Relevant bibliographies by topics / Obesity and metabolic disfunction

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  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Obesity and metabolic disfunction'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Obesity and metabolic disfunction"

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BĂLĂȘESCU, Elena, Larisa Diana PANDIA, Roxana Ioana NEDELCU, and Daniela Adriana ION. "Obesity – a closer look to cell mechanisms disfunction." Romanian Journal of Medical Practice 16, no. 2 (June 30, 2021): 129–34. http://dx.doi.org/10.37897/rjmp.2021.2.3.

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Obesity is a complex, multifactorial condition, a major public health problem with an increasing prevalence worldwide. Obesity is characterized by an excess of adipose tissue, a low degree of chronic inflammation and disorders in the synthesis of biologically active hormones and peptides which intervene in regulating appetite and energy balance, immunity, insulin sensitivity, angiogenesis, blood pressure, lipid metabolism and homeostasis of the body. The visceral adipose tissue accumulation is accompanied by metabolic disorders that have as a substrate subclinical inflammation and signaling by intracellular pathways that lead to irreversible cellular structural and functional changes. The long-term impact of overweight and obesity translates into shortening life expectancy and disability, due to association with severe comorbidities, such as cardiovascular diseases, diabetes, oncological conditions. Therefore, understanding the cellular mechanisms involved in obesity may facilitate the highlighting of new possible therapeutic targets.
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Lyasnikova, M. B., N. A. Belyakova, I. G. Tsvetkova, A. A. Rodionov, and N. O. Milaya. "Risks for development of metabolic disorders in alimentary constitutional obesity." Obesity and metabolism 18, no. 4 (February 19, 2022): 406–16. http://dx.doi.org/10.14341/omet12705.

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BACKGROUND: alimentary-constitutional obesity due to it’s high prevalence, is the key problem of modern healthcare system. However, obesity is not always accompanied with metabolic disorders, leading to early invalidization and mortality. That’s why it is important to study risks of metabolical nonhealth in obesity.AIM: to detect factors, increasing risks of development of metabolic disbalance in alimentary-constitutional obesity.MATERIALS AND METHODS: In patients with alimentary-constitutional obesity there was performed an examination including anthropometry (body mass index, Waist Circumference, Hip Circumference,waist to hip ratio), blood pressure measurement, laboratory tests – metabolic indexes: glucose, insulin, insulin resistance indexes, leptin, cholesterol, cholesterol of lipoproteins, triglycerides, aspartate aminotransferase, alanine aminotransferase, gamma-glutamiltransferase), body composition measurement by bioelectrical impedance analysis; patients were also interviewed on their behavior (food habits) and physical activity.RESULTS: There were formed two groups depending on metabolic health indexes: main group – metabolically non-healthy obesity (MNHO) - 241 persons (aged 41±12,09, duration of obesity 12,5±9,51 years) with alimentary-constitutional obesity and two or more signs of MS, a comparison group – of metabolically healthy obesity (MHO) – 120 persons (aged 35,5±10,03; p<0,05, duration of obesity 8,0±7,39 years; p<0,05) with alimentary-constitutional obesity and one sign of MS or without it. Data analysis of studied risk factors for development of metabolically non-healthy alimentary-constitutional obesity confirmed that most relevant factor in development of MNHO is abdominal fat mass distribution (increasing of Waist Circumference over 88 sm in females and over 102 sm in mails). At the same time MNHO had correlation not only with classical signs of MS, but also with blood insulin level, insulin resistance indexes, fat metabolism disbalance and liver disfunction. More severed risk for appearance of metabolic disorders have patients over 45 years old with decreased active cell mass (less than 45%), duration of obesity above 10 years and obesity-burdened heredity. In food habits risk of development of metabolically non-healthy obesity was increased in taking of fat milk food, and, on the contrary, - frequent snacks, alcohol free sweet drinks didn’t affect it.CONCLUSION: Development of MNHO is associated not only with the age of patient, duration of obesity, carbohydrate and fat metabolism indexes, but also with decreased percentage of metabolically active tissues and some food habits.
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Li, Linghuan, Guangyao Zhu, Gaohang Fu, Weiwei Zha, and Hanbing Li. "Metabolic Syndrome Ameliorated by 4-Methylesculetin by Reducing Hepatic Lipid Accumulation." International Journal of Molecular Sciences 23, no. 18 (September 9, 2022): 10465. http://dx.doi.org/10.3390/ijms231810465.

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Obesity is a chronic metabolic disease caused by an imbalance between energy intake and expenditure during a long period and is characterized by adipose tissue disfunction and hepatic steatosis. The aim of this study was to investigate the effect of 4-methylesculetin (4-ME), a coumarin derivative, upon adipose microenvironment and hepatic steatosis in mice induced by a high-fat diet (HFD), and to explore potential mechanisms of its beneficial effect on metabolic disorders. HFD-fed mice displayed visceral obesity, insulin resistance, and hepatic lipid accumulation, which was remarkably ameliorated by 4-ME treatment. Meanwhile, 4-ME ameliorated adipocyte hypertrophy, macrophage infiltration, hypoxia, and fibrosis in epididymal adipose tissue, thus improving the adipose tissue microenvironment. Furthermore, 4-ME reversed the increase in CD36, PPAR-γ, SREBP-1, and FASN, and the decrease in CPT-1A, PPAR-α, and Nrf2 translocation into the nucleus in livers of HFD mice and in FFA-incubated hepatocytes. Moreover, the beneficial effects of 4-ME upon lipid deposition and the expression of proteins related to lipid metabolism in FFA-induced LO2 cells were abolished by ML385, a specific Nrf2 inhibitor, indicating that Nrf2 is necessary for 4-ME to reduce hepatic lipid deposition. These findings suggested that 4-ME might be a potential lead compound candidate for preventing obesity and MAFLD.
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Gaysina, L. R., A. I. Safina, and Farida Vadutovna Valeeva. "Funktsional'noe sostoyanie pochek u detey i podrostkov s ozhireniem." Obesity and metabolism 8, no. 2 (June 15, 2011): 52–55. http://dx.doi.org/10.14341/2071-8713-4953.

