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Bickerton, Alex Sam Thomas. "Fat metabolism and the metabolic syndrome." Thesis, University of Oxford, 2008. http://ora.ox.ac.uk/objects/uuid:9108a8ca-8b3e-4e45-98e2-4765c009774f.
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Background: The metabolic syndrome is associated with an increased risk of diabetes and vascular disease. In order to understand the pathophysiological processes underlying such risk, it is necessary to develop a better understanding of normal fat metabolism and abnormalities associated with the syndrome. The hypothesis tested in this thesis is that specific abnormalities in adipose tissue and muscle fat metabolism characterise the metabolic syndrome. Methods: Fasting biochemical parameters were measured in a cohort of overweight men with and without the metabolic syndrome. Stable-isotope labeling and arterio-venous difference measurements were conducted in 18 men to elucidate pathways of exogenous and endogenous fat metabolism under fasting and postprandial conditions in adipose tissue and skeletal muscle. In addition, a pilot study of the effects of heat and electrical stimulation on adipose tissue metabolism was undertaken. Results: Cohort study - The prevalence of the metabolic syndrome depended on the definition used. Total cholesterol and apoB were greater in those with the metabolic syndrome than in those without. There was no difference in fasting NEFAs. Metabolic investigation - There was significant postprandial uptake of NEFA from the circulating NEFA pool by adipose tissue. Chylomicrons were confirmed as the preferred substrate of LPL. There was preferential uptake of FAs derived from chylomicron hydrolysis. There was release of NEFA across muscle. In the metabolic syndrome, adipose tissue NEFA output is lower during fasting and falls less following a meal than in the healthy obese. Clearance of dietary-derived TG is lower across both adipose tissue and muscle in the metabolic syndrome. Pilot study – Heat increased measures of lipolysis whereas electrical stimulation had no effect. Conclusions: Fat metabolism in individuals with the metabolic syndrome is characterised by metabolic inflexibility but not insulin resistance.
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Tsai, I.-Jung. "Perturbations of arachidonic acid metabolism in the metabolic syndrome." University of Western Australia. School of Medicine and Pharmacology, 2009. http://theses.library.uwa.edu.au/adt-WU2010.0065.
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[Truncated abstract] Arachidonic acid is oxidised in vivo by non-enzymatic (free radical) or enzymatic pathways (cyclooxygenase, lipoxygenase, and cytochrome P450) to form a range of biologically active eicosanoids. Specifically, arachidonic acid is metabolised by cytochrome P450 -hydroxylase to produce vasoactive 20-hydroxyeicosatetraenoic acid (20-HETE), and by 5-lipoxygenase to produce proinflammatory leukotriene B4 (LTB4), which can further be metabolised by -hydroxylase to from 20-OH-LTB4 and 20-COOH-LTB4. F2-Isoprostanes (F2-IsoPs) are produced through free radical attack on arachidonic acid and have been recognised as the most reliable markers of lipid peroxidation in vivo. The metabolic syndrome (MetS) is characterised by abdominal obesity, hypertension, insulin resistance, glucose intolerance, and dyslipidemia. It is associated with low-grade inflammation and oxidative stress and an increased risk of developing cardiovascular diseases. Dietary weight loss is strongly recommended for the management of the MetS and can potentially minimise the risk of cardiovascular diseases and diabetes in individuals with the MetS. Little is known regarding the role of these arachidonic acid metabolites in the MetS and the effect of weight loss on their metabolism. Chapter three comprised of three in vitro studies aimed to examine 20-HETE synthesis in human blood cells. 20-HETE acts as a second messenger for vasoconstrictor actions of angiotensin II (Ang II) and endothelin-1 (ET-1) in renal and mesenteric beds. Human neutrophils and platelets are integral to the inflammatory process. ... Production of LTB4 and 20-OH-LTB4 was significantly lower compared with controls (P<0.005) and remained so after adjustment for neutrophil count (P<0.05).The weight loss intervention resulted in a 4.6kg reduction in body weight and a 6.6cm decrease in waist circumference and a significant increase in LTB4 and 20-OH- LTB4 in the weight loss group. Chapter Five continued to investigate the role of other arachidonic acid metabolites, 20-HETE and F2-IsoPs in the MetS and the effect of weight loss. In the case-control study (Human study 1), plasma and urinary 20-HETE and F2-IsoPs were significantly elevated in the MetS group, but no significant difference was found in stimulated-neutrophil 20-HETE. A significant gender x group interaction was observed in that women with the MetS had higher urinary 20-HETE and F2-IsoPs compared to controls (P<0.0001). In a randomised controlled trial (Human study 2), relative to the weight- maintenance group, a 4.6 kg loss in weight resulted in a 2 mmHg fall in blood pressure but did not alter the production of 20-HETE or F2-IsoPs. No significant differences were shown in 20-HETE released from stimulated-neutrophils before and after weight loss. 20-HETE and oxidative stress may be important mediators of cardiovascular disease risk in the MetS. Although a 4% reduction in body weight reduced BP, there were no changes in plasma or urinary 20-HETE or F2-IsoPs. In summary, in vitro studies show that human neutrophils and platelets can produce 20-HETE in response to Ang II and ET-1, and human studies demonstrate that the presence of MetS has a significant impact on arachidonic acid metabolism and effective weight loss can restore leukocyte synthesis of LTB4.
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Zibadi, Sherma. "Metabolic Syndrome-Induced Cardiac Fibrosis." Diss., The University of Arizona, 2009. http://hdl.handle.net/10150/195321.
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Recent studies support the association between metabolic syndrome (MetS), a cluster of cardiovascular risk factors, and diastolic dysfunction. Disproportionate collagen accumulation, particularly cross-linking of collagen, plays a key role in translating interstitial fibrosis into mechanical chamber stiffness and diastolic dysfunction. Characteristic changes in the expression and activity of myocardial lysyl oxidase (LOX), a matrix modifying enzyme that catalyzes cross-linked collagen, are unclear in MetS. We established a diet-induced MetS model to study diastolic dysfunction by treating male C57BL/6 mice a high-fat high-simple carbohydrate (HFHSC) diet for 6 months. Despite blunted gene expression of LOX isoforms, MetS mice demonstrated significant increase in the ratio of protein expression of mature to proenzyme LOX, enhanced LOX activity, and increased cardiac cross-linked collagen compared with controls. This fibrotic response coincided with marked increase in left ventricular end-diastolic pressure and stiffness and impaired diastolic filling pattern. Our data demonstrate that diet-induced MetS alters the remodeling enzyme LOX, thereby increasing the amount of crosslinking and inducing diastolic dysfunction.Furthermore we examined the role of T-lymphocytes in myocardial LOX regulation in diet-induced fibrotic hearts. Female SCID mice which are devoid of functional T-lymphocytes and C57BL/6 mice were treated with HFHSC diet for 12 months. Similar to male C67BL/6, female HFHSC-fed C57BL/6 mice demonstrated significant increase in maturation and catalytic activity of myocardial LOX, cross-linking, ventricular stiffness and diastolic dysfunction. Whereas induction of LOX protein was minimal in SCID mice compared with wild-type counterparts. Correspondingly fibrillar cross-linked collagen formation and diastolic dysfunction were less prominent in SCID mice. Our results suggest a potential role of T-lymphocytes in induction of myocardial stiffness and diastolic dysfunction through modulation of LOX-dependent collagen maturation.Moreover we studied the role of leptin, an adipokine over-produced in MetS with fibrotic effects in non-cardiac tissues, as a key mediator of profibrogenic responses in the heart by administrating leptin to C57BL/6 and leptin-deficient ob/ob mice. With exogenous leptin administration ob/ob mice displayed passive diastolic filling dysfunction that coincided with increase in myocardial collagen compared with ob/ob controls. Our findings suggest profibrotic effects of leptin in the heart, primarily through predominance of collagen synthesis over degradation.
