Gotowe bibliografie tematyczne / Metabolic syndrome

Gotowa bibliografia na temat „Metabolic syndrome”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 27 lipca 2024

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Artykuły w czasopismach na temat "Metabolic syndrome"

Karimova, Maksuda Ahmedjanovna, i Dilnoza Kakhramanovna Kurbanbaeva. "Problems Of Metabolic Syndrome". American Journal of Medical Sciences and Pharmaceutical Research 03, nr 06 (10.06.2021): 52–55. http://dx.doi.org/10.37547/tajmspr/volume03issue06-08.

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At the beginning of the third millennium, for mankind, which overcame the epidemic of life-threatening infections during its centuries-old history, the problem of cardiovascular diseases (CVD) came to the fore in relevance among all causes of morbidity and mortality. A significant role in this was played by lifestyle modification associated with limiting physical activity, increasing the calorie content of food, and a steady increase in emotional stress. All of this potentiates the main risk factors for CVD, which are a “negative asset of progress,” namely increased blood pressure (BP), dyslipidemia, diabetes mellitus (DM) and obesity. Since 1988, after G. Reaven's Banting lecture, it is customary to designate the interconnected combination of these pathologies by the single term "metabolic syndrome X".

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Vazira, Ashrabova, i Saidov Saidamir. "METABOLIC SYNDROME: LITERATURE ANALYSIS". International Journal of Modern Medicine 03, nr 07 (1.07.2024): 12–23. http://dx.doi.org/10.55640/ijmm-03-07-03.

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MetS is a significant public health concern due to its association with severe health outcomes. Early identification and comprehensive management of MetS components are crucial in reducing the global burden of this syndrome. Further research is needed to refine diagnostic criteria, understand the underlying mechanisms, and develop more effective prevention and treatment strategies. The metabolic syndrome (MetS) is a group of illnesses that together better predict a person's risk of cardiovascular disease than any one of the illnesses alone. Human MetS risk is influenced by a combination of environmental and genetic variables. As MetS is a complex disorder with a startlingly high incidence rate these days, developing suitable experimental animal models that closely resemble the illness state in people is essential to resolving the challenges associated with assessing the pathophysiology of MetS in humans. The objective of this study is to provide an overview of the pathophysiology of dietary, genetic, and pharmaceutical models of metabolic syndrome. We will also go over the applicability, advantages, and disadvantages of various animal models. Despite the establishment of many animal models of MetS, more research on.

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Jeengar, Pooja, i Madhubala Chauhan. "Association of metabolic syndrome in polycystic ovarian syndrome". New Indian Journal of OBGYN 3, nr 2 (styczeń 2017): 90–94. http://dx.doi.org/10.21276/obgyn.2017.3.2.5.

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STĂNESCU, Ana Maria Alexandra, Ana Maria GOANŢĂ, Roxana IGNĂTESCU, Ekua Asafoaba APPIAH, Ioana Veronica GRĂJDEANU i Lucian IONIŢĂ. "COMPARISON BETWEEN HUMANS AND ANIMAL DIAGNOSED WITH METABOLIC SYNDROME AND OBESITY ASSOCIATED METABOLIC PROBLEMS". Romanian Journal of Medical Practice 12, nr 4 (31.12.2017): 250–55. http://dx.doi.org/10.37897/rjmp.2017.4.14.

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Metabolic syndrome is an increasingly recognised problem worldwide. The diagnostic criteria may vary from country to country and between humans and animals. It is therefore essential to have a globally regulated diagnostic criteria for both animals and humans.

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Wikiera, Beata, Agnieszka Zubkiewicz-Kucharska, Julita Nocoń-Bohusz i Anna Noczyńska. "Metabolic disorders in polycystic ovary syndrome". Pediatric Endocrinology Diabetes and Metabolism 23, nr 4 (2017): 204–8. http://dx.doi.org/10.18544/pedm-23.04.0094.

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Sapna Devi, A. "Metabolic Syndrome and VDR Gene Polymorphism". International Journal of Science and Research (IJSR) 13, nr 2 (5.02.2024): 610–12. http://dx.doi.org/10.21275/sr24205120015.

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Siddharth Bharatbhai, Rajpura, i Desai Archish Ishvarbhai. "Metabolic Syndrome among Polycystic Ovarian Syndrome: A Cross Sectional Study". Indian Journal of Obstetrics and Gynecology 7, nr 1 (2019): 65–71. http://dx.doi.org/10.21088/ijog.2321.1636.7119.12.

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Shalaby, Adel. "Metabolic Syndrome". Al-Azhar Medical Journal 47, nr 4 (1.10.2018): 1. http://dx.doi.org/10.21608/0053052.

