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Artykuły w czasopismach na temat „Metabolic syndrome mechanism”

Autor: Grafiati

Data publikacji: 2 czerwca 2025

Data aktualizacji: 31 lipca 2025

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1

Ogawa, Yoshihiro. "2. Molecular Mechanism of Metabolic Syndrome." Nihon Naika Gakkai Zasshi 105, Suppl (2016): 101b—102a. http://dx.doi.org/10.2169/naika.105.101b.

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Ogawa, Yoshihiro. "2. Molecular Mechanism of Metabolic Syndrome." Nihon Naika Gakkai Zasshi 105, no. 9 (2016): 1632–36. http://dx.doi.org/10.2169/naika.105.1632.

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McNamara, Anthony. "Metabolic syndrome." InnovAiT: Education and inspiration for general practice 12, no. 10 (2019): 582–88. http://dx.doi.org/10.1177/1755738019864615.

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Metabolic syndrome is the name given to a combination of cardiovascular risk factors. These include hyperinsulinaemia, impaired glucose tolerance, hypertension, central obesity and dyslipidaemia. People with metabolic syndrome have a high risk of developing type 2 diabetes, non-alcoholic fatty liver disease, and vascular conditions including coronary artery disease, peripheral vascular disease, and stroke. Central obesity can predispose to sleep apnoea and restrictive lung disease. For many years, it has been taught that the underlying mechanism of metabolic syndrome is insulin resistance seco

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Khairutdinov, V. R., and A. V. Samtsov. "Features of treatment of patients with psoriasis with metabolic syndrome." Vestnik dermatologii i venerologii 94, no. 4 (2018): 68–72. http://dx.doi.org/10.25208/0042-4609-2018-94-4-68-72.

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The article provides information on the prevalence of metabolic syndrome in patients with psoriasis. The criteria for the diagnosis of metabolic syndrome are presented. The General mechanisms of inflam - mation development in psoriasis and diseases forming the metabolic syndrome are described. Systemic subclinical inflammatory process developing in psoriasis and metabolic syndrome is considered as the main pathogenetic mechanism of their mutual negative influence. The difficulties of treatment of patients with psoriasis with metabolic syndrome are largely associated with the choice of a safe a

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Shimabukuro, Michio. "Clinical Diagnosis of Metabolic Syndrome 2. Lipotoxicity as a Mechanism of the Metabolic Syndrome." Internal Medicine 46, no. 16 (2007): 1285. http://dx.doi.org/10.2169/internalmedicine.46.1904.

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Hashim, Khairun-Nisa, Kok-Yong Chin, and Fairus Ahmad. "The Mechanism of Honey in Reversing Metabolic Syndrome." Molecules 26, no. 4 (2021): 808. http://dx.doi.org/10.3390/molecules26040808.

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Metabolic syndrome is a constellation of five risk factors comprising central obesity, hyperglycaemia, dyslipidaemia, and hypertension, which predispose a person to cardiometabolic diseases. Many studies reported the beneficial effects of honey in reversing metabolic syndrome through its antiobesity, hypoglycaemic, hypolipidaemic, and hypotensive actions. This review aims to provide an overview of the mechanism of honey in reversing metabolic syndrome. The therapeutic effects of honey largely depend on the antioxidant and anti-inflammatory properties of its polyphenol and flavonoid contents. P

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Ferraioli, Anthony, Kara Lee Shirley, and Panakkal David. "The Role of Atypical Antipsychotics in Glucose/Insulin Dysregulation and the Evolving Role of the Psychiatrist in a New Era of Drug Treatment Options." CNS Spectrums 9, no. 11 (2004): 849–61. http://dx.doi.org/10.1017/s1092852900002261.

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ABSTRACTThis article examines the issue of atypical antipsychotics, glucose/insulin, and other metabolic derangements (ie, metabolic syndrome), including a general introduction to the health, concerns of our patients, a review of the literature, possible mechanisms of antipsychotic induced glucose dysregulation, monitoring approaches, and management and prevention of metabolic syndrome. Literature review leads to mechanism hypotheses and risk estimations, leading to guidelines for monitoring and treatment. The patient population suffers from a higher degree of baseline metabolic dysregulation

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Canale, Maria Paola, Simone Manca di Villahermosa, Giuliana Martino, et al. "Obesity-Related Metabolic Syndrome: Mechanisms of Sympathetic Overactivity." International Journal of Endocrinology 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/865965.