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Tweedy, Maureen P. Guarnaccia Charles Anthony. "Metabolic syndrome and psychosocial factors." [Denton, Tex.] : University of North Texas, 2009. http://digital.library.unt.edu/permalink/meta-dc-11005.
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Gobin, Reeta Rukmini Devi. "Metabolic syndrome and cardiovascular disease." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610102.
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Hodge, Stephanie Jean. "Psychosocial underpinnings of metabolic syndrome." Thesis, Ulster University, 2018. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.737993.
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The rate of obesity throughout Europe has more than doubled over the past 20 years. It was hypothesised that certain patterns of adiposity and associated co-morbidity metabolic parameters were related to certain psychological traits and neurochemical markers. The study aim was to measure associations between adiposity, metabolic markers, psychological traits and the neurochemicals whole blood serotonin and salivary cortisol, in a single study. Participants were healthy (n=102), males (n=35) and females (n=67), aged 20-65 years (mean 39.7 years). The literature review found that some patterns of adiposity were associated with metabolic risk factors more strongly than were others. Gynoid fat may be a healthier state of adiposity in terms of cardiovascular health. Negative emotional traits, such as anxiety were associated with greater risk for metabolic syndrome/obesity, whilst positive measures such as optimism were linked with lower risk. Experimental findings showed optimism being linked with lower adiposity and life satisfaction associated with greater high density lipoprotein (HDL) cholesterol. Associations between whole blood (WB) serotonin and anthropometric measures found lower WB serotonin being associated with greater adiposity, and that this may be sex-linked. The theory that adiposity may be linked to salivary cortisol and certain psychological factors showed positive associations between gynoid fat, BMI and resilience. Higher salivary cortisol was also correlated with greater perceived stress, and with lower trait mood. These data imply a link between cortisol, adiposity and psychological factors. There are few studies in the literature linking these cross-disciplinary fields. Results suggest that serotonin could be an antecedent and/or a consequence of obesity. Data also suggest that psychometric and salivary cortisol factors, particularly resilience, may interplay together to contribute towards adiposity. This study also implies that the positive traits of optimism, resilience and life satisfaction are related to better metabolic health and more “healthy” patterns of fat deposition.
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Selig, Patricia Marie. "Factors Associated with Metabolic Syndrome." VCU Scholars Compass, 2003. https://scholarscompass.vcu.edu/etd/5960.
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The metabolic syndrome, a clinical condition linked to diabetes and cardiovascular disease is a powerful predictor for overall mortality, and is present in more than 20% of the US. population (Ford, Giles, & Dietz, 2002). This study examines gender differences as well as other factors associated with metabolic syndrome as defined by the Adult Treatment Panel III of the National Cholesterol Education Program.
A sample of 10,134 adults between 20-64 years of age was selected from the Third National Health and Nutrition Survey. Metabolic syndrome was present in 19.6 % of this sample. An ecological model of health services was used to analyze metabolic syndrome. The four model domains include population characteristics, environmental factors, health behaviors, and utilization of health care services.
The descriptive results showed statistically significant differences in individuals with metabolic syndrome and without metabolic syndrome. Those with metabolic syndrome were proportionately more older, reported a past medical history of cardiovascular disease and family history of diabetes, had lower levels of education and a lower annual household income. There were no differences between men and women in age, geographic residence, education or health insurance coverage. However, there were higher proportions of women with metabolic syndrome in all race categories when compared to men with metabolic syndrome with the exception of Caucasians. A family history of diabetes, a family history of cardiovascular disease, a past personal history of cardiovascular disease, level of income, habitual activity and having a usual source of health care were found to be statistically significant between men and women with metabolic syndrome.
Results of the logistic regression analysis revealed that overall, women were 30% less likely to have metabolic syndrome, yet African American women and Hispanic American women were nearly twice as likely to have metabolic syndrome than Caucasian women. Further research on gender differences for shared medical conditions is needed.
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Tweedy, Maureen P. "Metabolic Syndrome and Psychosocial Factors." Thesis, University of North Texas, 2009. https://digital.library.unt.edu/ark:/67531/metadc11005/.
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Metabolic syndrome is a constellation of risk factors, including abdominal obesity, hypertriglyceridemia, low HDL cholesterol, high blood pressure, and high fasting glucose, that commonly cluster together and can result in cardiovascular disease. The prevalence of metabolic syndrome and the components that comprise the syndrome vary by age and by racial/ethnic group. In addition, previous research has indicated that the risk factors contributing to metabolic syndrome may be exacerbated by exposure to perceived stress. This study utilized data from the 2002, 2004, and 2006 Health and Retirement Study (HRS) and National Health and Nutrition Examination Survey (NHANES) data sets. It was hypothesized that depression and anxiety (conceptualized as stress in this study) increase the risk of presenting with metabolic syndrome while social support decreases the risk of metabolic syndrome. While results of cross-sectional analysis do not indicate a significant relationship between depression and metabolic syndrome (t = -.84, ns), longitudinal analysis does indicate a significant relationship between depression and metabolic syndrome over time (t = -5.20, p <.001). However, anxiety is not significantly related to metabolic syndrome when the relationship is examined through cross-sectional analysis (t = -1.51, ns) and longitudinal analysis (χ² = 13.83, ns). Similarly, social support is not significantly related to metabolic syndrome when examined in cross-sectional (χ² = .63, ns) and longitudinal (t = 1.53, ns) analysis. Although level of stress is not significantly related to metabolic syndrome as a whole, there is a significant relationship between stress and both triglyceride level (t = -2.94, p = .003) and blood glucose level (t = -3.26, p = .001).
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Bowman, Thomas A. "Hepatic CEACAM1 Protects Against Metabolic Abnormalities Associated with Metabolic Syndrome." University of Toledo Health Science Campus / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=mco1271358149.
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Yasmin, Ephia. "Metabolic aspects of polycystic ovary syndrome." Thesis, University of Leeds, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.545722.
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Chaudhuri, Abhijit. "Metabolic changes in chronic fatigue syndrome." Thesis, University of Glasgow, 2003. http://theses.gla.ac.uk/6542/.
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Metabolic functions are one of the principal determinants of energy expenditure and are exquisitely susceptible to the effects of circulating hormones and chemical changes. Consequently, clinical experiments based on energy expenditure and metabolic functions were considered to be valid approaches to the present research. Significant abnormalities were found in the proton magnetic resonance spectroscopy of basal ganglia in CFS patients. Automatic cardiovascular responses to exercise are also impaired in a subset of CFS patients. Finally, plasma membrane injury appears to be a possible explanation for a range of observations made in this research. Subjective fatigue is a complex symptom. It is the outcome of a variable combination of physiological and neuropsychological changes induced by the primary disease process. Downstream links between brain, neuromuscular and the cardiorespiratory functions are implicated in the neural control of force output during exercises in health and disease. Higher perceived fatigue in CFS is probably caused by the central mechanisms while the sensory input to these neural regulatory mechanisms may limit endurance to maximal and submaximal exercises. Based on these findings and more indirect evidence from other studies, changes in cell membrane properties affecting neuronal signalling in the basal ganglia seem to emerge as one of the likely pathophysiological mechanisms in CFS. There is also evidence of an imbalance of the central autonomic tone in a subset of CFS patients. Surely, research in CFS has the potential to unravel the biology of central fatigue and may bridge the gap that exists between the borderland of neurology and psychiatry.
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Parr, Heather Joy. "Psychosocial factors associated with metabolic syndrome." Thesis, Ulster University, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.650080.