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Overweight and obesity are the most actual problems nowadays. Number of overweight patients steadily raises and duplicates every three decades. Obesity is associated with some factors of cardiovascular risk like diabetes mellitus and arterial hypertension, frequently leads to kidney disfunction. Obesity itself can result in poor renal hemodynamics, well-known risk factor of kidney disease. We studied impact of overweight and obesity in children and adolescents on renal tubular function and glomerular filtration rate.
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Fanelli, Elvira, Federico Abate Daga, Marco Pappaccogli, Elisabetta Eula, Anna Astarita, Giulia Mingrone, Chiara Fasano, et al. "A structured physical activity program in an adolescent population with overweight or obesity: a prospective interventional study." Applied Physiology, Nutrition, and Metabolism 47, no. 3 (March 2022): 253–60. http://dx.doi.org/10.1139/apnm-2021-0092.

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Obesity is a significant health problem, with increasing involvement of young population worldwide. The aim of this study was to evaluate the effects of 2 different types of physical exercise (resistance vs. combined aerobic-resistance) on cardiovascular and anthropometric profile of a sample of sedentary adolescents with overweight and obesity. After undergoing clinical, cardiovascular and anthropometric-metabolic evaluation (T0), subjects with overweight and obesity were randomized to a 6-month resistance or combined aerobic-resistance training program. Clinical, cardiovascular and anthropometric-metabolic evaluations were repeated after 6 months of training (T1) and after 3 months of detraining (T2). Thirty adolescents with overweight/obesity were enrolled and 20 subjects completed training program. A significant improvement in body composition was detected after 6 months, with a reduction of body mass index (32.1 [30.5 to 34.4] vs. 31.1 [29.6 to 33.4] kg/m2, p = 0.02) and adipose tissue (45.5 [41.1 to 49.7] vs. 41.6 [37.0 to 49.2] kg, p < 0.01). A reduction in diastolic blood pressure (75.5 ± 8.9 vs. 68.2 ± 6.4 mm Hg, p = 0.02) and pulse wave velocity (5.7 [5.1 to 5.9] vs. 5.2 [4.7 to 5.7] m/s, p = 0.04) was also observed. Persistence of the effect on the most important parameters was observed also after detraining period. In conclusion, regular physical exercise induces positive metabolic and cardiovascular effects, persisting even after brief discontinuation. Novelty: Physical exercise induces positive effect on cardiovascular risk profile. Positive effects persist also after brief discontinuation. Physical exercise reduces early signs of autonomic disfunction.
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Reguero, Marina, Marta Gómez de Cedrón, Sonia Wagner, Guillermo Reglero, José Carlos Quintela, and Ana Ramírez de Molina. "Precision Nutrition to Activate Thermogenesis as a Complementary Approach to Target Obesity and Associated-Metabolic-Disorders." Cancers 13, no. 4 (February 18, 2021): 866. http://dx.doi.org/10.3390/cancers13040866.

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Obesity is associated to increased incidence and poorer prognosis in multiple cancers, contributing to up to 20% of cancer related deaths. These associations are mainly driven by metabolic and inflammatory changes in the adipose tissue during obesity, which disrupt the physiologic metabolic homeostasis. The association between obesity and hypercholesterolemia, hypertension, cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM) is well known. Importantly, the retrospective analysis of more than 1000 epidemiological studies have also shown the positive correlation between the excess of fatness with the risk of cancer. In addition, more important than weight, it is the dysfunctional adipose tissue the main driver of insulin resistance, metabolic syndrome and all cause of mortality and cancer deaths, which also explains why normal weight individuals may behave as “metabolically unhealthy obese” individuals. Adipocytes also have direct effects on tumor cells through paracrine signaling. Downregulation of adiponectin and upregulation of leptin in serum correlate with markers of chronic inflammation, and crown like structures (CLS) associated to the adipose tissue disfunction. Nevertheless, obesity is a preventable risk factor in cancer. Lifestyle interventions might contribute to reduce the adverse effects of obesity. Thus, Mediterranean diet interventional studies have been shown to reduce to circulation inflammatory factors, insulin sensitivity and cardiovascular function, with durable responses of up to 2 years in obese patients. Mediterranean diet supplemented with extra-virgin olive oil reduced the incidence of breast cancer compared with a control diet. Physical activity is another important lifestyle factor which may also contribute to reduced systemic biomarkers of metabolic syndrome associated to obesity. In this scenario, precision nutrition may provide complementary approaches to target the metabolic inflammation associated to “unhealthy obesity”. Herein, we first describe the different types of adipose tissue -thermogenic active brown adipose tissue (BAT) versus the energy storing white adipose tissue (WAT). We then move on precision nutrition based strategies, by mean of natural extracts derived from plants and/or diet derived ingredients, which may be useful to normalize the metabolic inflammation associated to “unhealthy obesity”. More specifically, we focus on two axis: (1) the activation of thermogenesis in BAT and browning of WAT; (2) and the potential of augmenting the oxidative capacity of muscles to dissipate energy. These strategies may be particularly relevant as complementary approaches to alleviate obesity associated effects on chronic inflammation, immunosuppression, angiogenesis and chemotherapy resistance in cancer. Finally, we summarize main studies where plant derived extracts, mainly, polyphenols and flavonoids, have been applied to increase the energy expenditure.
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Savel'eva, L. V. "Sovremennaya kontseptsiya lecheniya ozhireniya." Obesity and metabolism 8, no. 1 (March 15, 2011): 51–56. http://dx.doi.org/10.14341/2071-8713-5191.

