional intake. These studies have provided further information about the optimal methods for assessment of insulin sensitivity and body composition as well as an insight into mechanisms underlying the association between body composition and insulin sensitivity.
18
Malik, Muhammad Omar. "Insulin resistance, ethnicity and cardiovascular risk." Thesis, University of Glasgow, 2015. http://theses.gla.ac.uk/6517/.
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Cardiovascular disease (CVD) is one of the leading causes of morbidity and mortality. The literature supports a series of established risk factors for CVD: age, gender, family history of CVD, ethnicity (un-modifiable); and high blood pressure, blood cholesterol, TGs, LDL, diabetes, pre-diabetes, obesity, smoking, physical inactivity, stress and unhealthy diet (modifiable). High blood pressure (hypertension) shares many of these risk factors. However, much of the variance/risk in both conditions cannot be explained. This has led to a search for novel risk factors, including insulin resistance and subclinical inflammation, the significance of which at present are controversial, particularly in relation to hypertension. There are also ethnic differences in the incidence, prevalence, risk factors and progression of cardiovascular disease. In some populations CVD occurs at an earlier age and progresses more rapidly. In this thesis I worked on two datasets in relation to hypertension, cardiovascular disease and their risk factors: (i) the RISC (Relationship between Insulin Sensitivity and Cardiovascular disease) study (chapters 2, 3, 5 and 6); and (ii) routinely-collected national data in Scotland via the SDRN (Scottish Diabetes Research Network) and SCI-Diabetes (chapter 2 and 7). Work on data from the RISC cohort focused on the relation between clamp-measured insulin sensitivity (its unique feature), inflammatory markers and hypertension; the SDRN work addressed ethnic differences in relation to diabetes and CVD. The first study (Chapter 3) examined the importance of insulin sensitivity/resistance in the development of hypertension and change in blood pressure over three years of follow-up in the healthy European (EU) RISC population. Systolic BP (SBP) was higher at baseline in insulin resistant (IR) women. There was no difference in BP in relation to IR in men. After adjustment for age, BMI, baseline BP and other covariates, low insulin sensitivity (M/I) predicted a longitudinal rise in SBP in women but not men, and SBP over time did not increase in insulin sensitive women. The second study (Chapter 4) was a systematic review of the relationships between two markers of low grade inflammation (IL-6 and CRP) and BP/hypertension, considering the roles of adiposity and insulin resistance. The systematic review showed evidence of considerable variation in the relationships amongst low grade inflammation, adiposity, insulin resistance and the development of hypertension. There appeared to be a positive association in the literature between CRP and DBP in younger individuals, although none of the studies were adjusted for insulin sensitivity determined by clamp technique. This association was further explored using RISC study data in Chapter 5 with stratification by sex and adjusting for clamp-derived insulin sensitivity. The third study (Chapter 5) examined the relationship of inflammatory markers with the development of hypertension and change in blood pressure over three years in the same healthy European population and whether any relationship was independent of clamp-measured insulin sensitivity (IS). High sensitivity C reactive protein (hsCRP) predicted prospective change in diastolic BP independent of insulin sensitivity and BMI whereas IL-6 had no relation with BP (both systolic and diastolic) or the incidence of hypertension. The fourth study (Chapter 6) evaluated all available predictors of BP rise over time (both systolic and diastolic) in a healthy EU population; moreover the significance of different predictors was examined within subgroups defined by age and sex. This analysis showed that baseline BP was the principal determinant of follow-up BP in all age and sex groups. Obesity was the second most important predictor (BMI in adults aged 30-44 years; percent change in BMI in middle age people aged 45-60 years). Lifestyle factors influenced BP via their effect on BMI. People who maintained their BMI during the three year follow-up did not exhibit a rise in BP (whether systolic or diastolic). Other important predictors identified in this analysis were insulin sensitivity in middle aged women and hsCRP in adult men. The fifth study (chapter 7) evaluated the role of ethnicity in the development of cardiovascular disease in people with type 2 diabetes living in Scotland. Over a follow-up of seven years, Pakistani people had increased risk of CVD and Chinese people had decreased risk of CVD as compared to White population. Pakistanis had an increased risk of CVD at a younger age independent of other conventional risk factors. In summary, insulin sensitivity and inflammation influence blood pressure, but their role is not generalised across different age and sex groups. BMI and change in BMI are important predictors of follow-up BP in adults and middle age healthy people, supporting a role for maintenance of BMI in preserving cardiovascular health. In addition to the known ethnic differences in the development of diabetes, I identified ethnic differences in the development of CVD.