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Rising levels of metabolic syndrome across Europe and India, and scant research on psychosocial determinants prompted these studies. Stress, depression and physical inactivity were hypothesized to predict obesity and metabolic syndrome; constant mood and increased resilience to confer protection. Abundant vegetable/fruit intake; lower saturated fat intake from dairy, meat and olive oil, and low/moderate wine intake were predicted determinants of health. Secondary modelling of representative data from GB and Portugal (Lipgene study) assessed psycho-social, dietary and lifestyle predictors of metabolic syndrome. Cultural adaptation of the Lipgene questionnaire was informed by qualitative research incorporating 24hr dietary recall for use in India (ChurpE). Qualitative themes suggested that urbanisation negatively impacted upon social structure, food choice, physical activity and health. Stress arising from the changing role of women was perceived to have affected familial wellbeing. Healthy eating referenced freshness, convenience, meal skipping, high fat/sugary foods, and nostalgia for tradition and rural lifestyle. Latent class analyses of the Indian and both European samples indicated three classes: 'healthier' lacking metabolic syndrome symptoms; 'metabolic syndrome' with comorbidities; and, 'obese/high blood pressure'. Additionally, an 'overweight' group in Europe was distinguished. In both studies older age, less sedentary behaviour and stress distinguished the 'healthier' from all other classes. Compared with the 'healthier', 'metabolic syndrome' members were more likely Portuguese experienced lower resilience and smoking cessation; and more British, younger and stressed members typified 'overweight' among Europeans. The 'obese' class were predominantly female with high BP. Among Indians, 'happier' mood characterised 'high BP' membership. That comorbidities varied between classes suggests disease progression from overweight/obesity to metabolic syndrome. Among Indians, alcohol, smoking, higher earnings, chatting to relax and dietary habits predicted obesity and comorbidities. Developing public health policy to prevent and treat obesity and metabolic syndrome should intervene to reduce sedentary behaviour, tackle stress, promote resilience and healthy eating.
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Bossé, Yohan. "Genetic Susceptibility to the Metabolic Syndrome." Thesis, Université Laval, 2004. http://www.theses.ulaval.ca/2004/22151/22151.pdf.
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Le syndrome métabolique est caractérisé par un regroupement de facteurs de risque présents chez un même individu et augmentant ainsi ses chances de développer le diabète de type 2 et les maladies cardiovasculaires. Il est donc important de comprendre l’étiologie génétique de ce trait. Dans cette thèse, une multitude d’approches génétiques ont été utilisées afin d’apporter un brin de connaissance sur l’architecture génétique du syndrome métabolique et de ses composantes individuelles. Trois gènes candidats ont été testés incluant le récepteur activé par les proliférateurs de péroxisomes (PPAR) α et PPARγ ainsi que la protéine de transfert des phospholipides (PLTP). Les gènes PPARα et PLTP ont tous deux été associés significativement avec plusieurs variables d’adiposité. Des effets significatifs d’interaction entre les gènes PPARα et PPARγ ont été obtenus pour les paramètres de glucose et d’insuline. Il a aussi été démontré que le polymorphisme PPARα L162V influence les changements de cholestérol-HDL2 suite à un traitement au gemfibrozil. Par la suite, des criblages génomiques ont été effectués sur les concentrations de lipides et de lipoprotéines plasmatiques. Plusieurs régions chromosomiques ont été identifiées incluant 1q43, 11q13 q24, 15q26.1, et 19q13.32 pour le cholestérol-LDL, 12q14.1 pour le cholestérol-HDL, 2p14, 11p13, et 11q24.1 pour les triglycérides, 18q21.32 pour l’apolipoprotéine (apo) B-LDL, et 3p25.2 pour l’apoAI. La contribution génétique à la variation du diamètre principal des particules LDL (DP-LDL) a aussi été étudiée. Les résultats démontrent une forte ressemblance familiale avec des coefficients d’héritabilité de plus de 50%, la présence d’un gène à effet majeur, et une forte évidence de liaison sur le chromosome 17q. Le gène de l’apoH, localisé à cet endroit, a par la suite été significativement associé au DP-LDL, suggérant que ce gène est responsable du signal de liaison observé sur le chromosome 17. Finalement, une variable quantitative du syndrome métabolique a été construite à l’aide d’une analyse factorielle. Un criblage génomique effectué sur cette variable a démontré une évidence de liaison sur le chromosome 15q, suggérant la présence d’un gène à cet endroit contribuant au regroupement des facteurs de risques caractérisant le syndrome métabolique. Plusieurs de ces résultats devront être répliqués, alors que d’autres méritent d’être suivis.The metabolic syndrome is a cluster of interrelated cardiovascular risk factors co-occurring in the same individual. People with this syndrome are at increased risk for developing diabetes mellitus and cardiovascular diseases. Accordingly, it is important to elucidate the genetic aetiology governing this trait in order to better comprehend its pathogenesis. In the present thesis, heritability and complex segregation analyses as well as candidate gene and genome-wide scan approaches have been applied to shed some lights on the genetic architecture of the metabolic syndrome and its individual components. A total of three candidate genes have been investigated including peroxisome proliferator-activated receptor (PPAR) α and PPARγ as well as phospholipid transfer protein (PLTP). It has been shown that polymorphisms in both PPARα and PLTP genes are significantly associated with several indices of adiposity. In addition, significant gene-gene interactions have been observed between PPARα and PPARγ on glucose/insulin parameters. It has also been shown that the HDL2-cholesterol response to gemfibrozil therapy is modulated by the PPARα L162V polymorphism. Genome-wide linkage scans have been performed on lipid and lipoprotein concentrations. Many chromosome regions harbouring lipoprotein/lipid genes have been identified including 1q43, 11q13 q24, 15q26.1, and 19q13.32 for LDL-cholesterol, 12q14.1 for HDL-cholesterol, 2p14, 11p13, and 11q24.1 for triglycerides, 18q21.32 for LDL-apolipoprotein (apo) B, and 3p25.2 for apoAI. The genetic contribution of the variation in LDL peak particle diameter (LDL-PPD) has been also investigated. Overall, the results indicate: 1) that LDL-PPD strongly aggregates within families with heritability estimate above 50%; 2) the existence of a major gene effect affecting the phenotype; and 3) the presence of a major quantitative trait locus located on chromosome 17q. The apo H gene, a positional candidate gene, was then significantly associated with LDL-PPD, suggesting that this gene is responsible for the linkage signal observed on 17q. Finally, factor analyses have been used to construct a quantitative metabolic syndrome variable and a genome-wide linkage scan has been conducted to identify the genomic regions underlying this trait. A major quantitative trait locus has been observed on chromosome 15q suggesting a gene within this region contributing to the clustering of the metabolic syndrome-related phenotypes. Many of these findings must go through independent replication, while others produced new leads that deserve follow-up.
Inscrit au Tableau d'honneur de la Faculté des études supérieures
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Navaneethan, Sankar. "METABOLIC SYNDROME AND CHRONIC KIDNEY DISEASE." Case Western Reserve University School of Graduate Studies / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=case1401967446.
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Kotwica, Aleksandra Olga. "Dietary nitrate and the modulation of energy metabolism in metabolic syndrome." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708924.
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Natanzon, Yanina. "METABOLIC SYNDROME IN AN IMMUNOSUPPRESSED POPULATION: GENETIC CONTRIBUTION TO METABOLIC SYNDROME TRAITS IN THE WOMEN'S INTERAGENCY HIV STUDY." Case Western Reserve University School of Graduate Studies / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=case1449252475.
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Cheng, K. K. "A metabolomic investigation of mouse models of atherosclerosis and the metabolic syndrome." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597571.