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Obesity is an unsolved problem of modern society, furthermore it is one of the main risk factors for type 2 diabetes mellitus, cardiovascular diseases and cancer, pathology of musculoskeletal and digestive systems, reproductive disfunction both for women and for men. It is known that treatment any chronic disease is rather complicated, not only for doctors but also for the patient, because it requires from the patient a careful self-control and substantial changes in lifestyle. In modern clinical practice, various methods of treatment of obesity are used: diet therapy, exercise therapy, physiotherapy, pharmacotherapy, psychotherapy and surgery. Modern methods of treatments of obesity are reviewed in this article
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Mikheev, R. K., E. N. Andreeva, E. V. Sheremetyeva, Yu S. Absatarova, T. A. Ponomareva, and O. R. Grigoryan. "Analysis of melatonin concentration and its correlation with ovarian disfunction among obese women of reproductive age." Problems of Endocrinology 67, no. 1 (February 12, 2021): 69–75. http://dx.doi.org/10.14341/probl12710.

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One of the new directions in the study of reproductive disorders in obese women is the effect and receptor sensitivity of melatonin on the gonadotropic function of the pituitary gland and ovariogenesis, taking into account the chronology of «light pollution». At the present stage, there is very little literature on the influence of the aspects of «light pollution» on the problem of obesity and reproductive disorders in the literature. This review is an attempt to combine the above problem in terms of the impact of «light pollution» and the level of receptor sensitivity of melatonin in women of reproductive age with obesity. The literature search was carried out in Russian (eLibrary, CyberLeninka.ru) and international (PubMed, Cochrane Library) databases in Russian and English. Free access to the full text of the articles was a priority. The selection of sources was prioritized for the period from 2015 to 2019. However, given the insufficient knowledge of the chosen topic, the choice of sources was dated from 1992. The work was carried out as part of the study «Central and peripheral pathophysiological mechanisms of development of adipose tissue diseases, taking into account clinical and hormonal characteristics» 2020–2022.
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Shyshkan-Shyshova, К. О., and O. V. Zinych. "Product of metabolic activity of intestinal microbium trimethylamine-N-oxide (TMAO) — biomarker of progression of atherosclerosis-copy in the heart of the heart." INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine) 18, no. 4 (June 30, 2022): 231–38. http://dx.doi.org/10.22141/2224-0721.18.4.2022.1177.

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The literature data on the importance of intestinal microbiota as an endocrine organ — producer of biologically active metabolites, which perform key functions to maintain metabolic homeostasis of the whole organism, in particular the condition of the cardiovascular system, are analyzed. Clinical and experimental studies using a metabolomical approach have shown that the development of atherosclerotic CVD is often associated with ele­vated levels of one of the microbial metabolites, trimethylamine N-oxide (TMAO). TMAO may be a sensitive prognostic biomar­ker of complications of type 2 diabetes, including atherosclerosis and cardiovascular disease. The precursor of TMAO is trimethy­lamine (TMA), formed by intestinal bacteria from food phosphatidylcholine and L-carnitine. In the liver, TMA is converted to TMAO under the influence of hepatic flavin monooxygenase 3. The mecha­nisms of the proatherogenic effect of elevated levels of TMAO include effects on bile acid and cholesterol metabolism, platelet hyperactivation, stimulation of inflammatory processes and oxidative stress, induction of endothelial disfunction and endoplasmic reticulum stress. It has been established that TMAO, in conditions of chronic elevation, can contribute to cardiome­tabolic diseases. Elevated le­vels of TMAO in dysmetabolic conditions (obesity, type 2 diabetes, atherosclerosis, or coronary heart disease) have been suggested to be largely associated with the gut microbiota profile. Therefore, regulating the ratio of intestinal microorganisms or their ability to form a precursor of TMAO — TMA, may be a way to develop new tools for the prevention and treatment of atherosclerosis and prevent the progression of cardiovascular complications, including in patients with type 2 diabetes. Studies have shown that inhibiting various stages of TMAO production can reduce TMAO levels and help treat atherosclerosis and diabetes.
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Branfield, Siobhan Laken, Benjamin Nieves Lopez, Matthew E. Poynter, and Anthony Valance Washington. "TLT-1, a Potential Regulator of Inflammatory Pathogenesis in Obesity and Non-Alcoholic Fatty Liver Disease (NAFLD)." Blood 138, Supplement 1 (November 5, 2021): 1005. http://dx.doi.org/10.1182/blood-2021-153403.