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The prevalence of the metabolic syndrome has increased worldwide over the past few years. Sympathetic nervous system overactivity is a key mechanism leading to hypertension in patients with the metabolic syndrome. Sympathetic activation can be triggered by reflex mechanisms as arterial baroreceptor impairment, by metabolic factors as insulin resistance, and by dysregulated adipokine production and secretion from visceral fat with a mainly permissive role of leptin and antagonist role of adiponectin. Chronic sympathetic nervous system overactivity contributes to a further decline of insulin sen

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Sharonova, L. A., S. V. Bulgakova, S. A. Burakshaev, et al. "Relationship between the main components of metabolic syndrome and oral diseases." Experimental and Clinical Gastroenterology, no. 8 (February 3, 2025): 131–42. https://doi.org/10.31146/1682-8658-ecg-228-8-131-142.

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The main components of the metabolic syndrome - obesity, insulin resistance and carbohydrate metabolism disorders, dyslipidemia, arterial hypertension - are comorbid, having a single pathogenetic mechanism for the formation of conditions. The prevalence of oral diseases exceeds the combined incidence of the five major non-communicable diseases. The article presents data on the relationship between oral diseases and the main components of metabolic syndrome. The relationship between adipose tissue dysfunction, chronic inflammation, oxidative stress, insulin resistance, atherogenesis, and the ro

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Mansilla, Eduardo, Vanina Díaz Aquino, Daniel Zambón, et al. "Could Metabolic Syndrome, Lipodystrophy, and Aging Be Mesenchymal Stem Cell Exhaustion Syndromes?" Stem Cells International 2011 (2011): 1–10. http://dx.doi.org/10.4061/2011/943216.

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One of the most important and complex diseases of modern society is metabolic syndrome. This syndrome has not been completely understood, and therefore an effective treatment is not available yet. We propose a possible stem cell mechanism involved in the development of metabolic syndrome. This way of thinking lets us consider also other significant pathologies that could have similar etiopathogenic pathways, like lipodystrophic syndromes, progeria, and aging. All these clinical situations could be the consequence of a progressive and persistent stem cell exhaustion syndrome (SCES). The main ou

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Kurniawati, Erna Yovi, Noor Pramono, Syarief Thaufik Hidayat, and Endang Mahati. "Polycystic Ovary Syndrome Markers and Mechanism." Syifa' MEDIKA: Jurnal Kedokteran dan Kesehatan 15, no. 1 (2024): 37. http://dx.doi.org/10.32502/sm.v15i1.7829.

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Polycystic ovary syndrome (PCOS) is a complex endocrine disorder characterized by hormonal imbalances, metabolic dysregulation, and reproductive abnormalities. This study aims to elucidate the significance of PCOS markers and their mechanisms while outlining the methodology employed. A comprehensive literature review was conducted from 2020 to 2023 using databases like PubMed, ScienceDirect, EMBASE, and Google Scholar. Key search terms included "pathophysiology," "pathogenesis," "PCOS," "marker," and "biomarker," aligned with the PICOT criteria. After removing duplicates, articles underwent a

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Pan, Chaolan, Anqi Zhao, and Ming Li. "A Topic Dermatitis-like Genodermatosis: Disease Diagnosis and Management." Diagnostics 12, no. 9 (2022): 2177. http://dx.doi.org/10.3390/diagnostics12092177.

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Eczema is a classical characteristic not only in atopic dermatitis but also in various genodermatosis. Patients suffering from primary immunodeficiency diseases such as hyper-immunoglobulin E syndromes, Wiskott-Aldrich syndrome, immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome, STAT5B deficiency, Omenn syndrome, atypical complete DiGeorge syndrome; metabolic disorders such as acrodermatitis enteropathy, multiple carboxylase deficiency, prolidase deficiency; and other rare syndromes like severe dermatitis, multiple allergies and metabolic wasting syndrome, Netherton synd

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Goh, Kah Kheng, Cynthia Yi-An Chen, Tzu-Hua Wu, Chun-Hsin Chen, and Mong-Liang Lu. "Crosstalk between Schizophrenia and Metabolic Syndrome: The Role of Oxytocinergic Dysfunction." International Journal of Molecular Sciences 23, no. 13 (2022): 7092. http://dx.doi.org/10.3390/ijms23137092.

