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Książki na temat „Metabolic syndrome mechanism”

Autor: Grafiati

Data publikacji: 2 czerwca 2025

Data aktualizacji: 31 lipca 2025

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1

C, Hansen Barbara, and Bray George A, eds. The metabolic syndrome: Epidemiology, clinical treatment, and underlying mechanisms. Humana Press, 2008.

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2

Gandhi, Tejal, and Anita Mehta, eds. Biochemical Mechanisms for Metabolic Syndrome. Springer Nature Switzerland, 2024. https://doi.org/10.1007/978-3-031-75686-3.

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Mantzoros, Christos S. Nutrition and metabolism: Underlying mechanisms and clinical consequences. Edited by SpringerLink (Online service). Humana, 2009.

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Lester, Packer, and Sies H. 1942-, eds. Oxidative stress and inflammatory mechanisms in obesity, diabetes, and the metabolic syndrome. CRC Press, 2008.

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Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Elsevier, 1996.

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6

Metabolic syndrome: Underlying mechanisms and drug therapies. John Wiley & Sons, 2011.

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7

Bray, George A., and Barbara C. Hansen. Metabolic Syndrome : : Epidemiology, Clinical Treatment, and Underlying Mechanisms. Humana Press, 2010.

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8

Bray, George A., and Barbara C. Hansen. The Metabolic Syndrome : : Epidemiology, Clinical Treatment, and Underlying Mechanisms. Humana, 2010.

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9

The Metabolic Syndrome:: Epidemiology, Clinical Treatment, and Underlying Mechanisms (Contemporary Endocrinology). Humana Press, 2008.

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10

Mukhopadhyay, Satinath, and Sunetra Mondal. Metabolic Syndrome: From Mechanisms to Interventions. Elsevier Science & Technology, 2022.

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11

Mukhopadhyay, Satinath, and Sunetra Mondal. Metabolic Syndrome: From Mechanisms to Interventions. Elsevier Science & Technology Books, 2022.

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12

Ruskin, David N. Metabolic Therapy and Pain. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0022.

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Chronic pain is associated strongly with poor quality of life. Drug treatments for pain can be problematic; with the understanding that chronic pain syndromes often involve derangement of homeostasis, there is an increased interest in applying nonpharmacological metabolic therapies. This chapter surveys clinical and animal research into the effects of fasting, calorie restriction, ketogenic diet, and polyunsaturated fatty acid supplementation on pain. These dietary treatments can significantly ameliorate pain in inflammatory and neuropathic disorders. The choice among these treatments might de

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13

Wang, Minghan. Metabolic Syndrome: Underlying Mechanisms and Drug Therapies. Wiley & Sons, Incorporated, John, 2011.

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14

Wang, Minghan. Metabolic Syndrome: Underlying Mechanisms and Drug Therapies. Wiley & Sons, Incorporated, John, 2010.

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Wang, Minghan. Metabolic Syndrome: Underlying Mechanisms and Drug Therapies. Wiley & Sons, Incorporated, John, 2011.

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Wang, Minghan. Metabolic Syndrome: Underlying Mechanisms and Drug Therapies. Wiley & Sons, Incorporated, John, 2011.

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17

Mantzoros, Christos S. Nutrition and Metabolism: Underlying Mechanisms and Clinical Consequences. Humana Press, 2016.

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Strasburger, Victor C., and Susan M. Coupey, eds. AM:STARs: Metabolic Challenges to Adolescent Health, Vol. 19, No. 3. American Academy of Pediatrics, 2005. http://dx.doi.org/10.1542/9781581104103.

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This widely respected resource includes "The Adolescent Obesity Epidemic," "Adolescent Obesity: Etiology, Office Evaluation, and Treatment," "Medical Intervention in Adolescent Obesity," "Dietary Approaches to Healthy Weight Management for Adolescents," "Does Adolescent Media Use Cause Obesity and Eating Disorders?" "Bariatric Surgery in Adolescents: Mechanics, Metabolism, and Medical Care," "The Metabolic Syndrome: A Gathering Challenge in a Time of Abundance," "Type 2 Diabetes Mellitus," "Screening Adolescents for Lipid Disorders: What Is the Best Approach?" "Body Image, Eating Disorders, an

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19

Sies, Helmut, ed. Oxidative Stress and Inflammatory Mechanisms in Obesity, Diabetes, and the Metabolic Syndrome. CRC Press, 2007. http://dx.doi.org/10.1201/9781420043792.

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Oxidative stress and inflammatory mechanisms in obesity, diabetes, and the metabolic syndrome. CRC Press, 2008.

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21

Sies, Helmut. Oxidative Stress and Inflammatory Mechanisms in Obesity Diabetes and the Metabolic Syndrome. Taylor & Francis Group, 2019.