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1n NMR spectroscopy and gas chromatography (GC) based metabolimics approaches were used to characterize the metabolic profiles of a selection of mouse models of atherosclerosis, including the wildtype C57BL/6 mice, the low-density lipoprotein receptor null (LDLR-/-) mice, and the Apolipoprotein E null (ApoE-/-) mice. The LDLR-/- mice demonstrated a profound perturbation in lipid and choline metabolism, notably the choline oxidation pathway, which results in reduced concentrations of choline derivatives in urine. A consistent change in this pathway was also observed in the ApoE-/- mice. The ApoE-/- mice exhibited significant changes in energy metabolism, favouring the utilisation of fatty acids for energy production. These findings were also compared with the ApoE-/- mice that are haplodeficient for the Ataxia telangiectasia mutated (ATM) gene. The ATM+/-/ApoE-/- mice demonstrated accelerated atherosclerosis and more severe abnormalities in energy metabolism, as compared with the ATM+/+/ApoE-/- mice. Finally, a metabolomic study on an inducible Akt1 transgenic mouse model was conducted. These mice exhibit inducible muscle hypertrophy, as well as a significant reduction in fat mass. The muscle-specific Akt1 activation caused increased glycolysis in gastronemius muscle, as well as increased gluconeogenesis, glycogenolysis and ketogenesis in the liver of the mice. These data demonstrate how hypertrophic muscle affects systemic metabolism, and influences distant organs to feed its active cell growth. The studies demonstrated the impact of a muscle-specific Akt1 activation on systemic metabolism, which leads to a reduction in risks associated with cardiovascular disease.
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Lindholm, Åsa Maria. "Metabolic Aspects in the Polycystic Ovary Syndrome." Doctoral thesis, Uppsala universitet, Institutionen för kvinnors och barns hälsa, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-120235.
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Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders among women of childbearing age and is associated with a number of metabolic disturbances. It has been hypothesised these women carry an increased risk of developing cardiovascular diseases (CVD) with advancing age. The first aim of this thesis was to establish the prevalence of PCOS-related symptoms in Northern Sweden. The Northern part of the WHO MONICA project was used for this purpose. Based on self-reported menstrual disturbances and hirsutism together with biochemical analyses of free androgen index, the estimated prevalence of PCOS in Northern Sweden was 4.8%, which corresponded with previous prevalence studies. Disturbances in the fibrinolytic system are predictors of future cardiovascular events and measurements of plasminogen activator inhibitor 1 (PAI-1) activity and tissue plasminogen activator (tPA) mass concentration may be used to assess fibrinolytic activity in women with PCOS. From the findings, over-weight women with PCOS had impaired fibrinolysis, especially if they displayed objective biochemical markers of hyperandrogenism. Conversely, lean women with PCOS, displayed no signs of disturbed fibrinolysis. The adipose tissue is an active endocrine organ that produces and releases hormones, pro- and anti-inflammatory cytokines, and chemoattractant cytokines. Proinflammatory molecules produced by adipose tissue can be active participants in the development of insulin resistance and the increased risk of cardiovascular disease associated with obesity. The findings suggested being overweight, rather than the PCOS diagnosis per se, was the main explanatory variable for elevated adipose tissue inflammation in PCOS patients. Weight reduction is the primary target for intervention in overweight and obese women with PCOS. When this thesis was planned, no placebo-controlled trials on anti-obesity drugs in women with PCOS had been conducted. Sibutramine in combination with lifestyle intervention resulted in significant weight reduction in overweight women with PCOS. In addition to the weight loss, sibutramine appeared to have a beneficial effect on metabolic and cardiovascular risk factors.
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Lindholm, Åsa Maria. "Metabolic Aspects in the Polycystic Ovary Syndrome." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-120235.
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Kannisto, Katja. "The metabolic syndrome : studies on thrifty genes /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-051-6/.
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Atiomo, William Usinode. "Polycystic ovary syndrome coagulation and metabolic studies." Thesis, University of Plymouth, 1998. http://hdl.handle.net/10026.1/2828.
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The polycystic ovary syndrome (PCOS) is a heterogeneous disorder in women characterised by chronic ovulatory failure, hyperandrogenaemia, and insulin resistance. Some women are completely asymptomatic and others present with extreme menstrual disturbance, severe hirsutism, infertility and recurrent miscarriage. The pathophysiology of PCOS is not completely understood, but it is thought that insulin resistance plays a central role. In normal subjects, non-diabetic obese patients and patients with non-insulin dependent diabetes, insulin resistance is associated with elevated plasminogen activator inhibitor-1 (PAI-1) levels. PAI-1 is a glycoprotein, which inhibits the formation of plasmin (a proteolytic enzyme). Plasmin aids fibrinolysis and extracellular proteolysis. High PAI-1 and low plasmin levels increase the risk of thrombosis and impair extracellular proteolysis required in ovarian follicle growth, ovulation and embryo implantation. This study was designed to determine whether elevated plasminogen activator inhibitor-1 (PAI-1) was associated with the insulin resistance present in PCOS, investigate its possible role in the causation of anovulation and recurrent pregnancy loss in these women and ascertain whether it was an additional thrombotic risk factor so that clinicians and patients could take appropriate measures to reduce this risk In a pilot study, systemic PAI-1 activity was significantly elevated in oligomenorrhoiec women with PCOS. A larger study supported these findings, but demonstrated that obesity was a significant confounding factor, as the increase in PAI-1activity disappeared when standardised for weight. Activated Protein-C (APC) resistance was subsequently tested in these women because of the unexpected finding of an increased prevalence of a positive family history of thrombosis in women with PCOS compared with controls, but there was no increase in the prevalence of APC-resistance in PCOS. In another project, the cellular distribution of PAI-1 protein in human ovaries was described for the first time using immunohistochemistry. It was localised to the granulosa and theca cell compartments in both polycystic and normal ovaries, however there was no significant difference in the intensity of PAI-l staining between both groups on image analysis. PAI-1 messenger RNA expression was also evaluated in these biopsies by in-situ hybridisation, but no signal was detected suggesting that there was either a low overall RNA preservation in the tissues, or an insufficient sensitivity of the cocktail of oligonucleotide probes used. This study did not support the hypothesis that elevated PAI-1 was a feature of PCOS, however the in-situ location of PAI-1 protein was demonstrated for the first time in the human ovary and consistent with a previously suspected role in ovulation. The results did not support a role for PAI-1 in anovulation, recurrent miscarriage or increased thrombosis in PCOS.
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Benjamin, Boben. "Metabolic syndrome and psychosis in Alzheimer's disease." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/metabolic-syndrome-and-psychosis-in-alzheimers-disease(eedebc61-9cbb-4d8d-9e60-a025f054278a).html.
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The metabolic syndrome is a constellation of vascular risk factors including abdominal obesity, hypertension, diabetes, hypertriglyceridaemia and low high density lipoprotein cholesterol. The aim of the study was to explore the link between the metabolic syndrome and its components, and psychosis in Alzheimer’s disease. The participants were selected from the Human Serum Metabolome Project. 246 participants with Alzheimer’s disease were assessed at baseline and 151 were followed up a year later. The neuropsychiatric inventory was used to capture information about psychiatric symptoms including delusions and hallucinations. The vascular risk factors were determined from the history from the participant and carer; abdominal obesity however was measured during the study. Hypertriglyceridaemia and high density lipoprotein cholesterol data were unavailable and so the study focuses on the link between the metabolic syndrome components of obesity, hypertension and diabetes, and psychosis in Alzheimer’s disease. Although not part of the metabolic syndrome criteria, a history of hypercholesterolaemia was used in conjunction with the available metabolic syndrome components and the link between the resulting vascular syndrome and psychosis in Alzheimer’s disease was studied. Two measure of psychosis were used for the research. First of all, a factor representing psychosis was derived by factor analysis of the neuropsychiatric inventory data. Secondly, a direct measure of psychosis using the delusions and hallucinations items from the neuropsychiatric inventory was used. Cross-sectional and longitudinal analyses were conducted. The majority of the analyses conducted failed to find a significant link between the measures. Male sex, a lower Mini Mental State Examination score as well as the use of antipsychotics and memantine were found to be significantly associated with psychosis at baseline. Overall this study does not support the link between the metabolic syndrome or its components and psychosis in Alzheimer’s disease. Future research looking at subsets of Alzheimer’s patients with more clearly defined lipid triglyceride and high density lipoprotein cholesterol data will be useful.