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The high prevalence of metabolic syndrome in persons with schizophrenia has spurred investigational efforts to study the mechanism beneath its pathophysiology. Early psychosis dysfunction is present across multiple organ systems. On this account, schizophrenia may be a multisystem disorder in which one organ system is predominantly affected and where other organ systems are also concurrently involved. Growing evidence of the overlapping neurobiological profiles of metabolic risk factors and psychiatric symptoms, such as an association with cognitive dysfunction, altered autonomic nervous syste

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Tashtemirova, Irodakhon Makhkambaevna. "State Of Purine Exchange And Microalbuminuria In Patients With Metabolic Syndrome." American Journal of Medical Sciences and Pharmaceutical Research 03, no. 01 (2021): 46–54. http://dx.doi.org/10.37547/tajmspr/volume03issue01-08.

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The aim of the given work was study interactions of impairments sympa-thetic – adrenal systems functional condition and processes of peroxidal oxida-tion of lipids in woman with metabolic syndrome. 107women at the age of 25-49 were observation. They were randomized into 3 groups: I (control) – 15 healthy persons, II – 43 patients with arterial hypertension, III – 49 women with arterial hypertension in combination with metabolic syndrome. The results of carried investigations showed that activation of sympathetic adrenal system and processes of peroxidal oxidation of lipids took place in metabo

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Song, Ming, Miriam Vos, and Craig McClain. "Copper-Fructose Interactions: A Novel Mechanism in the Pathogenesis of NAFLD." Nutrients 10, no. 11 (2018): 1815. http://dx.doi.org/10.3390/nu10111815.

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Compelling epidemiologic data support the critical role of dietary fructose in the epidemic of obesity, metabolic syndrome and nonalcoholic fatty liver disease (NAFLD). The metabolic effects of fructose on the development of metabolic syndrome and NAFLD are not completely understood. High fructose intake impairs copper status, and copper-fructose interactions have been well documented in rats. Altered copper-fructose metabolism leads to exacerbated experimental metabolic syndrome and NAFLD. A growing body of evidence has demonstrated that copper levels are low in NAFLD patients. Moreover, hepa

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Chang, Huan-Cheng, Tien-Mu Hsiao, Mei-Huei Lien, Chih-Jung Yeh, and Hao-Jan Yang. "Metabolic syndrome and depression are not correlated: results from a community sample exploring the unique and common correlates for the two diseases." Neuropsychiatry (London) 7, no. 2 (2017): 7. https://doi.org/10.5281/zenodo.14676997.

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Aim: More and more studies are suggesting evidence for the comorbidity of cardiovascular disease and depressive disorders, yet the mechanism is obscure. Our study aimed to identify correlates common and unique to metabolic syndrome and depression, in order to clarify the relationship between the two diseases in terms of their taxonomy and potential overlapping mechanisms. Methods: Data from a large-scale community sample of 30-year-old or older residents of a Taiwanese city (N=11,258) were analyzed to compare sociodemographic and lifestyle factors between four groups: metabolic syndrome only,

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Lotti, Francesco, Sara Marchiani, Giovanni Corona, and Mario Maggi. "Metabolic Syndrome and Reproduction." International Journal of Molecular Sciences 22, no. 4 (2021): 1988. http://dx.doi.org/10.3390/ijms22041988.

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Metabolic syndrome (MetS) and infertility are two afflictions with a high prevalence in the general population. MetS is a global health problem increasing worldwide, while infertility affects up to 12% of men. Despite the high prevalence of these conditions, the possible impact of MetS on male fertility has been investigated by a few authors only in the last decade. In addition, underlying mechanism(s) connecting the two conditions have been investigated in few preclinical studies. The aim of this review is to summarize and critically discuss available clinical and preclinical studies on the r

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Nishikawa, Hiroki, Akira Asai, Shinya Fukunishi, Shuhei Nishiguchi, and Kazuhide Higuchi. "Metabolic Syndrome and Sarcopenia." Nutrients 13, no. 10 (2021): 3519. http://dx.doi.org/10.3390/nu13103519.