19
Nowak, 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.
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The worldwide increasing number of persons affected by largely preventable diseases like diabetes demands better prevention and treatment. Insulin is required for effective utilisation of circulating nutrients. Impaired responsiveness to insulin (insulin resistance, IR) is a hallmark of type 2 diabetes and independently raises the risk of heart attack and stroke. The pathophysiology of IR is incompletely understood. High-throughput measurement of large numbers of circulating biomarkers may provide new insights beyond established risk factors. The aims of this thesis were to (i) use proteomics, metabolomics and genomics methods in large community samples to identify biomarkers of IR; (ii) assess biomarkers for risk prediction and insights into aetiology and consequences of IR; and (iii) use Mendelian randomisation analysis to assess causality. In Study I, analysis of 80 circulating proteins in 70-to-77-year-old Swedes identified cathepsin D as a biomarker for IR and highlighted a tentative causal effect of IR on raised plasma tissue plasminogen activator levels. In Study II, nontargeted fasting plasma metabolomics was used to discover 52 metabolites associated with glycaemic traits in non-diabetic 70-year-old men. Replication in independent samples of several thousand persons provided evidence for a causal effect of IR on reduced plasma oleic acid and palmitoleic acid levels. In Study III, nontargeted metabolomics in plasma samples obtained at three time points during an oral glucose challenge in 70-year-old men identified associations between a physiologic measure of IR and concentration changes in medium-chain acylcarnitines, monounsaturated fatty acids, bile acids and lysophosphatidylethanolamines. Study IV provided evidence in two large longitudinal cohorts for causal effects of type 2 diabetes and impaired insulin secretion on raised coronary artery disease risk. In conclusion, the Studies in this thesis provide new insights into the pathophysiology and adverse health consequences of IR and illustrate the value of combining traditional epidemiologic designs with recent molecular techniques and bioinformatics methods. The results provide limited evidence for the role of circulating proteins and small molecules in IR and require replication in separate studies and validation in experimental designs.
20
Barber, Collin. "SIRT3: Molecular Signaling in Insulin Resistance." Thesis, The University of Arizona, 2014. http://hdl.handle.net/10150/315823.
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A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.<br>Post-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.
21
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/.
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Insulin resistance is a disease state characterised by the reduced ability of insulin to exert its effects in peripheral tissues, skeletal muscle and adipose tissue. This condition has been associated with a number of other disease states including obesity and hypertension. The hypertensive Milan rat has previously been shown to be insulin resistant. Unlike any other hypertensive, insulin resistant model, the Milan rat has a normotensive, isogenic control which responds normally to insulin. As GLUT-4, the insulin-stimulated glucose transporter, had been implicated in insulin resistance I examined the levels of GLUT-4 present in the Milan rat. Results suggest that the insulin resistance experienced by this hypertensive strain may be due to a reduction in GLUT-4 within the intracellular membranes of skeletal muscle. This is due to the nature of insulin-stimulated glucose transport, which arises as a result of GLUT-4 translocatlng to the cell surface from an intracellular pool, and therefore increasing the rate of glucose uptake. Consequently, any reduction in intracellular GLUT-4may account for the insulin resistance observed. Further studies eXamined the stroke-prone spontaneously hypertensive rat, and the stroke-prone spontaneously hypertensive rat F2 generation. The F2 generation contains individuals that are extremely hypertensive and others which are normotensive. This was done to determine if the decrease in GLUT-4 observed in the hypertensive Milan rat correlated with increasing blood pressure. The results suggest that GLUT-4 levels in the stroke-prone spontaneously hypertensive rat are not altered by an increase in blood pressure. This result is in agreement with most studies on skeletal muscle GLUT-4, and highlights the complex nature of insulin resistance associated with hypertension. The concluding chapter discusses the effects of oestrogen, and derivatives, on insulin-stimulated glucose uptake in 3T3-L1 adipocytes. Previous studies have shown that females taking steroid hormones, either by means of the contraceptive pill, of hormone replacement therapy, tend to suffer from insulin resistance. In 3T3-L1 adipocytes a 48 hour treatment with 30nM oestrogen significantly reduces insulin-stimulated glucose transport. This demonstrates that the cells have developed insulin resistance. However these cells do not have reduced GLUT-4 levels and the insulin resistance, induced by oestrogen, occurs by an as yet unknown mechanism.