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Abstract Background: Obesity, a nationwide health issue, has related medical costs ranging between $147-210 billion per year in United States and has been associated with a 3.5-fold increased risk of developing NAFLD. In obesity, platelets work in a pleotropic manner with vascular and immune cells to amplify the chronic inflammatory process. Interestingly, studies have demonstrated that platelet numbers and reactivity are increased in obese individuals. The emerging role of activated platelets during obesity induced inflammation introduces the novel concept of platelet targeted therapeutic interventions. Kopec et al, further supports the idea that the mechanism underlying the progression of obesity lies in a platelet mediated pro-inflammatory state, illustrating that there is extravascular fibrin(ogen) deposition, macrophages and inflammatory cytokines within white adipose tissue and liver of mice on western diet. Kopec et al uses a fibrinogen mutant mouse (Fiby390-396 ) which lacks the binding motif for Mac-1 and inhibits the ligand interaction with leukocytes, diminishing inflammation, reducing macrophage counts, reducing weight, protects mice from NAFLD and glucose dysmetabolism. Taken together, all evidence points towards a platelet/fibrinogen/leukocyte pathophysiological mechanism underlying the development of obesity. TREM-Like Transcript-1 (TLT-1) is a platelet specific receptor found in the a-granules of platelets and released to the surface upon platelet activation. TLT-1 is a type 1 receptor that, like the integrin a2bb3, binds fibrinogen and facilitates platelet aggregation . However, although TLT-1 may assist in clot formation and hemostasis to arrest bleeding in a non-inflammatory/nonimmune mediated setting, TLT-1's main association is with regulating inflammatory-derived bleeding. This is demonstrated by increased hemorrhage after inflammatory treatments such as lipopolysaccharide LPS in the treml1 -/- mice as compared to controls. Considering the emerging evidence in support of a platelet-fibrinogen receptor ligand interaction as a key mechanism underlying the development of obesity and that TLT-1, a platelet specific receptor binds fibrinogen and mediates leukocyte trafficking, our laboratory set out to determine whether TLT-1 could be implicated as the main culprit underlying this mechanism. When placed on a western diet, treml1 -/-mice are more prone to weight gain, based on these finding we hypothesize that: The TLT-1/Fibrinogen molecular interaction regulates metabolic inflammation in obesity Aims: Evaluate the effects of western diet on obesity and NAFLD in the treml1 -/- mouse model Methods: TLT-1 (treml1 -/-) - apolipoprotein E (apoe -/-) double null (AT-DKO;n=11) mice and control apoe +/-/treml1 +/- littermate controls (AT-Hets;n=20) were fed western diet for 20 weeks. Plasma samples were collected for adipokine, glucose, insulin, liver enzyme and lipid profiling. Mouse were perfused, liver and adipose tissue were collected for histological analysis. Results: Overall AT-DKO mice gained more weight compared to AT-Hets (12.94±1.90 vs 8.51±1.70 grams p=0.02). Plasma analysis demonstrates that the AT-DKO have higher levels of TNF-a (0.54±0.60 vs 0.118±0.17 pg/ml p=0.03), and IL-10 (2.50±1.40 vs 1.50±2.10 pg/ml p=0.004) compared to littermate controls. Histological analysis of livers illustrates increased lipid vacuoles and inflammatory foci in the AT-DKO mice as compared to controls, while preliminary data is not significant for these differences, liver damage in the AT-DKO was significantly greater as demonstrated by increased AST levels (166.21±91.00 vs 102±68.10 U/L p=0.02). Moreover, the AT-DKO mice had higher levels of ALT, direct bilirubin, cholesterol, pai-1 , triglycerides and lower IL-6 and Adiponectin (Table 1 data not significant). These findings suggest that in the absence of TLT-1 these mice are more prone to liver disfunction , hyperlipidemia and inflammatory alterations. Conclusions: Mutant AT-DKO mice are more prone to obesity and NAFLD compared to littermate controls, suggesting that TLT-1, a platelet gene, plays a surprising role in metabolism. Further investigation could adjudicate TLT-1 administration as a potential therapeutic intervention for prevention and amelioration of Obesity and related pathologies. The current state of this project will be reported here. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.
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Dissertations / Theses on the topic "Obesity and metabolic disfunction"

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Bonacina, F. "ROLE OF THE LONG PENTRAXIN 3 (PTX3) IN CARDIOMETABOLIC DISEASES." Doctoral thesis, Università degli Studi di Milano, 2016. http://hdl.handle.net/2434/353808.

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PTX3 is a biomarker of cardiovascular diseases and exerts protective functions in acute myocardial infarction and atherosclerosis. Here we aimed at investigating the role of PTX3 in cardiovascular diseases. First we studied the role of PTX3 in arterial thrombosis induced by FeCl3 injury: PTX3 KO mice showed a 60% reduction in carotid artery blood flow with a greater thrombus formation compared to 20% of WT mice (p<0.01) following arterial thrombosis, an effect mediated by PTX3 derived from non-hematopoietic cells: indeed, PTX3 KO mice transplanted with bone marrow from WT or PTX3 KO mice presented a significant increased carotid occlusion compared to WT mice transplanted with bone marrow from WT or PTX3 KO mice (p<0.01). This effect was independent of altered hemostatic properties, impaired platelet activation, modulation of P-selectin activity as P-selectin KO/PTX3 KO mice showed a significant reduction in carotid artery blood flow and increased arterial thrombus formation compared to P-selectin KO (p<0.01). PTX3 was shown to localize between the damaged artery and thrombus and to reduced platelet aggregation induced by collagen and fibrinogen (p>0,01), an effect related mainly to the C-terminal and N-terminal domain respectively. Finally, exogenous administration of hrPTX3 reverted the pro-thrombotic phenotype in PTX3 KO mice and improves the outcomes in WT (p<0.01). In conclusion, PTX3 deficiency is associated with increased arterial thrombosis via modulation of collagen and fibrinogen thrombogenicity. In parallel, we investigated the role of PTX3 in the immune-inflammatory response associated to obesity and metabolic disorders, a condition deeply associated with the incidence of cardiovascular events. After 20 weeks of high fat diet (HFD,45% of calories from fat), PTX3 KO mice compared to WT, showed a decreased weight gain (p<0.05), coupled to a decreased accumulation of fat at both 10 and 20 weeks in the visceral (VAT,p<0.05) and subcutaneous adipose depots (SCAT,p<0.05) measured by magnetic resonance for imaging. Basal glycaemia at both 10 and 20 weeks was similar between groups as well as glucose and insulin tolerance measured by glucose (GTT) and insulin tolerance test (ITT), excluding a direct role of PTX3 on glucose homeostasis. As PTX3 is a key component of innate immunity, we focused our attention on the inflammatory response in VAT of PTX3 KO: adipocyte size was significantly smaller (p<0.01) and associated with a decreased infiltration of leukocytes and expression of pro-inflammatory cytokines (MCP-1, IL-6, p<0.05) compared to WT. These data show that deficiency of PTX3 results in reduced HDF-induced obesity as a consequence of a decreased inflammatory state of PTX3 KO VAT. Concluding, we have shown the dual role of PTX3 which plays a protective role in arterial thrombosis, while in a model of diet-induced obesity is associated with the promotion of inflammation and fat deposition in adipose tissue. This dual role suggests that PTX3 may play different functions depending on the origin and the site of action.
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Rahman, Olaiwola. "Metabolic studies in leanness and obesity." Thesis, University of Surrey, 1986. http://epubs.surrey.ac.uk/2728/.