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Countryman, Amanda. "Cardiovascular Reactivity and the Metabolic Syndrome in Adolescents." Scholarly Repository, 2008. http://scholarlyrepository.miami.edu/oa_theses/169.
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The association between cardiovascular reactivity and the metabolic syndrome, as well as individual metabolic syndrome criterion variables, was investigated in adolescents. Cardiovascular reactivity has been examined as a risk marker or factor in the pathogenesis of hypertension or cardiovascular disease, but few studies have looked at its relationship with the metabolic syndrome. Blood pressure (BP) and heart rate (HR) cardiovascular reactivity to three tasks, evaluated speaking, mirror star tracing, and cold pressor, were assessed in 148 adolescents. Using the American Heart Association (AHA) adult definitional criteria, individuals were classified into metabolic syndrome groups (presence vs. absence of metabolic syndrome), and 16% of individuals met criteria for the metabolic syndrome. In logistic regression analyses, the occurrence of the metabolic syndrome was negatively associated with HR reactivity to the cold pressor (OR = 0.920, 95% CI = 0.873, 0.969), and positively associated with diastolic blood pressure (DBP) reactivity to the star tracing task (OR = 1.089, 95% CI = 1.008, 1.177). Results of multiple regression analyses that included individual metabolic syndrome risk variables indicated that cold pressor reactivity explained 7% of the variance in casual BP, while star tracing reactivity accounted for 7% of the variance waist circumference and 6% of the variance triglycerides (ps < .05). The findings indicate that cardiovascular reactivity to physical or behavioral challenge is associated with the metabolic syndrome in a sample of adolescents. Cardiovascular reactivity may be an important clinical tool for identifying individuals at risk of the metabolic syndrome and cardiovascular disease.
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Jacobsson, Annelie. "Comparing NR Expression among Metabolic Syndrome Risk Factors." Thesis, University of Skövde, Department of Computer Science, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-814.
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The metabolic syndrome is a cluster of metabolic risk factors such as diabetes type II, dyslipidemia, hypertension, obesity, microalbuminurea and insulin resistance, which in the recent years has increased greatly in many parts of the world. In this thesis decision trees were applied to the BioExpress database, including both clinical data about donors and gene expression data, to investigate nuclear receptors ability to serve as markers for the metabolic syndrome. Decision trees were created and the classification performance for each individual risk factor were then analysed. The rules generated from the risk factor trees were compared in order to search for similarities and dissimilarities. The comparisons of rules were performed in pairs of risk factors, in groups of three and on all risk factors and they resulted in the discovery of a set of genes where the most interesting were the Peroxisome Proliferator Activated Receptor - Alpha, the Peroxisome Proliferator Activated Receptor - Gamma and the Glucocorticoid Receptor. These genes existed in pathways associated with the metabolic syndrome and in the recent scientific literature.
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Sjögren, Per. "Cardiovascular risk factors, diet and the metabolic syndrome /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-894-0/.
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Castro, Mora Milena. "Evidence synthesis and decision modelling for Metabolic Syndrome." Thesis, University of Leicester, 2013. http://hdl.handle.net/2381/28451.
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Metabolic Syndrome (MetS) may be defined as a clustering of risk factors for diabetes mellitus (T2DM) and cardiovascular disease (CVD) which puts individuals at increased risk of developing these conditions and consequently leads to a reduction in life expectancy and increased morbidity. Although there are a number of definitions of MetS, essentially having any three of the following five risk factors confers a diagnosis of MetS; (i) impaired fasting glucose levels, (ii) raised blood pressure, (iii) raised triglycerides, (iv) low levels of high-density lipoprotein cholesterol (HDLC), and (v) increased waist circumference. A comprehensive decision model has been developed to combine different levels of evidence in a Markov model. This model is based in the behavior of MetS and its possible progression to T2DM and CVD, in order to evaluate the potential impact of a MetS based intervention at population level. Evidence synthesis methods are going to be incorporated in the model to integrate different levels of information. Firstly, a Mixed Treatment Analysis (MTC) of Randomized Controlled Trials (RCTs), which have evaluated a number of lifestyle and pharmacological interventions in individuals with MetS was undertaken. This information also assessed the possibility of reversing a diagnosis of MetS. Secondly, a systematic review of published literature was conducted to assess the evidence related with the association between the MetS and development of T2DM and/or CVD. A Bayesian approach to the problem has also been advocated which enables flexibility to develop a Markov model of this complexity. WinBugs offers a comfortable solution for the evaluation of a Markov model, given its Gibbs sampler. Main findings of this thesis are related with large amount of uncertainty, presuming a difficulty to provide a clear decision related to the application of MetS for prevention of T2DM and CVD.
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Okafor, Chika Emelda. "Educational Intervention on Metabolic Syndrome for Psychiatric Providers." ScholarWorks, 2019. https://scholarworks.waldenu.edu/dissertations/7417.
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Statistics show a high prevalence of metabolic syndrome (MetS) in patients with mental illness receiving second-generation antipsychotic medications. MetS is associated with elevation of obesity, truncal obesity, blood pressure, cholesterol, and fasting glucose. The purpose of this project was to educate psychiatric providers about the importance of MetS screening, early detection, management, and referral for better treatment and management. The project was guided by Lewin's theory of change model. The project inquired if educational intervention on MetS improved providers' knowledge and intent to adopt MetS guidelines. A literature review and established guidelines of the American Psychiatric Association and American Diabetic Association about MetS in psychiatric patients directed the educational content. Five expert panelists with over 10 years of experience in psychiatric mental health reviewed the educational content using a Likert-type questionnaire. Findings resulted in the acceptance of the educational content without further recommendation. Twelve staff attended the educational session presented on MetS. Comparison of the pretest and posttest questionnaires that has 5 multiple choice questions indicated some positive effects. The good knowledge of MetS, how to screen for MetS, health promotion activities with consumers, metabolic profile of different neuroleptic medications, providers' roles in MetS. The participants' overall knowledge about MetS screening improved from 8.3% pretest to 83.3% after receiving the educational program. The educational project for MetS screening might foster positive social change by improving continuity and quality of care, which will lead to better patient outcomes, reduce healthcare cost, and impact positive patient outcomes.
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Morris, Tiffany J. "Investigating the molecular mechanisms of the metabolic syndrome." Thesis, University of Cambridge, 2010. https://www.repository.cam.ac.uk/handle/1810/237703.