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Skeletal muscle is a major organ of insulin-induced glucose metabolism. In addition, loss of muscle mass is closely linked to insulin resistance (IR) and metabolic syndrome (Met-S). Skeletal muscle loss and accumulation of intramuscular fat are associated with a variety of pathologies through a combination of factors, including oxidative stress, inflammatory cytokines, mitochondrial dysfunction, IR, and inactivity. Sarcopenia, defined by a loss of muscle mass and a decline in muscle quality and muscle function, is common in the elderly and is also often seen in patients with acute or chronic m

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Zhou, Jingyu, Xiao Guo, Xiaoli Liu, et al. "Intrinsic Therapeutic Link between Recuperative Cerebellar Con-Nectivity and Psychiatry Symptom in Schizophrenia Patients with Comorbidity of Metabolic Syndrome." Life 13, no. 1 (2023): 144. http://dx.doi.org/10.3390/life13010144.

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Components of metabolic syndrome might be predictors of the therapeutic outcome of psychiatric symptom in schizophrenia, whereas clinical results are inconsistent and an intrinsic therapeutic link between weaker psychiatric symptoms and emergent metabolic syndrome remains unclear. This study aims to reveal the relationship and illustrate potential mechanism by exploring the alteration of cerebellar functional connectivity (FC) in schizophrenia patients with comorbidity metabolic syndrome. Thirty-six schizophrenia patients with comorbidity of metabolic syndrome (SCZ-MetS), 45 schizophrenia pati

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Matsuzawa, Yuji, Tohru Funahashi, and Tadashi Nakamura. "Molecular mechanism of vascular disease in metabolic syndrome X." Journal of Diabetes and its Complications 16, no. 1 (2002): 17–18. http://dx.doi.org/10.1016/s1056-8727(01)00194-5.

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Mironov, Nikolay, Mainul Haque, Azeddine Atfi, and Mohammed S. Razzaque. "Phosphate Dysregulation and Metabolic Syndrome." Nutrients 14, no. 21 (2022): 4477. http://dx.doi.org/10.3390/nu14214477.

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Phosphorus is one of the most abundant minerals in the human body. It is essential for almost all biochemical activities through ATP formation, intracellular signal transduction, cell membrane formation, bone mineralization, DNA and RNA synthesis, and inflammation modulation through various inflammatory cytokines. Phosphorus levels must be optimally regulated, as any deviations may lead to substantial derangements in glucose homeostasis. Clinical studies have reported that hyperphosphatemia can increase an individual’s risk of developing metabolic syndrome. High phosphate burden has been shown

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Yamada, Eijiro, Ryota Uehara, Yasuyo Nakajima, et al. "Identifying a New Mechanism of Sarcopenia by Autophagy." Journal of the Endocrine Society 5, Supplement_1 (2021): A50. http://dx.doi.org/10.1210/jendso/bvab048.099.

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Abstract Sarcopenia is one of the critical factors in reducing Activity of Daily Life and associated with morbidity and mortality. Sarcopenia has also been linked to metabolic syndrome. In recent years, it has been reported that autophagy is one of the mechanisms as a cause of sarcopenia. Therefore, we focused on autophagy as a system that can regulate both sarcopenia and metabolic syndrome in skeletal muscle and revealed that non-receptor tyrosine kinase Fyn not only participates in metabolic syndrome but also regulates autophagy regulating sarcopenia through STAT3 regulation, mainly using tr

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Mumusoglu, Sezcan, and Bulent Okan Yildiz. "Metabolic Syndrome During Menopause." Current Vascular Pharmacology 17, no. 6 (2019): 595–603. http://dx.doi.org/10.2174/1570161116666180904094149.

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The metabolic syndrome (MetS) comprises individual components including central obesity, insulin resistance, dyslipidaemia and hypertension and it is associated with an increased risk of cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM). The menopause per se increases the incidence of MetS in aging women. The effect(s) of menopause on individual components of MetS include: i) increasing central obesity with changes in the fat tissue distribution, ii) potential increase in insulin resistance, iii) changes in serum lipid concentrations, which seem to be associated with increasing

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Bowles, Nicole P., Ilia N. Karatsoreos, Xiaosong Li, et al. "A peripheral endocannabinoid mechanism contributes to glucocorticoid-mediated metabolic syndrome." Proceedings of the National Academy of Sciences 112, no. 1 (2014): 285–90. http://dx.doi.org/10.1073/pnas.1421420112.