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Oxidative Stress and Inflammatory Mechanisms in Obesity, Diabetes, and the Metabolic Syndrome. Taylor and Francis, 2007.

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Oxidative stress and inflammatory mechanisms in obesity, diabetes, and the metabolic syndrome. CRC Press/Taylor & Francis, 2007.

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24

Sies, Helmut. Oxidative Stress and Inflammatory Mechanisms in Obesity, Diabetes, and the Metabolic Syndrome. Taylor & Francis Group, 2007.

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25

Karon, Barry L., and Naveen L. Pereira. Heart Failure and Cardiomyopathies. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0046.

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Heart failure is a clinical syndrome characterized by the inability of the heart to maintain adequate cardiac output to meet the metabolic demands of the body while still maintaining normal or near-normal ventricular filling pressures. Heart failure may be present at rest, but often it is present only during exertion as a result of the dynamic nature of cardiac demands. For correct treatment of heart failure, the mechanism, underlying cause, and any reversible precipitating factors must be identified. Typical manifestations of heart failure are dyspnea and fatigue that limit activity tolerance

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Packer, Lester, and Helmut Sies. Oxidative Stress and Inflammatory Mechanisms in Obesity, Diabetes, and the Metabolic Syndrome. Oxidative Stress and Disease. Taylor & Francis Group, 2010.

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27

(Editor), Lester Packer, and Helmut Sies (Editor), eds. Oxidative Stress and Inflammatory Mechanisms in Obesity, Diabetes, and the Metabolic Syndrome (Oxidative Stress and Disease). CRC, 2007.

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28

Miller, Michelle A. Sleep, inflammation, and disease. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198778240.003.0012.

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Sleep is a fundamental requirement for living individuals. Sleep disturbances and sleep disorders have extensive effects on the immune system, affecting one’s susceptibility to, and ability to fight off, infections—both bacterial and viral—and the subsequent development of different diseases. This is mediated by the increase in pro-inflammatory cytokines associated with sleep loss and disruption. A number of common conditions, such as obesity, cardiovascular disease, metabolic syndrome, obstructive sleep apnoea syndrome, rheumatoid arthritis, and systemic lupus erythematosus, all share pro-inf

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29

Eddouks, Mohamed, Adolfo Andrade-Cetto, Michael Heinrich, Vincenzo De Feo, and William C. Cho, eds. Action Mechanisms of Traditional Medicinal Plants used to Control Type 2 Diabetes or Conditions of Metabolic Syndrome. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88966-469-6.

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Wordsworth, B. P. Skeletal dysplasias. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0150.

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Bone is metabolically active throughout life and metabolic disturbances may have wide-ranging consequences that are not restricted to altering its mechanics. The study of some genetic bone diseases has already provided remarkable insights into the normal regulation of bone metabolism. Skeletal dysplasias are developmental disorders of the chondro-osseous tissues commonly resulting in short stature, which is often disproportionate. The underlying mutations are often in the structural genes encoding components of the matrix but may also involve growth factors or cell signalling. In contrast, the

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31

Hsieh, David T., and Elizabeth A. Thiele. Ketogenic Diet for Other Epilepsies. Edited by Eric H. Kossoff. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0007.

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The ketogenic diet is the treatment of choice for epilepsy in certain disorders of brain metabolism, in particular glucose transporter protein 1 deficiency and pyruvate dehydrogenase deficiency. The International Ketogenic Diet Study Group has listed several other conditions for which the ketogenic diet has been reported as being particularly beneficial and could be offered earlier. Whether efficacy in these conditions is due in part to the broad-spectrum efficacy of the ketogenic diet or to specific mechanisms specific to these conditions is still under investigation. This chapter discusses t

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COVID-19 Severity in Obese Patients : Potential Mechanisms and Molecular Targets for Clinical Intervention: SARS-CoV-2 COVID-19 Obesity Inflammation Coronavirus Metabolic Syndrome. Independently Published, 2021.

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33

Menon, Ashok, and Haris A. Khwaja. Complications of Jejunoileal Bypass. Edited by Tomasz Rogula, Philip Schauer, and Tammy Fouse. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190608347.003.0035.

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Jejunoileal bypass (JIB) was a malabsorptive bariatric procedure developed in the 1950s based on pioneering work in canine models. All described variants involved anastomosis between the proximal jejunum and terminal ileum. Long-term weight loss and improvement in hyperlipidemia were found to be particularly impressive. However, it became clear by the 1980s that morbidity and mortality associated with JIB were unacceptably high. The procedure was abandoned, and many patients underwent reversal to normal intestinal continuity, or revision to other bariatric procedures. Two main mechanisms under

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34

Hodgkiss, Andrew. Psychiatric consequences of particular cancers. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0004.