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This thesis aims to highlight molecular mechanisms that have been altered by prenatal undernutrition and may be involved in the metabolic syndrome. Two separate studies were conducted both using a rat model developed through manipulation of the maternal diet to provoke the key features of the metabolic syndrome in adult offspring. Microarray technology was used to detect changes in gene expression in target tissues between offspring of control (normally fed, AD) and undernourished (UN) mothers to obtain a broader picture of the cellular functions and genetic pathways that may be implicated in the metabolic syndrome. The rst study compared gene expression differences in liver, skeletal muscle, and white adipose tissue between 55 day old male offspring of AD and UN mothers. No significant changes were found in muscle or adipose tissue; however, the differences in the liver suggested the UN animals had been metabolically programmed to favour fat as an energy source. To investigate whether DNA methylation might be responsible for the observed transcriptional changes, pooled liver samples from the rat study were used with the McrBC restriction enzyme assay to determine full, partial, incomplete, or no methylation between AD and UN. Two differentially expressed genes (Zfand2a and Mapk4) showed methylation changes. The same liver samples were hybridised to a miRNA array. Two miRNAs showed a nearly 2-fold upregulation in the UN livers. Both were found to be either directly or indirectly associated with the metabolic syndrome. MiR-335 has been shown to be upregulated in the livers of obese/diabetic mice. By association with miR-27a, miR-451 might be involved in aspects of lipid metabolism in adipose tissue. A second study used microarray to analyse the liver tissues of day 170 female offspring of the same rat model with additional insults (neonatal leptin treatment and post-weaning high-fat (HF) diet). Leptin has been shown to reverse the programming effects of the restricted maternal diet and this study aimed to highlight mechanisms that could be involved in this reversal. The results revealed the importance of the interaction between treatments. Significant gene expression changes were only present when two or more treatments were combined. This study revealed significantly, differentially expressed genes involved in immune function, regulation of the circadian rhythm, and metabolism. These findings provide a number of interesting genes and pathways for further studies and also highlight the need to conduct a thorough study in multiple tissues at different time-points to pinpoint the window of developmental plasticity.
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García, Bravo Gabriela. "Milk and dairy intake and the metabolic syndrome." Thesis, Linnéuniversitetet, Institutionen för naturvetenskap, NV, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-11113.
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The overall aim of this master thesis was to get an overview on how milk and dairy consumption affect development of the metabolic syndrome, and from this review to formulate a milk product with potentially beneficial effects. A cluster of metabolic abnormalities such as insulin resistance and type 2 diabetes, hypertension, obesity and dyslipidaemia are known as the metabolic syndrome. Epidemiological studies performed to investigate the relation between milk and dairy intake and the metabolic syndrome, suggests that low-fat milk and dairy intake have a positive effect in the prevention of the disease. Many dairy components might contribute to this effect. There are promising effects seen by whey amino acids on the glucose and insulin control, but the long-term effects are warranted. Low-fat milk and dairy as part of a diet rich in fruits and vegetables have the most blood pressure reducing effect. This beneficial effect is in part believed to be due to the calcium content of milk and dairy products. In addition, it is also hypothesised that calcium plays an important roll in weight management. However, the evidence up to date is contradictorily. Weight control, on the other hand, can be improved by affecting satiety. Acute intervention studies show that whey, in particular, alfa-lactalbumin, is more satiating than other proteins, resulting in a lower energy intake in a subsequent meal. It is of interest to the dairy industry to provide milk and dairy consumers with milk products that have beneficial effects on wellness and health. Therefore, based on the literatured reviewed on milk and dairy intake and the metabolic syndrome, a milk product with beneficial effects on weight was formulated and developed.
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Lam, Chung-mei Jamie. "Obstructive sleep apnea and cardiometabolic complications." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43085854.
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Bollinger, Lance Thyfault John P. Thomas Tom R. "A proposed scoring system for quantification of metabolic syndrome severity." Diss., Columbia, Mo. : University of Missouri--Columbia, 2008. http://hdl.handle.net/10355/5621.
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The entire thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file; a non-technical public abstract appears in the public.pdf file. Title from PDF of title page (University of Missouri--Columbia, viewed on September 16, 2009). Thesis advisor: Dr. John Thyfault, Dr. Tom Thomas. Includes bibliographical references.
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Hatch, Anthony Ryan. "The politics of metabolism the metabolic syndrome and the reproduction of race and racism /." College Park, Md.: University of Maryland, 2009. http://hdl.handle.net/1903/9629.
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Thesis (Ph. D.) -- University of Maryland, College Park, 2009.Thesis research directed by: Dept. of Sociology. 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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Ong, Kwok-leung. "Metabolic syndrome its prevalence and association with urotensin II /." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B3723058X.
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Ong, Kwok-leung, and 王國良. "Metabolic syndrome: its prevalence and association with urotensin II." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B3723058X.
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Hudecova, Miriam. "Reproductive and Metabolic Consequences of the Polycystic Ovarian Syndrome." Doctoral thesis, Uppsala universitet, Institutionen för kvinnors och barns hälsa, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-123248.
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Polycystic ovary syndrome (PCOS) is a complex clinical condition characterized by hyperandrogenism and chronic oligo/anovulation. Infrequent ovulation and metabolic alterations in women with PCOS are associated with subfertility and probably increased miscarriage rates compared with normal fertile women. The overall risk of developing type 2 diabetes and impaired glucose tolerance (IGT) is three- to sevenfold higher in PCOS women, and the onset of glucose intolerance seems to occur at an earlier age than in healthy controls. Women with PCOS also have several risk factors for cardiovascular disease, although it is unclear whether they actually experience more cardiovascular events than other women. Very few studies assessing the long-term reproductive and metabolic consequences in older women with previously confirmed PCOS have been conducted. In this long-term follow-up of women with PCOS, 84 women with a diagnosis of PCOS between 1987 and 1995 and age at the follow-up > 35 years and an age-matched population-based group of control women participated. Data on reproductive outcome, ovarian reserve, endothelial function, insulin sensitivity and beta-cell function were collected. According to our results most women with PCOS had given birth and the rate of spontaneous pregnancies was relatively high. The rate of miscarriages was not increased in PCOS patients and the ultrasound findings together with increased levels of anti-müllerian hormone suggested that their ovarian reserve is superior to women of similar age. PCOS women displayed signs of endothelial dysfunction, but this was largely due to the increased prevalence of independent risk factors for cardiovascular disease such as increased BMI, triglycerides and blood pressures. IGT and type 2 diabetes occurred more often in PCOS women. Free androgen levels and beta-cell function decreased over time whereas insulin sensitivity remained unchanged. Obesity at young age and progressive weight-gain rendered them more prone to be insulin resistant at the follow-up. Beta-cell function was increased in PCOS women in comparison with control subjects but declined over time. Independent of PCOS phenotype at the index assessment and persistence of PCOS symptoms at the follow-up investigation, premenopausal women with PCOS had lower insulin sensitivity and increased beta cell function in comparison with control subjects. Conclusion: The long-term reproductive outcomes of PCOS are similar compared to women with normal ovaries. Although symptoms and androgen levels are normalized over time, women with PCOS continue to display reduced insulin sensitivity and increased beta-cell function and they also have an increased risk of IGT and type 2 diabetes.
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Hettne, Kristina. "Using nuclear receptor interactions as biomarkers for metabolic syndrome." Thesis, University of Skövde, Department of Computer Science, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-813.
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Metabolic syndrome is taking epidemic proportions, especially in developed countries. Each risk factor component of the syndrome independently increases the risk of developing coronary artery disease. The risk factors are obesity, dyslipidemia, hypertension, diabetes type 2, insulin resistance, and microalbuminuria. Nuclear receptors is a family of receptors that has recently received a lot of attention due to their possible involvement in metabolic syndrome. Putting the receptors into context with their co-factors and ligands may reveal therapeutic targets not found by studying the receptors alone. Therefore, in this thesis, interactions between genes in nuclear receptor pathways were analysed with the goal of investigating if these interactions can supply leads to biomarkers for metabolic syndrome. Metabolic syndrome donor gene expression data from the BioExpressä, database was analysed with the APRIORI algorithm (Agrawal et al. 1993) for generating and mining association rules. No association rules were found to function as biomarkers for metabolic syndrome, but the resulting rules show that the data mining technique successfully found associations between genes in signaling pathways.