22
Kershner, David. "Oral Glucose Insulin Secretion Test for Identifying Patients with Insulin Resistance." ScholarWorks, 2018. https://scholarworks.waldenu.edu/dissertations/5634.
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Insulin resistance is an increasing public health issue with the current literature, suggesting reduced sensitivity of insulin leads to adult onset diabetes and associated downstream pathologies that reduce life expectancy. The main objectives of this study were to evaluate the ability of the Oral Glucose Insulin Secretion Test (OGIST) to identify insulin resistance and examine differences in the insulin sensitivity based on gender, age, and ethnicity. This study was supported by the insulin resistance theory which focuses on the reduced ability of insulin to bind to the cellular insulin receptor, reducing the sensitivity of insulin. The OGIST lab results of a total of 250 patients, aged 18-65, were included in this study from a major city in the midwestern United States. Binomial logistic regression was used to evaluate the relationship between the dependent variables and the validation independent variables and analyze the possible differences seen in insulin, proinsulin, C-peptide, and HbA1c with age. The OGIST demonstrated the ability to identify elevated levels of insulin, proinsulin, and C-peptide at the end of the first phase insulin secretion to glucose. The results of this study demonstrated patients with insulin resistance exhibited a greater reduction in insulin production with age compared to those without insulin resistance. There were no changes observed between gender or ethnicity. The OGIST was the only test that demonstrated the ability to identify the individual's insulin sensitivity, β-cell function, and progression to diabetes. The ability of the OGIST to identify both insulin resistance and β-cell function can contribute to positive social change by encouraging further research for the early diagnosis and treatment of insulin resistance and the reduction in adult onset diabetes.
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Frangioudakis, 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.
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Insulin resistance is the major metabolic defect in obesity and Type 2 diabetes. Increased lipid accumulation is strongly associated with insulin resistance. A significant component of insulin resistance is thought to be a reduced ability of insulin to activate the cascade of phosphorylation events that lead to the metabolic effects of this hormone. The broad aims of this thesis were to examine the effect of high-fat diets containing different fat subtypes on in vivo insulin signalling, under conditions normally used to detect whole body insulin resistance, and to compare the effects of acute and chronic lipid oversupply on insulin signalling in vivo. Time-course and dose-response effects of insulin stimulation on site-specific phosphorylation of key signalling proteins were studied in rat tissues in vivo, to establish an appropriate experimental system to examine the onset of activation of the insulin signalling pathway. It was determined that short insulin infusions with concurrent glucose infusion, similar to the beginning of a euglycaemic-hyperinsulinaemic clamp, significantly increased the phosphorylation of major intermediates of the insulin signalling pathway in important tissues of insulin action (skeletal muscle [RQ], liver [LIV] and white adipose tissue [EPI]). These experiments provided a platform to study insulin signalling under the same conditions used to study lipid-induced insulin resistance. The provision of diets enriched in polyunsaturated or saturated fatty acids (FA) resulted in the corresponding enrichment of these fat subtypes in rat plasma and tissues. However, the effects on insulin signalling were essentially the same. Both fat diets induced defects in sitespecific phosphorylation of insulin receptor substrate (IRS)-1 and protein kinase B (PKB) in RQ and LIV, but not EPI. This suggests that the amount of fat in the diet, rather than enrichment in a particular fat subtype, had a greater impact on the development of signalling defects and that the response to high-fat feeding was tissue-specific. A 3hr elevation of circulating FA (using a lipid/heparin infusion), to a level that is relevant in clinical Type 2 diabetes, impaired insulin-stimulated PKB phosphorylation with no significant effect on IRS-1 phosphorylation. This suggests that there may be differences in the way acute and chronic exposure to increased FA impair insulin signalling. The phosphorylation defects observed in both chronic and acute studies did not seem to be associated with activation of major stress signalling pathways (JNK and NFkB), which have been suggested to have a role in lipidinduced insulin resistance. In conclusion, these studies demonstrate that impaired IRS-1 and PKB phosphorylation do have a role in the reduced insulin action observed with lipid oversupply in vivo, because the changes were detected under similar conditions as those used to determine whole body insulin resistance.