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Glucocorticoids are known to promote the development of metabolic syndrome through the modulation of both feeding pathways and metabolic processes; however, the precise mechanisms of these effects are not well-understood. Recent evidence shows that glucocorticoids possess the ability to increase endocannabinoid signaling, which is known to regulate appetite, energy balance, and metabolic processes through both central and peripheral pathways. The aim of this study was to determine the role of endocannabinoid signaling in glucocorticoid-mediated obesity and metabolic syndrome. Using a mouse mod

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Singh, Himadri, Samuel Joshua Pragasam, and Vijayalakshmi Venkatesan. "Emerging Therapeutic Targets for Metabolic Syndrome: Lessons from Animal Models." Endocrine, Metabolic & Immune Disorders - Drug Targets 19, no. 4 (2019): 481–89. http://dx.doi.org/10.2174/1871530319666181130142642.

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Background: Metabolic syndrome is a cluster of medical conditions that synergistically increase the risk of heart diseases and diabetes. The current treatment strategy for metabolic syndrome focuses on treating its individual components. A highly effective agent for metabolic syndrome has yet to be developed. To develop a target for metabolic syndrome, the mechanism encompassing different organs - nervous system, pancreas, skeletal muscle, liver and adipose tissue - needs to be understood. Many animal models have been developed to understand the pathophysiology of metabolic syndrome. Promising

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Nolan, Christopher J., and Marc Prentki. "Insulin resistance and insulin hypersecretion in the metabolic syndrome and type 2 diabetes: Time for a conceptual framework shift." Diabetes and Vascular Disease Research 16, no. 2 (2019): 118–27. http://dx.doi.org/10.1177/1479164119827611.

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While few dispute the existence of the metabolic syndrome as a clustering of factors indicative of poor metabolic health, its utility above that of its individual components in the clinical care of individual patients is questioned. This is likely a consequence of the failure of clinicians and scientists to agree on a unifying mechanism to explain the metabolic syndrome. Insulin resistance has most commonly been proposed for this role and is generally considered to be a root causative factor for not only metabolic syndrome but also for its associated conditions of non-alcoholic fatty liver dis

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Dustova, Gulzoda Komiljonovna, and Umida Rustamovna Malikova. "MORPHOLOGY OF THE SMALL INTESTINAL WALL ADRENERGIC NERVOUS SYSTEM IN A MODEL OF METABOLIC SYNDROME." Multidisciplinary Journal of Science and Technology 5, no. 5 (2025): 837–40. https://doi.org/10.5281/zenodo.15465077.

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This article describes the morphological changes in the adrenergic nervous system of the small intestine wall of experimental animals that have created a metabolic syndrome model. At the same time, the involvement of the nervous system in the development of metabolic syndrome is also demonstrated.

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Lazarev, V. V., S. A. Daryin, G. P. Brusov, L. E. Tsypin, and T. G. Popova. "PROPOFOL-INDUCED METABOLIC DISTRESS SYNDROME." Russian Journal of Pediatric Surgery, Anesthesia and Intensive Care 8, no. 2 (2018): 65–69. http://dx.doi.org/10.30946/2219-4061-2018-8-2-65-69.

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Introduction. The obtained experience of using propofol under clinical conditions and in experimental studies discover the mechanism of a negative drug effect at the level of mitochondrial enzymes which is currently treated as the propofol infusion syndrome.Purpose. To demonstrate the cases of creatine phosphokinase level variation during the intraoperative pediatric use of propofol in anesthesia.Materials and methods. Three cases of intraoperative use of propofol in 2–17‑years-old patients with different dosages and dose schedules.Results. The level of creatine phosphokinase was increased 9–4

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Wells, Greg D., Michael D. Noseworthy, Jill Hamilton, Mark Tarnopolski, and Ingrid Tein. "Skeletal Muscle Metabolic Dysfunction in Obesity and Metabolic Syndrome." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 35, no. 1 (2008): 31–40. http://dx.doi.org/10.1017/s0317167100007538.

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ABSTRACT:Obesity and the related metabolic syndrome have become a worldwide epidemic. Inactivity appears to be a primary causative factor in the pathogenesis of this obesity and metabolic syndrome. There are two possible, perhaps not mutually exclusive, events that may lead to intramyocellular lipid accumulation and mitochondrial dysfunction in patients with obesity. First, obesity, with high intake-associated lipid accumulation in muscle may interfere with cellular mitochondrial function through generation of reactive oxygen species leading to lipid membrane peroxidative injury and disruption

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Rahmariani, Fitri. "The Relationship Between Metabolic Syndrome and Depression: A Literature Review." Scientia Psychiatrica 3, no. 3 (2022): 293–97. http://dx.doi.org/10.37275/scipsy.v3i3.109.