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Bennett, Amanda Jane. "Genes and environment in the aetiology of metabolic syndrome." Thesis, Imperial College London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.444179.
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Aghilla, Mohamed M. "Inflammation and cardio-metabolic risks in polycystic ovary syndrome." Thesis, University of Warwick, 2012. http://wrap.warwick.ac.uk/50038/.
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Polycystic Ovary Syndrome (PCOS) is the most common reproductive and endocrine disorder in females during their reproductive life. The syndrome is characterized by a constellation of symptoms and signs including menstrual disturbance, hyperandrogenism and polycystic ovaries. Other features of PCOS include obesity, metabolic syndrome, insulin resistance and an increased risk of developing diabetes mellitus and cardiovascular disease. Recently, PCOS has been recognized as a low grade inflammatory condition. Several inflammatory markers have been found to be raised in PCOS, such as interleukin-6, tumour necrosis factor-alpha and Interleukin-18. Low grade inflammation may potentially produce an insulin resistant state and promote the development of atherosclerosis. Insulin sensitzers such as metformin and pioglitazone have been shown to have a favourable effect not only on the symptoms of PCOS, but also on the hormonal and metabolic parameters in those subjects. In my thesis I primarily focussed on IL-18, B cells activating factor (BAFF), and the hepatokine, Fetuin-A, all linked to insulin resistance. IL-18 has a strong affinity towards its natural inhibitor, IL-18 binding protein (BP) and binding of IL-18 to IL-18 BP results in neutralization of IL-18, and consequently reduced free IL-18; the active form of the molecule. I have shown that PCOS women have a higher free IL-18, with hyperinsulinaemia the main factor that determines IL-18 in vitro. Furthermore, I have shown that Pioglitazone treatment for 12 weeks decreased both the total and free IL-18 in PCOS women. The reduction of IL-18 was accompanied by an improvement in IR. On the other hand, metformin treatment for six months failed to improve insulin sensitivity and did not influence IL-18 levels. BAFF, a novel adipokine, was studied in PCOS subjects, and I found lower BAFF levels in this cohort of patients. In vivo, BAFF correlated negatively with androgens, and in vitro work revealed that androstenedione as a negative regulatory factor for BAFF production Fetuin-A also known human protein α2-Heremans-Schmid glycoprotein, is a known natural inhibitor for insulin and abundantly expressed and secreted by the liver; fetuin-A has been suggested to act as a link between obesity, insulin resistance and MS. The circulating levels of Fetuin A are increased in women with PCOS, which is more pronounced when associated with MS. Metformin decreases Fetuin A in vivo, and also decreases both the expression and secretion of Fetuin A from HepG2 cells.
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Strahorn, Pamela. "The metabolic syndrome : the role of the Y chromosome." Thesis, University of Glasgow, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414106.
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Laprano, Nicola. "Metabolic alterations in a murine model of Barth syndrome." Thesis, University of Glasgow, 2018. http://theses.gla.ac.uk/9105/.
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Barth syndrome (BTHS) is a rare monogenic disease characterized by cardiomyopathy, skeletal myopathy and neutropenia, caused by mutations in the Xq28 locus. Mutations in the locus result in the loss of function of the Tafazzin protein (Taz), a transacylase responsible for the final step in the production of mature cardiolipin (CL). CL is a fundamental component of the inner mitochondrial membrane, where it cooperates in the maintenance of membrane stability and in various cellular processes such as mitochondrial respiration, autophagy and reactive oxygen species sensing. Using a novel murine model of BTHS, we investigated the mitochondrial phenotype, the metabolic signature and the gene expression profile in the heart of Taz knockout (KO) mice. We identified extensive heart-specific changes in the structure and composition of the mitochondria accompanied by alterations of the metabolome and gene expression. The alterations are specific to the adult, so probably derive from a developmental process happening after birth. The alteration of the gene expression seems to indicate activation of the unfolded protein response, suggesting an effect of stress response pathways in the cellular processes which underlie Barth syndrome.
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Ma, Man Chun John. "Genetic determinants of Metabolic Syndrome in Lyon Hypertensive rats." Diss., University of Iowa, 2013. https://ir.uiowa.edu/etd/1987.
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Metabolic Syndrome (MetS) is a collective term for a cluster of disorders, including dysglycemia, central obesity, dyslipidemia, hypertension, and eventual end organ damage. The combination of these disorders increases the risk of many kinds of end organ damages, including coronary heart disease, kidney failure, and cirrhosis. MetS is highly prevalent in the United States, affecting one third of the U.S. population in a 2009 estimate.
The Lyon strains are three rat strains selectively inbred from the same colony of outbred rats for different blood pressure levels. The Lyon Hypertensive (LH) strain, in addition to its essential hypertension phenotype, also harbors many disorders found in MetS. The Lyon Normotensive (LN) rat strain is completely devoid of these symptoms, while Lyon Low-pressure (LL) is obese but is resistant to other traits of MetS.
Rat chromosome 17 (RNO17) has previously been linked with many of MetS' phenotypes in Lyon Hypertensive (LH). In this project, we are using a mixture of genetical genomics and systems biology methods to identify genetic elements that may cause the LH phenotype.
Divergent haplotype blocks between the Lyon strains were first identified by the analysis of the distribution of observed strain differences (OSD) calculated from the result of genome resequencing. Divergent haplotype regions totaling less than 16% of the rat genome that contain more than 95% of the identified SNPs in each of the three pairwise comparisons between the Lyon strains have been identified; in particular, there are 14 divergent haplotype blocks between LH and LN spanning 7.7% of RNO17 that harbor more than 97% of SNPs identified on RNO17. Twenty-five genes in these regions were thus identified as potential genetic determinants for MetS.
Phenotypic QTLs (pQTL) and expression QTLs (eQTL) mapping from a cohort of male LH × LN F2 rats were performed by putting the cohort on a 15-week phenotyping protocol and genome-wide genotyping. Total liver RNA from 36 individuals from the cohort were sequenced to provide expression data for eQTL mapping. We have mapped 22 pQTLs that are statistically linked to 15 traits, with RNO17 linked to 15 traits associated with blood pressure, leptin and body weight. We have also identified 1,200 eQTLs from this cohort, including 11 eQTLs with cis-linkage with one or more genes. On RNO17, we have identified two SNPs between 29-39 Mb which are significantly linked to the expression of 85 genes; the only gene with cis-linkage with these SNPs, RGD1562963, was hence identified as a putative master regulator.
Transcriptome analyses were then performed on the Lyon parental animals; the total liver and kidney of RNA from 6 each of LH, LL and LN strains that were subjected to the same 15-week phenotyping protocol were sequenced for differential expression analysis, gene coexpression network analysis and quantitative trait transcript analysis. Differential expression analysis identified 4 genes on RNO17's divergent haplotype regions: Cul2 and the aforementioned RGD1562963 for liver, Amph and Bambi for kidney. Quantitative trait transcript analyses have shown significant correlations between the expressions of these four genes with one or more of the traits of the animals treated, validating their status as potential genetic determinants for MetS. However, out of the 84 genes that RGD1562963 potentially regulates, only two other genes (Cul2 and Supt4h1) have significant correlations with one or more traits. Gene coexpression network analyses have shown a relationship between genes on the TGF-β pathway and the differentially expressed genes in the kidney, supporting our speculation on the hyperactivity of the TGF-β system in the etiology of the LH phenotypes.