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Wiggam, 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.
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Verchere, 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.
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The effect of varying concentrations of glucose or the gastrointestinal hormones, gastric inhibitory polypeptide (GIP) and somatostatin (SS-14), on the in vitro immunoreactive insulin (IRI) response to the parasympathetic neurotransmitter, acetylcholine (ACh) was investigated. The isolated, vascularly perfused rat pancreas was used in all experiments.
Acetylcholine (1.0 µM) did not stimulate IRI secretion in the presence of 2.2 mM glucose. However, in the presence of 4.4, 6.6, or 8.9 mM glucose, ACh (1.0 µM) potently stimulated IRI secretion (approximately fourfold). At a higher glucose concentration (17.8 mM), the IRI response to ACh was reduced. GIP also potentiated the IRI response to 1.0 µM ACh. This potentiation was most marked in the presence of 1.0 nM GIP, whereas the effect of concomitant infusion of 0.2 nM GIP and 1.0 µM ACh was only slightly greater than additive. SS-14 potently inhibited ACh-stimulated IRI secretion. These results demonstrated the glucose dependency of cholinergically stimulated IRI secretion, and that physiological levels of glucose and GIP increased B-cell sensitivity to cholinergic stimulation. It was suggested that the parasympathetic stimulation of IRI secretion associated with food intake could be affected by postprandial increases in glucose, GIP, and SS-14.
The idea that endogenously released somatostatin may have influenced glucose or GIP-stimulated IRI secretion was not supported by the present experiments, since neither glucose (8.9 mM) nor GIP (2.0 nM) were found to have a significant effect on the release of pancreatic somatostatin-like immunoreactivity (SLI). Both atropine (1.0 µM) and hexamethonlum (100 µM) inhibited the IRI response to ACh. This suggested that the parasympathetic stimulation of IRI secretion was mediated not only by muscarinic receptors on the B-cell, but also by nicotinic receptors on intrapancreatic ganglia. Neither atropine nor hexamethonlum had a significant effect on glucose- or GIP-stimulated IRI secretion, indicating that the IRI response to these stimuli was not mediated by cholinergic receptors.
Both SS-14 and the synthetic somatostatin analog SMS 201-995 (SMS; Sandostatin®) inhibited IRI secretion stimulated by 8.9 mM glucose, 2.0 nM GIP, or 1;.0 µM ACh, but not 17.8 mM glucose. The most potent inhibition by both SS-14 and SMS was observed in the presence of the weakest IRI stimuli (8.9 mM glucose and 1.0 µM ACh). These results suggested that the inhibitory effects of somatostatin on the B-cell could be overcome by the presence of strong stimuli. In addition, the inhibitory effects of the native hormone and the analog were found to be approximately equipotent (weight basis), indicating that the increased potency of SMS previously observed in vivo was due to its longer half-life in plasma, and not due to a more potent direct effect on the B-cell.<br>Medicine, Faculty of<br>Cellular and Physiological Sciences, Department of<br>Graduate
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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.