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Metabolic rate and the proportion of carbohydrate, fat and protein oxidised at rest and during exercise were established in lean large eaters consuming 12843 + 1888 kJ per day and lean small eaters consuming 7090 +1568 kJ per day. Ther average resting metabolic rate in the lean large eaters was 330 + 47 ml oxygen/min. and in the lean small eaters was 285 + 54 ml oxygen/min. The average exercise metabolic rate in the lean large eaters was 1269 + 94 ml oxygen/min and in the lean small eaters was 1253 + 102 ml oxygen/min. In another group of lean large and small eaters, the average post prandial metabolic rate in lean large eaters consuming on average 13875 + 1562 kJ/day was 314 + 45 ml oxygen/min and in lean small eaters consuming 6372 + 1691 kJ/day was 278 + 40 ml oxygen/min. 24 hr energy expenditure in lean large eaters consuming on average 13005 ± 2004 kJ/day was 10191 + 34 kJ/day, and in lean small eaters consuming on average 7529 + 2228 kJ/day was 7156 + 461 kJ/day. However, none of these differences were statistically significant because of wide individual variation and the relatively small number of subjects. The adaptation of metabolic rate to a restricted energy intake was investigated in a group of obese women and a group of obese diabetic women. In the obese women, low metabolic rate observed during food restriction was associated with low nitrogen excretion. Long term metabolic rate measurements (up to 17 weeks) in the obese women who had lost weight indicated that metabolic rate was restored to previous values once feeding had commenced. Clinical studies indicated weight loss was achieved in the obese women without any damage to their health and there was a lowering of blood glucose levels in the obese diabetic women. A survey of 855 very low calorie diet (VLCD) users with relatively little clinical contact but helped by lay personnel confirmed the earlier clinical study that weight loss can readily be achieved by using a VLCD and that weight maintenance for up to a year was good probably because of the improved dietary behaviour as reported by the dieters. The proportion of dieters suffering from side-effects, such as halitosis, postural hypotension, constipation, weakness, hunger and headache were established, these sideeffects were not regarded as serious by most dieters. 88% claimed to feel well while on the diet and 71% claimed an Improvement in their health, while 2.8% consulted their doctor for symptoms which arose while they were on the diet.
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Kempen, Kitty Petronella Gertruda. "Metabolic effects of weight cycling in obesity." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1996. http://arno.unimaas.nl/show.cgi?fid=6679.

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Boyle, Kristen E. Houmard Joseph A. "Metabolic inflexibility in skeletal muscle with obesity." [Greenville, N.C.] : East Carolina University, 2009. http://hdl.handle.net/10342/1904.

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Thesis (Ph.D.)--East Carolina University, 2009.
Presented to the faculty of the Department of Exercise and Sports Science. Advisor: Joseph A. Houmard. Title from PDF t.p. (viewed Apr. 30, 2010). Includes bibliographical references.
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Camerotto, C. "OBESITY AND METABOLIC SYNDROME: PLASMA LIPOPROTEINS ALTERATIONS." Doctoral thesis, Università degli Studi di Milano, 2011. http://hdl.handle.net/2434/151781.

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Obesity, especially if associated with metabolic syndrome, promotes oxidative stress, a low grade chronic inflammatory state, and modify the composition and function of plasma lipoproteins. Oxidative damage to lipoproteins not only make LDL atherogenic but can also alter HDL reducing their anti-atherogenic properties. The possibility of monitoring the lipid peroxidation of the individual regions of LDL and HDL could lead to more detailed information on the molecular mechanisms that are the basis of the increased risk of cardiovascular diseases observed in obesity and metabolic syndrome. The object of this study was to investigate the susceptibility to peroxidation of plasma and of the hydrophobic core and the surrounding envelope of LDL and HDL in obese male (BMI between 25 and 35 Kg mq) with (SM, n=20)) or without (OB, n =40) metabolic syndrome. The susceptibility of plasma to peroxidation was higher in SM and OB than in normo-weight controls (CT, n=60), but not significant differences were observed between these two obese groups. Also the susceptibility to peroxidation of isolated LDL and HDL was higher in both obese groups than in CT. LDL and HDL in SM presented an higher content of triacylglicerols than the corresponding HDL of OB. Moreover, the hydrophobic core of HDL showed a risk of peroxidation significantly higher in SM than in OB. This last parameter was inversely correlated with the waist to hip ratio, an index of visceral obesity. This last evidence seems to indicate that the increase of inflammation typical of the visceral adipose tissue could be one of the major causes of the higher susceptibility to peroxidation found in the hydrophobic core of HDL. The evaluation of the susceptibility to peroxidation of the core and the envelope of LDL and HDL might contribute to the identification of a subset of patients at increased risk of metabolic and cardiovascular complications. Future “ad hoc” randomized clinical trials should be designed to address the effects of weight reduction and /or different diet and/or nutritional supplementation on these parameters.
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Porras, Jordi Sanz. "Obesity surgery : an ethnography of metabolic im/balance." Thesis, Lancaster University, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.662193.