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Certain tumour types can cause psychopathology through direct biological mechanisms such as metastatic spread to the brain, release of onconeuronal antibodies, ectopic hormone secretion, or release of pro-inflammatory cytokines. Lung cancers, adenocarcinoma of the pancreas, brain tumours, and ovarian tumours are considered in detail. Confusional states due to brain metastases, syndrome of inappropriate ADH secretion, hypercalcaemia of malignancy, and anti-Hu encephalitis are found in lung cancers. Severe depression, due to interleukin-6 release and its actions on the HPA axis and tryptophan me

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35

Gaitanis, John, Phillip L. Pearl, and Howard Goodkin. The EEG in Degenerative Disorders of the Central Nervous System. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0013.

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Nervous system alterations can occur at any stage of prenatal or postnatal development. Any of these derangements, whether environmental or genetic, will affect electrical transmission, causing electroencephalogram (EEG) alteration and possibly epilepsy. Genetic insults may be multisystemic (for example, neurocutaneous syndromes) or affect only the brain. Gene mutations account for inborn errors of metabolism, channelopathies, brain malformations, and impaired synaptogenesis. Inborn errors of metabolism cause seizures and EEG abnormalities through a variety of mechanisms, including disrupted e

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36

Sever, Mehmet Şükrü, and Raymond Vanholder. Acute kidney injury in polytrauma and rhabdomyolysis. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0252_update_001.

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The term ‘polytrauma’ refers to blunt (or crush) trauma that involves multiple body regions or cavities, and compromises physiology to potentially cause dysfunction of uninjured organs. Polytrauma frequently affects muscles resulting in rhabdomyolysis. In daily life, it mostly occurs after motor vehicle accidents, influencing a limited number of patients; after mass disasters, however, thousands of polytrauma victims may present at once with only surgical features or with additional medical complications (crush syndrome). Among the medical complications, acute kidney injury (AKI) deserves spec

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37

Bentham, James R. The genetics of congenital heart disease. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, et al. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0022.

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Congenital heart disease (CHD) is defined as a structural cardiac malformation resulting from an abnormality of development; 8% of CHD is inherited in a Mendelian fashion and 12% results from chromosomal imbalance. Recurrence risk and new research suggest that even the remaining 80% of patients without an identifiable familial or syndromic basis for disease may have an identifiable genetic cause. The potential to understand these mechanisms is increasing with the advent of new sequencing techniques which have identified multiple or single rare variants and/or copy number variants clustering in

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(Editor), Sayed Ali, Francesco Fornai (Editor), and Yossef Itzhak (Editor), eds. Cellular and Molecular Mechanisms of Drugs of Abuse and Neurotoxicity: Cocaine, GHB, and Substituted Amphetamines (Annals of the New York Academy of Sciences). Blackwell Publishing Limited, 2006.

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Coates, Laura C., and Philip S. Helliwell. Psoriatic arthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0114.

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Psoriasis is a chronic skin condition affecting about 3% of Europeans and North Americans. About 15% of people afflicted with psoriasis will develop psoriatic arthritis—cutaneous risk factors for this are psoriasis of the nails, scalp, and flexures. Since most cases of arthritis develop in people with psoriasis, new screening tools, both clinical and imaging, are available. Some genetic factors may also explain susceptibility and severity. Historically, five clinical subgroups have been described but these may be simplified to axial and peripheral involvement, the latter dividing into oligo- a

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Coates, Laura C., and Philip S. Helliwell. Psoriatic arthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0114_update_003.

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Psoriasis is a chronic skin condition affecting about 3% of Europeans and North Americans. About 15% of people afflicted with psoriasis will develop psoriatic arthritis—cutaneous risk factors for this are psoriasis of the nails, scalp, and flexures. Since most cases of arthritis develop in people with psoriasis, new screening tools, both clinical and imaging, are available. Some genetic factors may also explain susceptibility and severity. Historically, five clinical subgroups have been described but these may be simplified to axial and peripheral involvement, the latter dividing into oligo- a

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41

Ellinson, Michelle, and Tommy Rampling. Normal nutritional function. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0331.

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Normal nutritional function requires a healthy diet. Healthy eating incorporates a variety of nutrients that are essential for energy expenditure, prevention of disease, and maintenance of normal physiological function. An unhealthy diet can result in malnutrition, and this contributes to illness and death throughout the world. The core principle of healthy eating is obtaining an adequate balance, and the diseases resulting from overnourishment differ greatly from those resulting from undernourishment. In the third world, diets tend to rely heavily on staple crops, and can be very seasonal. En

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(Editor), T. Kumazawa, L. Kruger (Editor), and K. Mizumura (Editor), eds. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.

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