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Thesis (Ph.D.)--East Carolina University, 2008.<br>Presented 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.
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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.
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Hale, 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.
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Pang, Shengru [Verfasser], and Marco [Akademischer Betreuer] Prinz. "Microglial activation during obesity-induced insulin resistance." Freiburg : Universität, 2017. http://d-nb.info/1187132764/34.
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Winter, 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.
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Pickavance, 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.
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Shmueli, 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.
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Eason, Robert C. "Treating type 2 diabetes through insulin resistance." Thesis, Aston University, 2002. http://publications.aston.ac.uk/10953/.
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Type 2 diabetes is an insidious disorder, with micro and/or macrovascular and nervous damage occurring in many patients before diagnosis. This damage is caused by hyperglycaemia and the diverse effects of insulin resistance. Obesity, in particular central obesity, is a strong pre-disposing factor for type 2 diabetes. Skeletal muscle is the main site of insulin-stimulated glucose disposal and appears to be the first organ that becomes insulin resistant in the diabetic state, with later involvement of adipose tissue and the liver. This study has investigated the use of novel agents to ameliorate insulin-resistance in skeletal muscle as a means of identifying intervention sites against insulin resistance and of improving glucose uptake and metabolism by skeletal muscle. Glucose uptake was measured in vitro by cultured L6 myocytes and isolated muscles from normal and obese diabetic ob/ob mice, using either the tritiated non-metabolised glucose analogue 2-deoxy-D-glucose or by glucose disposal. Agents studied included lipoic acid, isoferulic acid, bradykinin, lipid mobilising factor (provisionally synonymous with Zinca2 glycoprotein) and the trace elements lithium, selenium and chromium. The putative role of TNFa in insulin resistance was also investigated. Lipoic acid improved insulin-stimulated glucose uptake in normal and insulin resistance murine muscles, as well as cultured myocytes. Isoferulic acid, bradykinin and LMF also produced a transient increase in glucose uptake in cultured myocytes. Physiological concentrations of TNFa were found to cause insulin resistance in cultured, but no in excised murine muscles. The effect of the M2 metabolite of the satiety-inducing agent sibutramine on lipolysis in excised murine and human adipocytes was also investigated. M2 increased lipolysis from normal lean and obese ob/ob mouse adipocytes. Arguably the most important observation was that M2 also increased the lipolytic rate in adipocytes from catecholamine resistant obese subjects. The studies reported in this thesis indicate that a diversity of agents can improve glucose uptake and ameliorate insulin resistance. It is likely that these agents are acting via different pathways. This thesis has also shown that M2 can induce lipolysis in both rodent and human adipocytes. M2 hence has potential to directly reduce adiposity, in addition to well documented effects via the central nervous system.
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Al-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.
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Blond, 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.