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Several intemet sites sucp as 'Live Well' run by the National Health Service of the United Kingdom promote a 'healthy lifestyle' among citizens by providing information on how to avoid weight gain. A common recommendation to achieve and maintain a 'healthy' body weight is to balance body metabolism. That is, the energy we put in our body (calories we eat) must be the same as the energy we spend (physical activity). This thesis questions the universality of this recommendation and explores the complexity of balancing metabolism in daily life. In order to tackle this issue, this dissertation is premised by posthuman Science, Technology and Society studies (STS). This implies understanding metabolic balance as a set of practices that involve the association of human and non-humans actors. An attention to everyday practices is the guiding principle as this dissertation locates a study of metabolic balance in a case study of how people who suffer from morbid obesity live with bariatric surgery. Empirically this thesis demonstrates that in practice metabolism needs to be continuously re-balanced in daily life to avoid weight (re )gain. I suggest that the process of balancing metabolism may include sets of practices which are beyond the decision making of an informed individual. Metabolic balance, in the case of bariatric surgery, is shared work, an effect of collaborative work by the collective of cure (' healthy' lifestyle recommendations) and secondary care practices (coping with aspects of embodied living such as eating, masticating, drinking, buying, digesting or exercising). Theoretically, it argues that when metabolic balance after a gastric bypass is achieved, it is an effect of tinkering with secondary care practices of body metabolism. Thus, instead of putting big efforts into patient's adherence to a set of general healthy lifestyle recommendations, more attention should be given to care practices which (im)balance metabolism.
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Benrick, Anna. "Cytokines in metabolic functions /." Göteborg : Section of Endocrinology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, 2008. http://hdl.handle.net/2077/9608.

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LaPensee, Christopher Ryan. "METABOLIC FUNCTIONS OF PROLACTIN IN THE MOUSE." University of Cincinnati / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1172587296.

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Berg, Erika L. "Endocrinology of equine metabolic pathophysiology." Diss., Columbia, Mo. : University of Missouri-Columbia, 2006. http://hdl.handle.net/10355/4472.

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Thesis (Ph. D.) University of Missouri-Columbia, 2006.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on July 31, 2007) Includes bibliographical references.
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Juanola, Falgarona Martí. "Glycemic index in the management of Obesity and Metabolic syndrome." Doctoral thesis, Universitat Rovira i Virgili, 2014. http://hdl.handle.net/10803/319948.