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Mychka, Viktoriya Borisovna, Irina Evgen'evna Chazova, V. B. Mychka i I. E. Chazova. "Metabolic syndrome". Systemic Hypertension 6, nr 1 (15.03.2009): 50–53. http://dx.doi.org/10.26442/sg33062.

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Lee, L., i R. A. Sanders. "Metabolic Syndrome". Pediatrics in Review 33, nr 10 (1.10.2012): 459–68. http://dx.doi.org/10.1542/pir.33-10-459.

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Rozprawy doktorskie na temat "Metabolic syndrome"

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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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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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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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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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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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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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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Książki na temat "Metabolic syndrome"

E, Batone Thomas, red. Metabolic syndrome research trends. New York: Nova Science Publishers, 2008.

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Ahima, Rexford S., red. Metabolic Syndrome. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-12125-3.

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Farooqui, Akhlaq A. Metabolic Syndrome. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7318-3.

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Wang, Minghan, red. Metabolic Syndrome. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470910016.

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The metabolic syndrome. Wyd. 2. Chichester, West Sussex: Wiley-Blackwell, 2011.

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Scott, Isaacs. Overcoming metabolic syndrome. Omaha, Neb: Addicus Books, 2006.

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Byrne, Christopher D., i Sarah H. Wild, red. The Metabolic Syndrome. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470025131.

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Hansen, Barbara Caleen, i George A. Bray, red. The Metabolic Syndrome. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-116-5.

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Beck-Nielsen, Henning, red. The Metabolic Syndrome. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1331-8.

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Byrne, Christopher D., i Sarah H. Wild, red. The Metabolic Syndrome. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444347319.

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Części książek na temat "Metabolic syndrome"

Farooqui, Akhlaq A. "Essential Fatty Acid Metabolism in Metabolic Syndrome and Neurological Disorders". W Metabolic Syndrome, 67–101. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7318-3_3.

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Wang, Minghan. "Gut as an Endocrine Organ: The Role of Nutrient Sensing in Energy Metabolism". W Metabolic Syndrome, 1–28. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470910016.ch1.

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Wang, Minghan. "Current Antidiabetic Therapies and Mechanisms". W Metabolic Syndrome, 253–78. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470910016.ch10.

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Burcelin, Remy, Cendrine Cabou, Christophe Magnan i Pierre Gourdy. "GLP-1 Biology, Signaling Mechanisms, Physiology, and Clinical Studies". W Metabolic Syndrome, 279–325. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470910016.ch11.

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McIntosh, C. H. S., S. J. Kim, R. A. Pederson, U. Heiser i H. U. Demuth. "Dipeptidyl Peptidase IV Inhibitors for Treatment of Diabetes". W Metabolic Syndrome, 327–58. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470910016.ch12.

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Ryan, Margaret, i Serge A. Jabbour. "Sodium Glucose Cotransporter 2 Inhibitors". W Metabolic Syndrome, 359–75. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470910016.ch13.

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Micanovic, Radmila, James D. Dunbar i Alexei Kharitonenkov. "Fibroblast Growth Factor 21 as a Novel Metabolic Regulator". W Metabolic Syndrome, 377–89. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470910016.ch14.

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Tong, Qiang. "Sirtuins as Potential Drug Targets for Metabolic Diseases". W Metabolic Syndrome, 391–422. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470910016.ch15.

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Hale, Clarence, i David J. St. Jean. "11β-Hydroxysteroid Dehydrogenase Type 1 as a Therapeutic Target for Type 2 Diabetes". W Metabolic Syndrome, 423–58. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470910016.ch16.

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Yan, Hai, Wei Gu i Murielle Veniant-Ellison. "Monoclonal Antibodies for the Treatment of Type 2 Diabetes: A Case Study with Glucagon Receptor Blockade". W Metabolic Syndrome, 459–67. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470910016.ch17.

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Streszczenia konferencji na temat "Metabolic syndrome"

Cosmescu, Adriana, i Doina Felea. "P67 Metabolic syndrome: case report". W 8th Europaediatrics Congress jointly held with, The 13th National Congress of Romanian Pediatrics Society, 7–10 June 2017, Palace of Parliament, Romania, Paediatrics building bridges across Europe. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313273.155.

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Muñoz-Diosdado, A., L. Ramírez-Hernández, A. M. Aguilar-Molina, J. A. Zamora-Justo, R. A. Gutiérrez-Calleja i C. D. Virgilio-González. "Holter registers and metabolic syndrome". W XIII MEXICAN SYMPOSIUM ON MEDICAL PHYSICS. AIP Publishing LLC, 2014. http://dx.doi.org/10.1063/1.4901381.

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Savira, Maya, Rusdiana, Sry Suryani Widjaja i M. Syahputra. "Comparison Malondialdehyde (MDA) Level between Obesity Non Metabolic Syndrome and Obesity with Metabolic Syndrome Patients". W International Conference of Science, Technology, Engineering, Environmental and Ramification Researches. SCITEPRESS - Science and Technology Publications, 2018. http://dx.doi.org/10.5220/0010081806440647.