An LH-17LN consomic strain was also generated by introgressing an LN copy of RNO17 onto the LH genomic background to validate in vivo the role of RNO17 in the etiology of MetS symptoms in LH. We have observed that the consomic strain has significantly decreased body weight, adiposity, blood pressure, and inter-week blood pressure differences that may be a surrogate for salt sensitivity. Thus, the role of RNO17 on the LH genotype is validated.
In summary, we have been able to identify, by in vivo and in silico methods, that RNO17 is related to the MetS traits in LH; that 4 genes, Amph, Bambi, Cul2, and RGD1562963, are potential genetic contributors to RNO17's effects; and that their effects may include, but are not limited to, the activation of TGF-Β signals.
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Lu, Ran [Verfasser]. "Metabolic syndrome, olfactory dysfunction, and brain morphology / Ran Lu." Bonn : Universitäts- und Landesbibliothek Bonn, 2019. http://d-nb.info/1240761252/34.
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Bryant, Lynda P. "HIV and the metabolic syndrome." Thesis, 2008. http://hdl.handle.net/10413/1188.
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Paredes, Sílvia Cristina de Sousa. "Cortisol: the villain in Metabolic Syndrome?" Dissertação, 2013. https://repositorio-aberto.up.pt/handle/10216/82811.
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Liang, Yen-Huei, and 梁妍慧. "Metabolic syndrome, cardiovascular disease and employment." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/37200229783722024318.
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碩士淡江大學
產業經濟學系碩士班
99
The prevalence of cardiovascular diseases and its risk factors (including overweight/obesity, diabetes, hypertension and hyperlipidemia) has been on the rise in the past decade in developing countries. These chronic health problems not only place a huge burden on health care and welfare systems, but may also affect labor market performance. We hence examine the negative impact of metabolic syndrome on the probability of cardiovascular disease and also on the probability of employment through increase of the risk of cardiovascular disease by analyzing the 2005 National Health Interview Survey (NHIS) of Taiwan. It uses an endogenous trivariate probit model with a recursive structure, and the instrumental variables include prevalence rate of disease and genetic factors. The empirical results indicate that cardiovascular disease has a significantly negative effect on both male’s and female’s employment probability. For men, the effect of cardiovascular disease is to reduce labor force participation by 44.31% while for women the effect is 26.98%. On the other hand, the results confirm that metabolic syndrome increases the risk for cardiovascular disease significantly. Metabolic syndrome will increase the incidence rate of cardiovascular disease by 17.01% for men and 30.37% for women. If metabolic syndrome can be avoided, the employment rates will rise by 5.8% and 7.73% for men and women, respectively. Therefore, given the significant increase in the incidence of metabolic syndrome, it is imperative that a multifaceted approach to combat this trend be undertaken. For example, enhance the education level will reduce the risk for metabolic syndrome and cardiovascular disease for women, and hence it would improve the social productivity. In addition, the prevention and treatment of cardiovascular disease should improve the probability of individuals finding and retaining employment.
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Paredes, Sílvia Cristina de Sousa. "Cortisol: the villain in Metabolic Syndrome?" Master's thesis, 2013. https://repositorio-aberto.up.pt/handle/10216/82811.
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Hradecká, Michaela. "Přírodní látky vhodné k léčbě metabolického syndromu." Master's thesis, 2019. http://www.nusl.cz/ntk/nusl-405193.
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Hradecká M.: Natural compounds applicable for the treatment of metabolic syndrome, Diploma thesis 2018/2019, Charles University, Faculty of Pharmacy in Hradec Králové, Department of Pharmaceutical Botany, pp. 60. Occurence of metabolic syndrome is increasing worldwide in children and adults. The use of natural compounds is one of possibilities in the prevention and treatment of metabolic syndrome. These compounds may act complexly or affect individual risk factors associated with metabolic syndrome. Selected plants with these effects are incorporated into my diploma thesis (for example Allium sativum, Crataegus laevigata, Hibiscus sabdariffa, Persea americana, Rosmarinus officinalis, Silybum marianum and Vaccinium myrtillus). The alga Undaria pinnatifida and fungus Pleurotus sajor-caju are also mentioned. It is necessary to carry out other clinical studies, where the positive effect of mentioned constituents will be confirmed, which could be added to the list of phytopharmaceuticals used to prevent, slow down or treat the metabolic syndrome in the future. Keywords: natural compounds, metabolic syndrome
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Dlabajová, Denisa. "Antioxidanty přírodního původu ovlivňující metabolický syndrom." Master's thesis, 2016. http://www.nusl.cz/ntk/nusl-344075.
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Dlabajová D., Antioxidants of natural origin influencing metabolic syndrome, Diploma thesis 2015/2016, Charles University in Prague, Faculty of Pharmacy in Hradec Králové, pp. 61. Large amounts of substances are extracted from plants found all over the world that show antioxidant activity, which prohibits the formation of free radicals. This activity could be beneficial in preventing and curing risk factors of metabolic syndrome. The selection of plants with this effect is shown in my diploma thesis (for example Salvia limbata, Lupinus luteus, Rosmarinus officinalis, Pueraria lobata etc.), which is divided into plant extracts, culinary plants and substances with significant antioxidant activity. Keywords: plants, antioxidants, metabolic syndrome
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Hartmann, Riley James. "The altered gut microbiome in metabolic syndrome." 2015. http://hdl.handle.net/1993/30345.
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Metabolic syndrome is a disease affecting 25% of North America’s population causing strain on the medical systems. With diet and exercise, genetics, environment, and the gut microbiota all being targeted as potential causes of the disease, there is a lack of consensus on the exact aetiology and pathophysiology. With improved methods in bioinformatic sequencing of faecal bacterial DNA in recent years, our research indicates that a dysbiosis in the gut microbiome is both necessary and sufficient in causing immunological changes in the host in order for the development of metabolic syndrome, T1Ds, and T2Ds. Specifically, our data indicates these shifts in microbiota occur prior to the onset of disease, and produce the disease regardless of diet and genetics. The findings in the current study indicate that future research towards manipulating the gut microbiota to prevent disease, as well as using the faecal bacteria as a screening tool should be pursued.
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Kaur, Sonya Sarjit. "Cortical thickness and inflammation in Metabolic Syndrome." Thesis, 2012. http://hdl.handle.net/2152/29158.
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Metabolic Syndrome (MetS), the clustering of obesity, high blood pressure, and disordered glucose and lipid/lipoprotein metabolism within a single individual, is associated with poorer cognitive function and dementia in later life. It has been hypothesized that cognitive impairment in MetS occurs primarily within the context of inflammation. MetS risk factors are also associated with thinning of the cerebral cortex. However, the mechanisms by which MetS and inflammation affect the brain are poorly understood. The present study used statistical mediation to examine the relationship between MetS risk factors, cortical thickness in a priori regions of interest (ROIs) and inflammation. ROIs in the inferior frontal, superior temporal, middle frontal, supra marginal, anterior cingulate and middle occipital regions were chosen from the previous literature. Serum levels of pro-inflammatory markers (interleukin 1, interleukin 2, interleukin 6 and C-Reactive Protein) were measured using enzyme-linked immunosorbent assays. Forty-three adults between the ages of 40 and 60 years underwent a health screen, neuropsychological testing and structural magnetic resonance imaging. A higher number of MetS risk factors was associated with thinning in the inferior frontal ROI (β=-0.35, p = 0.019). A higher number of MetS risk factors was also associated with higher levels of serum interleukin 2 (β=0.31, p=0.04). A higher level of serum interleukin 2 was also associated with reduced thickness in the inferior frontal ROI (β=-0.41, p=0.013). After accounting for the effects of interleukin 2, the number of MetS risk factors was no longer associated with cortical thickness in the inferior frontal ROI indicating successful statistical mediation and pointing towards a potentially important role for imflammation in linking MetS to cortical thinning and cognitive vunlerability.text