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L'insulino-résistance est un des mécanismes physiopathologiques associé au diabète de type II et à l'obésité. Améliorer la compréhension de ce mécanisme est nécessaire pour essayer de limiter l'extension de ces maladies considérées à l'heure actuelle comme de véritables épidémies. Une des causes de l'insulino-résistance réside dans l'accumulation intrahépatique et intramusculaire de lipides due à la rupture de la balance entre oxydation mitochondriale et lipogenèse de novo, perturbant la signalisation insulinique à l'origine de l'insulino-résistance. Connaître les facteurs induisant la modification de cette balance et la manière dont ceux-ci la déséquilibrent permettrait de prévenir l'insulino-résistance hépatique et musculaire. Nous avons souhaité approfondir, grâce à des études in vivo et in vitro, le rôle de l'acide nicotinique, agent hypolypémiant, des polyphénols, micronutriments présents dans les fruits et légumes et du fructose, molécule lipogénique. Ces composés agiraient comme modulateurs de la résistance à l'insuline et comme inducteurs du déséquilibre entre oxydation mitochondriale et lipogenèse de novo. Après avoir mis au point deux améliorations techniques (stabilité des solutions de [6,6-²H2]-glucose utilisées pour la mesure de la sensibilité à l'insuline et validation des mesures de dépenses énergétiques d'un nouveau calorimètre), nous avons montré que l'acide nicotinique est capable d'améliorer le profil lipidique plasmatique, tout en induisant une insulino-résistance hépatique dans une population d'hommes présentant une dyslipidémie mixte. Cette insulino-résistance, confirmée dans un modèle cellulaire d'hépatome humain, est reliée à l'inhibition d'une des enzymes « clés » de la lipogenèse de novo, la diacylglycérol acétyltransférase (DGAT). Cette inhibition enzymatique diminue les concentrations plasmatiques en triglycérides et induit une augmentation d'intermédiaires lipidiques à l'origine de l'insulino-résistance. Nous avons également mis en évidence le rôle insulinosensibilisateur d'un extrait de polyphénols de raisins rouges, lors d'un stress métabolique induit par la consommation de fructose dans une population de sujets à risque génétique de défaut d'oxydation mitochondriale. Cet effet insulino-sensibilisateur est dû à l'augmentation de l'activité et de la biogenèse mitochondriales réduisant l'effet lipogénique du fructose. Ces résultats montrent l'importance du lien entre rupture de la balance lipogenèse de novo oxydation lipidique et impact sur l'insulino-sensibilité. L'acide nicotinique est impliqué dans l'induction d'une insulino-résistance hépatique par inhibition de la DGAT, enzyme clé de la lipogenèse de novo. Les polyphénols sont impliqués dans l'augmentation de la sensibilité à l'insuline par amélioration de la fonctionnalité et de la biogenèse mitochondriales en réponse à une augmentation de la lipogenèse induite par le fructose
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Song, 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/.
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Danielsson, 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.
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Slevin, Karen Aoife. "Dietary fat and insulin sensitivity." Thesis, University of Surrey, 2000. http://epubs.surrey.ac.uk/843068/.
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Insulin resistance is associated with a number of metabolic abnormalities that increase the risk of developing coronary heart disease. Dietary fat has been linked with insulin resistance, with alterations in the quality as opposed to the quantity of dietary fat now thought be more important in instigating improvements in insulin resistance. The aim of this work was to investigate the effect of alterations in the dietary fat intakes of middle-aged men (n = 32) on the insulin sensitivity of glucose disposal and postprandial lipid metabolism and to explore the mechanistic links between these insulin responsive pathways. Three separate dietary interventions were conducted; the first involved an increase in the intake of n-3 polyunsaturated fat, the second a decrease in saturated fat and an increase in carbohydrate and the third a decrease in saturated fat and an increase in monounsaturated fat intake. Compliance was monitored by the measurement of red blood cell phospholipid fatty acid composition, postprandial lipid metabolism was measured over 9 hours following a high-fat breakfast (80 g fat), and insulin resistance was measured using the short insulin tolerance test. The results of the study showed that while insulin sensitivity was inversely correlated with red blood cell saturated fatty acid concentration at baseline, the insulin sensitivity of glucose disposal was unaffected by any of the dietary interventions conducted. In measurements of postprandial lipaemia, improvements were observed following the low-saturated fat / high-monounsaturated fat diet and the n-3 polyunsaturated enriched diet, however the low-saturated fat/ high-carbohydrate diet was associated with a worsening of postprandial lipaemia through an increase in the concentrations of triglyceride-rich-lipoproteins. Changes in fasting biochemical measurements were most evident in the low-saturated / high-monounsaturated diet, with an 11 % reduction in total cholesterol and a 15.4 % reduction in fasting triglycerides. There were no observed changes in the activity levels or the gene expression of lipoprotein lipase. There was an unexpected positive association between the degree of insulin sensitivity and the extent of postprandial lipaemia, indicating that the link between these pathways is complex and warrants further investigation. Overall this work supports the view that dietary guidelines should be directed towards a change in the composition of fat, to a lower saturated fat intake, a higher monounsaturated fat intake and a lower n-6 : n-3 ratio through an increase in the intake of long chain n-3 polyunsaturated fatty acids.