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Depressive disorders are a group of disorders with characteristics of loss of happiness, feeling useless or desperate, withdrawn or uninterested in common activity, and loss of energy or hypoactivity almost every day. Metabolic syndrome (MetS) is a clustering of conditions consist of central obesity, dyslipidemia, glucose intolerance, and hypertension. Both diseases are considered important risk factors of morbidity and cause of quality of life impairment. Some mechanisms are submitted to explain the correlated mechanism between MetS and depression.

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Kytikova, Oxana Y., Marina V. Antonyuk, Tatyana A. Gvozdenko, and Tatyana Р. Novgorodtseva. "Metabolic aspects of the relationship of asthma and obesity." Obesity and metabolism 15, no. 4 (2019): 9–14. http://dx.doi.org/10.14341/omet9578.

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Asthma and obesity are serious medical and social world problems, and their combined course is characterized by a decrease in the quality of life, an increase in the frequency and duration of hospitalization. The present review summarizes the current views on the mechanisms of formation of asthma phenotype combined with obesity, role of leptin and adiponectin imbalance in the development of systemic inflammation in obesity in the pathophysiology of asthma, its interrelations with metabolic syndrome. We present data that shows that syndrome is closely related not only to the debut of asthma, bu

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Kitov, S., and L. Kitova. "Electrocardiographic markers of proarrhythmogenicity in metabolic syndrome." Bulgarian Cardiology 31, no. 1 (2025): 22–30. https://doi.org/10.3897/bgcardio.31.e146569.

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The etiopathogenetic mechanisms of metabolic syndrome that affect cardiac electrophysiology and lead to myocardial remodelling are numerous. Cardiomyocyte changes induced by metabolic and proinflammatory factors impair repolarization, exacerbate the heterogeneity of the transmural dispersion of repolarization, and prolong the Tpeak-end interval. Tpeak-Tend interval has been described as a marker of arrhythmogenicity that is more sensitive than the standard QT interval. Multiple pathological conditions and their effect on myocardial repolarisation have been studied &ndash; coronary artery d

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Kitov, S., and L. Kitova. "Electrocardiographic markers of proarrhythmogenicity in metabolic syndrome." Bulgarian Cardiology 31, no. (1) (2025): 22–30. https://doi.org/10.3897/bgcardio.31.e146569.

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The etiopathogenetic mechanisms of metabolic syndrome that affect cardiac electrophysiology and lead to myocardial remodelling are numerous. Cardiomyocyte changes induced by metabolic and proinflammatory factors impair repolarization, exacerbate the heterogeneity of the transmural dispersion of repolarization, and prolong the Tpeak-end interval. Tpeak-Tend interval has been described as a marker of arrhythmogenicity that is more sensitive than the standard QT interval. Multiple pathological conditions and their effect on myocardial repolarisation have been studied – coronary artery disease, sl

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Diemieszczyk, Inna, Paulina Głuszyńska, Pawel Andrzej Wojciak, Jerzy Robert Ładny, and Hady Razak Hady. "METABOLIC SYNDROME. ETIOLOGY AND PATHOGENESIS." Wiadomości Lekarskie 74, no. 10 (2021): 2510–15. http://dx.doi.org/10.36740/wlek202110126.

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The aim of the study was to assess the impact of individual components of the metabolic syndrome on the human body, taking into account their etiology and pathogenesis. This article is analytical analysis of scientific and medical literature basing on aspects of the etiology and pathogenesis of the metabolic syndrome. The key role in the pathogenesis of the metabolic syndrome is played by insulin resistance, which may be a result of lifestyle conditions (low physical activity, overweight or obesity) or genetic background. A certain role in the pathogenesis of the metabolic syndrome is also att

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Shackelford, Rodney E., Maisoun Q. Abdelbaqi, Amal Anga, and James Cotelignam. "Nijmegen breakage syndrome 1 protein hyperacetylation as a molecular mechanism underlying metabolic syndrome." Bioscience Hypotheses 1, no. 6 (2008): 295–300. http://dx.doi.org/10.1016/j.bihy.2008.06.013.

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Stoian, Marilena, Victor Stoica, and Gabriela Radulian. "The Role of Distubances of Phosphate Metabolism in Metabolic Syndrome." Romanian Journal of Diabetes Nutrition and Metabolic Diseases 20, no. 3 (2013): 307–13. http://dx.doi.org/10.2478/rjdnmd-2013-0029.