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Senhorinha, Gláucia Maria, Arlys Emanuel Mendes da Silva Santos i Douglas Daniel Dophine. "The role of metabolic syndrome in Alzheimer’s disease". W XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.319.

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Background: Metabolic syndrome (MS) leads to the deposits formation of insoluble protein aggregates, neuroinflammation, oxidative stress, neuronal insulin resistance, progressive insulin resistance, desensitization and β-amyloid amyloidosis in the brain, besides direct ischemic effects which are closely associated with Alzheimer’s disease (AD).1 Objectives: The present study seeks to understand the role of the metabolic syndrome in the pathophysiology of Alzheimer’s disease and to describe preventive and therapeutic interventions. Methods: PUBMED and Web of Science were the databases used, the following descriptors were used to search the articles: “Alzheimer Disease” OR “Alzheimer Dementia” AND “Metabolic Syndrome”. Results: The studies in general have shown that MS is related to AD through brain insulin resistance, triggered by oxidative stress and neuroinflammation. It is related to the progressive atrophy of brain regions involved in the progression of AD. Insulin resistance in the brain is related to the progressive atrophy of the brain regions from initial progression of AD. These regions are cingulate cortices, medial temporal lobe, prefrontal gyri and other regions.³ Thus, there is an inhibition of the mechanisms of beta-amyloid removal, leading to its accumulation, which generates neuroinflammation, that in turn potentiates insulin resistance in the central nervous system, contributing to the genesis and progression of cognitive damage.2,3 Conclusions: Insulin resistance plays a major role in the initiation and perpetuation of cognitive impairment in AD. Furthermore, the components of the MS associated with AD, when treated with preventive and therapeutic measures, break this association by promoting rebalancing of the metabolism.

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Arsić, Aleksandra, Milica Kojadinović, Snjezana Petrović, Danijela Ristić Medić, Milena Žuža Praštalo i Vesna Vučić. "FFECTS OF POMEGRANATE JUICE ON LIPID METABOLISM IN WOMEN WITH DYSLIPIDEMIA AND METABOLIC SYNDROME". W 2nd International Symposium on Biotechnology. Faculty of Agronomy in Čačak, University of Kragujevac, 2024. http://dx.doi.org/10.46793/sbt29.79aa.

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The objective of this research was to evaluate the effects of the consumption of Pomegranate juice (PJ) on blood pressure and lipid metabolism in subjects with dyslipidemia and metabolic syndrome. Twelve females with established dyslipidemia and 12 females with metabolic syndrome consumed 300 mL of PJ daily for 2 and 6 weeks respectively. PJ consumption resulted in a significant decrease in diastolic blood pressure, and LDL-cholesterol, an increase in the estimated activity of stearoyl-CoA desaturase in the short study, and a significant decrease in the percentage of arachidonic acid and an increase in monounsaturated fatty acids in longer study. These results indicate a positive impact of the consumption of pomegranate juice, in both short and long periods, on lipid metabolism and suggest potential anti-inflammatory and cardio- protective effects

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Ekici, Aydanur, Emel Bulcun, Mehmet Ekici, Pinar Yildiz, Tulay Karakoc i Dilay Cimen. "Metabolic syndrome in interstitial lung diseases". W Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa3823.

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Midori Shinzato, Marcia, Pamela Judith Silva, Franciely Bueno Wigeneske i Elias Silva de Medeiros. "PAINFUL MUSCULOSKELETAL DISEASES IN METABOLIC SYNDROME". W Congresso Brasileiro de Reumatologia 2020. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2020.17344.

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Viégas, Jéssica de Vasconcelos Oliveira, Tainá Rodrigues Toqueton, Délio Guerra Drummond Júnior, Renata Ferreira Chagas, Lênio Airam de Pinho, Clara Araújo Montenegro Fonseca i Igor Costa Santos. "Clinical treatment of metabolic syndrome in pregnant women". W II SEVEN INTERNATIONAL MEDICAL AND NURSING CONGRESS. Seven Congress, 2023. http://dx.doi.org/10.56238/iicongressmedicalnursing-022.

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Metabolic syndrome is a medical condition characterized by a set of cardiovascular risk factors, including obesity, hypertension, insulin resistance, and dyslipidemia. During pregnancy, a woman's body undergoes complex metabolic and hormonal changes to facilitate fetal development. However, when the pregnant woman has metabolic syndrome, these changes can be exacerbated, increasing the risk of serious obstetric complications and having a potential impact on maternal-fetal health.

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Zaibi, Haifa, Sarra Maazaoui, Jihen Ben Amar, Ines Laaouini, Saloua Azzebi, M. Ali Baccar, Besma Dhahri i Hichem Aouina. "Metabolic syndrome in chronic obstructive pulmonary disease". W ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa719.