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La obesitat y la síndrome metabòlica (SMet) són una de les principals causes de mortalitat arreu del món. L’índex glucémic (IG) i la càrrega glucémica (CG) han estat associades a un augment del risc de desenvolupar obesitat, diabetis tipus 2, SMet i malalties cardiovasculars. Actualment la evidència científica suggereix possibles beneficis de l’IG/CG per a la prevenció i tractament de la obesitat i la SMet. El nostre objectiu va ser analitzar la associació entre IG/CG de la dieta i el risc de desenvolupar SMet i els seus components, a més a més de analitzar la relació entre l’IG/CG i marcadors d’inflamació perifèrics. Per altra banda, vam analitzar la efectivitat d’una dieta de alt IG/CG contra una dieta baixa amb IG/CG i una dieta baixa en greix sobre la pèrdua de pes i la millora del perfil metabòlic, a través de la modulació d’uns mecanismes relacionats amb la sacietat, la inflamació i altres marcadors metabòlics. Aquesta tesi ha estat realitzada en el marc de l’estudi PREDIMED, un assaig clínic nutricional, multicèntric i aleatoritzat; i de l’estudi GLYNDIET, un assaig clínic en paral•lel, aleatoritzat i controlat de 6 mesos de duració. Els resultats obtinguts mostren com les dietes amb alt IG/CG podrien jugar un paper important en el desenvolupament de la SMet i alguns dels seus components. A més, el consum d’aquestes dietes també podria modular alguns marcadors cardiometabolics que contribuirien al guany de pes i al desenvolupament de malalties cardiovasculars. Finalment, vam observar com el consum d’una dieta amb baix IG i un moderat contingut de carbohidrats era més efectiva per la pèrdua de pes i la millora de la sensibilitat i resistència a la insulina que una dieta de alt IG i un moderat contingut de carbohidrats o una dieta baix en greix.
La obesidad y el síndrome metabólico (SMet) son una de las principales causas de la mortalidad a nivel mundial. El índice glucémico (IG) i la carga glucémica (CG) han estado asociados a un mayor riesgo de obesidad, diabetes tipo 2, SMet y enfermedades cardiovasculares. Actualmente la evidencia científica sugiere posibles beneficios del IG/CG para la prevención y tratamiento de la obesidad y SMet. Nuestro objetivo fue analizar la asociación entre el IG/CG de la dieta y el riesgo de desarrollar SMet i sus componentes, además de analizar la relación del IG/CG y marcadores de inflamación periféricos. Por otro lado, analizamos la efectividad de una dieta de alto IG/CG contra una dieta baja en IG/CG y una dieta baja en grasa sobre la pérdida de peso i la mejora del perfil metabólico, a través de la modulación de mecanismos relacionados con la saciedad, la inflamación y otros marcadores metabólicos. Esta tesis se ha realizado dentro del marco del estudio PREDIMED, una ensayo clínico nutricional, multicéntrico i aleatorizado; y el estudio GLYNDIET, un ensayo clínico en paralelo, aleatorizado y controlado de 6 meses de duración. Los resultados obtenidos muestran como las dietas de alto IG/CG podrían jugar un papel importante en el desarrollo del SMet y alguno de sus componentes. Además, el consumo de estas dietas también podría modular algunos marcadores cardiometabólicos que contribuyen a la ganancia de peso y al desarrollo de enfermedades cardiovasculares. Finalmente, observamos como el consumo de una dieta de bajo IG y una moderada cantidad de carbohidratos era más efectiva para la pérdida de peso y la mejora de la sensibilidad y la resistencia a la insulina que una dieta de alto IG y una moderada cantidad de carbohidratos o una dieta baja en grasa.
Obesity and Metabolic Syndrome (MetS) are one of the main causes of disability and death worldwide. It has been proposed that high glycemic index (GI) and high glycemic load (GL) diets are associated with increased risks of obesity, type 2 diabetes mellitus, MetS and cardiovascular disease. To date, evidence suggests possible benefits of the GI/GL for the prevention and management of obesity and MetS. We aimed to analyze the association between dietary GI and GL and the risk of to develop MetS and its features, as well as, the relationship between dietary GI and GL, peripheral adipokines and inflammatory markers. Also, we aimed to analyze the effectiveness of a high GI/GL diet versus a low-GI/GL and a low-fat diet in body weight loss and the improvement of metabolic profile, through the modulation of some mechanisms related to satiety, inflammation and other metabolic risk markers. This thesis has been conducted in the framework of the PREDIMED Study, multicenter randomized nutrition trial, and the GLYNDIET study, a 6-month randomized, parallel, controlled clinical trial. Our results suggest that high dietary GI and GL have a potential role in the development of MetS and some of its components. The consumption of diets with high-GI foods or high dietary GL may also modulate some cardiometabolic markers thus contributing to weight gain and cardiovascular disease. Finally, we found that a moderate-CH low-GI diet may be more effective for weight loss than a moderate-CH high-GI diet or a conventional low-fat diet. The metabolic benefits observed for insulin resistance and sensitivity in those subjects following a low-GI diet, and the tendency to improve other inflammatory and associated metabolic risk markers, also indicate that low-GI diets are better tools for managing obesity and its associated comorbidities.
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Books on the topic "Obesity and metabolic disfunction"

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Ahima, Rexford S., ed. Metabolic Basis of Obesity. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-1607-5.

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Ordemann, Jürgen, and Ulf Elbelt, eds. Obesity and Metabolic Surgery. Berlin, Heidelberg: Springer Berlin Heidelberg, 2022. http://dx.doi.org/10.1007/978-3-662-63227-7.

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Metabolic basis of obesity. New York: Springer, 2011.

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J, Antel, ed. Obesity and metabolic disorders. Amsterdam: IOS Press, 2005.

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Agrawal, Sanjay, ed. Obesity, Bariatric and Metabolic Surgery. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-54064-7.

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Bray, George A. The Metabolic Syndrome and Obesity. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-431-5.

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Agrawal, Sanjay, ed. Obesity, Bariatric and Metabolic Surgery. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-04343-2.

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European Society for Clinical Investigation. Meeting. Stress, obesity, and metabolic syndrome. Boston, Mass: Blackwell Publishing on behalf of the New York Academy of Sciences, 2006.

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Kiess, W., Arya M. Sharma, Martin Wabitsch, and Claudio Maffeis. Metabolic syndrome and obesity in childhood and adolescence. Basel: Karger, 2015.

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Guide to obesity and the metabolic syndrome: Origins and treatment. Boca Raton: CRC Press, 2011.

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Book chapters on the topic "Obesity and metabolic disfunction"

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Batsis, John A. "Sarcopenic Obesity." In Metabolic Syndrome, 665–78. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-11251-0_38.

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Batsis, John A. "Sarcopenic Obesity." In Metabolic Syndrome, 1–17. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-12125-3_38-1.

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Ordemann, J., U. Elbelt, A. Stengel, and T. Hofmann. "Obesity." In Obesity and Metabolic Surgery, 1–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 2022. http://dx.doi.org/10.1007/978-3-662-63227-7_1.

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Frazier-Wood, Alexis C., and Zhe Wang. "Genetics of Obesity." In Metabolic Syndrome, 123–40. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-11251-0_10.

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Chan, Dick C., Jing Pang, and Gerald F. Watts. "Dyslipidemia in Obesity." In Metabolic Syndrome, 525–40. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-11251-0_30.

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Speakman, John R. "Evolution of Obesity." In Metabolic Syndrome, 103–22. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-11251-0_9.

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Frazier-Wood, Alexis C., and Zhe Wang. "Genetics of Obesity." In Metabolic Syndrome, 1–21. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-12125-3_10-1.

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Chan, Dick C., Jing Pang, and Gerald F. Watts. "Dyslipidemia in Obesity." In Metabolic Syndrome, 1–18. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-12125-3_30-1.