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Sundström, 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.
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<p>Left 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<sup> </sup>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.</p><p>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.</p>
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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.
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Spence, 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.
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Chapter one provides an overview of the regulation of insulin secretion/action, details normal insulin action, and, describes the concept of insulin resistance and its assessment. It specifically focuses on obesity (as the most important contributor to insulin resistance) and reviews dietary effects on insulin resistance and plasma lipids. Chapter two describes methods which are common to chapters 3, 4 and 5: assessment of habitual diet; formulation/practical administration of intervention diets; blood sampling; and assessment of body composition, insulin sensitivity, and vascular compliance. Chapter three compares the effects of a high versus low sucrose diet (25 vs. 10 %, respectively, oftotal energy intake) in 13 healthy subjects, in a randomised crossover design with sequential 6 week dietary interventions separated by a 4 week washout. Diets were weight maintaining with identical macronutrient and fibre content. The results demonstrated that a high sucrose intake, as part of an isocaloric weight maintaining diet, had no detrimental effect oninsulin resistance. Chapter four investigates the effects of a low carbohydrate versus low fat weight reduction diet (0.5 kg/week) on insulin sensitivity and cardiovascular risk in overweight/obese subjects (n = 24) using a parallel group randomised controlled trial design. Following similar weight loss, both diets were equally effective in improving insulin sensitivity. The low fat diet also had beneficial effects on augmentation index (a measure of arterial stiffness), a finding which was not evident within the low carbohydrate group. Chapter five explores whether adipokines (leptin, adiponectin and retinol binding protein 4) potentially mediate the effects of weight loss (induced by hypocaloric dieting in study 2) on insulin sensitivity. Results demonstrated that diet induced changes in adipokines did not correlate with the change in insulin sensitivity. Chapter six provides a general discussion and concluding remarks for the main body of the thesis.
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Nygren, Jonas. "The sites and mechanisms of postoperative insulin resistance /." Stockholm, 1997. http://diss.kib.ki.se/1997/91-628-2695-6.
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Sundström, 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/.
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Field, 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.
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Bradley, 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.
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Khoo, 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.
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Alzadjali, 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.
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Humphreys, 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.
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Biochemical characterisation of fibroblasts from patients with one sub-type of severe insulin resistance, pseudo-acromegalic insulin resistance, was undertaken in order to localise the site of defective insulin signalling. The studies which were carried out can be divided into 1) verification of normal insulin receptor function 2) measurement of metabolic and mitogenic end-point actions of insulin and 3) analysis of components of the signalling cascade. In brief, in most studies the response in patient cells was indistinguishable from normal controls. However, in patient cells there was reduced sensitivity to insulin-stimulation of the enzyme phosphatidylinositol 3-kinase(PI3-K). There is much evidence to support a role for PI3K in insulin's effects on the stimulation of glucose transport. Additionally, the purported inhibitor of the insulin receptor tyrosine kinase PC1 was modestly increased in insulin resistant patients cells. Defects which could be responsible for insulin resistance were also investigated genetically. Molecular scanning studies of two candidate genes, the major substrate of the insulin receptor tyrosine kinase, the insulin receptor substrate-1 (IRS-1) and the insulin-regulated glucose transported, Glut 4, were carried out in groups of severely insulin resistant patients. Silent polymorphisms were detected in both genes. No mutations were detected in the Glut 4, however one novel mutation (Met613Val) was detected in the IRS-1 gene, in addition to a previously described mutation (Gly972Arg). The mutation Gly972Arg has been reported in both NIDDM and control subjects. The patient with the mutation Met613Val in the IRS-1 gene inherited it from her deceased father. Met613Val was not found in a general Caucasian population studied and all additional family members studied had normal glucose tolerance and did not carry the mutation.
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Hunter, 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.
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Pickersgill, 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.
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