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Lobova, Tatyana Aleksandrovna. "Metabolic syndrome: pathogenetic aspects and prognostic value". W VIII International applied research conference. TSNS Interaktiv Plus, 2016. http://dx.doi.org/10.21661/r-111348.

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Raporty organizacyjne na temat "Metabolic syndrome"

Hawksworth, Dorota, i Arthur Burnett II. Metabolic syndrome and men’s health. BJUI Knowledge, sierpień 2019. http://dx.doi.org/10.18591/bjuik.0482.

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MOSKALENKO, O. L., R. A. YASKEVICH i E. V. KASPAROV. METABOLIC SYNDROME: PREVALENCE, DIAGNOSIS CRITERIA. Science and Innovation Center Publishing House, kwiecień 2022. http://dx.doi.org/10.12731/978-0-615-67340-0-3.

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This article presents a review of the literature and analyzes scientific research on the metabolic syndrome and diagnostic criteria. The authors conducted a scientific search using the relevant keywords in the PubMed and Google Scholar search engines, in the Scopus, Web of Science, MedLine, The Cochrane Library, EMBASE, Global Health, CyberLeninka, RSCI and others databases.

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Fu, Jia, Jinqiong Jiang i Kanghan Liu. Metabolic syndrome and survival of hepatocellular carcinoma. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, grudzień 2022. http://dx.doi.org/10.37766/inplasy2022.12.0113.

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Wang, Rui, Guanghua Chen, Xuan Zhang, Cheng Li i Yonghua Chen. The effect of bariatric surgery on pancreas fat accumulation: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, kwiecień 2023. http://dx.doi.org/10.37766/inplasy2023.4.0072.

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Review question / Objective: This systematic review and meta-analysis aimed to assess the effect of bariatric surgery on pancreas fat accumulation. Condition being studied: Pancreatic steatosis is characterized by increased accumulation of fat in the pancreas. The most common causes are obesity and metabolic syndrome. Due to this close association between obesity and metabolic syndrome, one can assume that, in addition to a rapid and sustained weight loss, bariatric surgery could affect metabolic syndrome and its components. However, it remains unclear whether bariatric surgery and weight loss can reverse abnormalities in pancreatic lipid metabolism in association with their effect on endocrine pancreatic dysfunction. This systematic review and meta-analysis aimed to measure the change of pancreatic fat in a group of patients with severe obesity before and after bariatric surgery.

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Kirby, Michael, i Jonny Coxon. The metabolic syndrome, erectile dysfunction and testosterone deficiency. BJUI Knowledge, wrzesień 2019. http://dx.doi.org/10.18591/bjuik.0484.

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Goddard, Clayton. SGLT2 Inhibitors and Potential Applications in Treating Metabolic Syndrome. Ames (Iowa): Iowa State University, maj 2022. http://dx.doi.org/10.31274/cc-20240624-1280.

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Li, Mengdie, Yating Yang, Haixia Wang i Tianhao Bao. Meta-analysis of risk factors for metabolic syndrome in schizophrenia. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, kwiecień 2021. http://dx.doi.org/10.37766/inplasy2021.4.0023.

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Mateș, Letiția, Marius Emil Rusu, Ionel Fizeșan, Daniela-Saveta Popa i Daniel Leucuța. Walnut intake interventions targeting biomarkers of metabolic syndrome and inflammation in middle-aged and older adults: a systematic review and meta-analysis of randomized controlled trials research protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, czerwiec 2022. http://dx.doi.org/10.37766/inplasy2022.6.0058.

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Review question / Objective: The aim of this study was to conduct a systematic review and meta-analysis of randomized controlled trials (RCTs) in order to properly examine the evidence on the effects of walnut consumption on chosen indicators of inflammation and metabolic syndrome in mature adults. Condition being studied: Metabolic syndrome (MetS), chronic, low-grade inflammation, and oxidative stress are all important risk factors for morbidity and death, with a higher frequency in the elderly population. Information sources: We conducted a comprehensive search in five databases: Pubmed, EMBASE, Scopus, Cochrane, ClinicalTrials, from inception.

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Wang, Xiaolan, Lijuan Ha, Bing Yan i Xiaona Liu. The Effectiveness of acupuncture for metabolic syndrome: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, styczeń 2022. http://dx.doi.org/10.37766/inplasy2022.1.0062.

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Voicehovska, Julija, Mila Vlaskovska, Jana Janovska, Sergejs Babikovs, Vladimirs Voicehovskis, Andrejs Skesters, Alise Silova i in. Oxidative Stress Markers Diagnostic Value in Metabolic Syndrome Dermal Manifestations: a Prospective Clinical Trial. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, luty 2018. http://dx.doi.org/10.7546/crabs.2018.02.15.

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