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Speakman, John R. "Evolution of Obesity." In Metabolic Syndrome, 1–23. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-12125-3_9-1.

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Hughes, Sheryl O., Thomas G. Power, Jayna M. Dave, and Teresia M. O’Connor. "Childhood Environment and Obesity." In Metabolic Syndrome, 243–59. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-11251-0_15.

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Conference papers on the topic "Obesity and metabolic disfunction"

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Savira, Maya, Rusdiana, Sry Suryani Widjaja, and M. Syahputra. "Comparison Malondialdehyde (MDA) Level between Obesity Non Metabolic Syndrome and Obesity with Metabolic Syndrome Patients." In 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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Osokina, Irina. "P289 Metabolic complications of obesity in children." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.639.

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Rychkova, Lyubov, Anna Pogodina, Lyudmila Grebenkina, Olga Berdina, Zhanna Ayurova, and Tatyana Astakhova. "P517 Metabolic features of adolescents with obesity." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.852.

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Nesterovska, Olga, Ganna Stupnytska, Oleksandr Fediv, Oksana Prituliak, and Iryna Nemish. "Evaluation of Systematic Inflammation, Oxidative Stress and Endothelial Disfunction in COPD, ASTHMATIC AND ACO Patients with Obesity." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2661.

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Oliveira, F. M., W. H. Tran, D. Lesser, R. Bhatia, R. Ortega, S. D. Mittelman, T. G. Keens, S. L. Davidson Ward, and M. C. Khoo. "Autonomic and metabolic effects of OSA in childhood obesity." In 2010 32nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC 2010). IEEE, 2010. http://dx.doi.org/10.1109/iembs.2010.5627789.

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Florentina, Nechita. "The Role Of Primary Kinetoprophilaxy In Metabolic Disorders – Exogenous Obesity." In EduWorld 2018 - 8th International Conference. Cognitive-Crcs, 2019. http://dx.doi.org/10.15405/epsbs.2019.08.03.109.

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Berenbaum, F. "SP0157 Metabolic phenotype: the two faces of obesity in osteoarthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.7120.

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Zaytouni, Tamara, Cory Dubois, Daniel Hitchcock, Nicholas Stylopoulos, Clary Clish, and Nada Kalaany. "Abstract IA26: Identifying metabolic liabilities in obesity-associated pancreatic cancer." In Abstracts: AACR Special Conference: Metabolism and Cancer; June 7-10, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.metca15-ia26.

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Singh, Mandeep, Raj Kumar, Shailendra Gaur, and Rajendra Prasad. "Effect of obesity and metabolic syndrome in patients with bronchial asthma." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa4582.

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Healy, LA, AM Ryan, L. Quinn, EM Connolly, MJ Kennedy, T. Boyle, and JV Reynolds. "Is metabolic syndrome the link between obesity and postmenopausal breast cancer?." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-5040.

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Reports on the topic "Obesity and metabolic disfunction"

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Jaganathan Geethalakshmi, Kruthica, Iyshwarya Bhaskar Kalarani, and Ramakrishnan Veerabathiran. Metabolic complications associated with lipodystrophic obesity and diabetes. Peeref, November 2022. http://dx.doi.org/10.54985/peeref.2211p4354869.

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Kim, Su-Jong. Understanding Obesity and the Influence of Acculturation on Metabolic Responses in East Asian Populations in the United States. Fort Belvoir, VA: Defense Technical Information Center, August 2007. http://dx.doi.org/10.21236/ad1014003.

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Chang, Yuwen, Tingting Du, Xiangling Zhuang, and Guojie Ma. Time-restricted eating can lead to weight loss due to energy restriction: A systematic review and meta-analysis based on randomized, controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2022. http://dx.doi.org/10.37766/inplasy2022.10.0098.

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Review question / Objective: P: Adults with overweight or obesity; I: Time restricted eating with eating window less than 10 hours and with or without calorie restriction; C: People with eating window more than 12 hours; O: Weight loss, body composition, metabolic risk factors, energy intake and eating window. Condition being studied: Adults with overweight and obesity. Information sources: We search four databases including PubMed, Embase, Scopus and the Cochrane library.
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Wang, Jiajie, Wei Huang, Yanji Zhang, Zhengrong Zhao, and Zhongyu Zhou. Acupuncture and related interventions for the treatment of obesity: protocol for a scoping review of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2022. http://dx.doi.org/10.37766/inplasy2022.3.0099.

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Review question / Objective: The purpose of this study is to summarize the characteristics of RCT in the treatment of obesity by acupuncture and other related intervention measures, so as to enhance evidence-based clinical practice about acupuncture for obesity. Condition being studied: Obesity is a chronic metabolic disease that is defined as a body's excessive accumulation or abnormal distribution of total or local fat content. Their complications such as Type II diabetes mellitus, hyperlipidemia, and cardiovascular diseases are strongly related to higher risks of mortality. In recent years, with the changes in diet structure and living habits, 1.9 billion adults were overweight and over 650 million were obese according to the report by the WHO in 2016. Acupuncture is a characteristic therapy of traditional Chinese medicine, which is effective and safe for the treatment of simple obesity. In recent years, many RCTs using acupuncture in simple obesity were carried out within and outside of China. But currently, acupuncture treatment has no uniform standard, and there are a number of problems with this current clinical application of modern Chinese Medicine. Unfortunately, there is an absence of high-quality data supporting their use. This scoping review aims to summarize the characteristics of RCT in the treatment of obesity by acupuncture and other related intervention measures, so as to enhance evidence-based clinical practice about acupuncture and moxibustion for obesity.
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