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Abstract Background and Aims: Metabolic syndrome represents a cluster of cardiovascular risk factors and reached epidemic proportions. It was hypothesized that disturbances in phosphate metabolism may represent a feature of the metabolic syndrome. The aim of the study was to investigate the relationship between phosphate levels and the presence of metabolic syndrome components, as well as the putative mechanism for reduced phosphate level in metabolic syndrome. Materials and Methods: We enrolled 155 subjects: 64 with metabolic syndrome and 91 controls. Biochemical parameters of the metabolic s

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Purohith, Raghunandan, Nagendra P. M. Nagalingaswamy, and Nanjunda S. Shivananju. "Dietary Carotenoids in Managing Metabolic Syndrome and Role of PPARs in the Process." Current Nutrition & Food Science 16, no. 6 (2020): 846–53. http://dx.doi.org/10.2174/1573401315666190619111557.

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Metabolic syndrome is a collective term that denotes disorder in metabolism, symptoms of which include hyperglycemia, hyperlipidemia, hypertension, and endothelial dysfunction. Diet is a major predisposing factor in the development of metabolic syndrome, and dietary intervention is necessary for both prevention and management. The bioactive constituents of food play a key role in this process. Micronutrients such as vitamins, carotenoids, amino acids, flavonoids, minerals, and aromatic pigment molecules found in fruits, vegetables, spices, and condiments are known to have beneficial effects in

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M., Elyasov, and Soltanova O. "METABOLIC SYNDROME AND ITS RISK FACTORS." International Journal of Multidisciplinary Research Transactions 5, no. 4 (2023): 124–25. https://doi.org/10.5281/zenodo.7782885.

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There are several definitions which are suggested to explain how metabolic syndrome is appeared. According to modern scientific information G. Reaven was one of the first who tried to explain the term of "syndrome X" or "metabolic syndrome" in 1988. He found out such symptoms as hyperinsulinemia, tissue-induced insulin resistance (IR), impaired glucose tolerance, high density of lipoprotein, hypertriglyceridemia that lowers cholesterol (HDL cholesterol) and arterial hypertension (AG) were cоmposition of metabolic syndrome. However, considering the metabolic syndrome it star

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Arshad, Nurul ‘Ain, Teoh Seong Lin, and Mohamad Fairuz Yahaya. "Metabolic Syndrome and Its Effect on the Brain: Possible Mechanism." CNS & Neurological Disorders - Drug Targets 17, no. 8 (2018): 595–603. http://dx.doi.org/10.2174/1871527317666180724143258.

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Background & Objective: Metabolic syndrome (MetS) is an interconnected group of physiological, biochemical, clinical and metabolic factors that directly increase the risk of cardiovascular disease, type 2 diabetes mellitus (T2DM) and mortality. Rising evidence suggests that MetS plays a significant role in the progression of Alzheimer’s disease and other neurodegenerative diseases. Nonetheless, the factors linking this association has not yet been elucidated. As we are facing an increasing incidence of obesity and T2DM in all stages of life, understanding the association of MetS and neurod

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Kseneva, Svetlana Igorevna, Elena Valentinovna Borodulina, Vladimir Vasilievich Udut, and Vladimir Petrovich Fisenko. "Mechanism Underlying the Formation of a Cluster of Metabolic Syndrome." Endocrine, Metabolic & Immune Disorders - Drug Targets 20, no. 4 (2020): 564–69. http://dx.doi.org/10.2174/1871530319666191007115214.

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Background: The concept of metabolic syndrome (MetS) as a cluster of risk factors of type 2 diabetes and cardiovascular diseases has undergone some evolutionary transformations over the past years. Integrating the autonomic dysfunction into the pathogenesis of MetS creates the possibility of including a range of nosologies affecting treatment and clinical manifestations of pathologies belonging to MetS into the MetS cluster. The purpose of this work is to determine the involvement of autonomic dysfunction in the pathogenesis of associated pathological conditions in patients and MetS. Methods:

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Li, Zexin, Lili Zhang, Yingshi Huang, Peixuan Yang, and Wencan Xu. "A Mechanism Exploration of Metabolic Syndrome Causing Nodular Thyroid Disease." International Journal of Endocrinology 2019 (November 26, 2019): 1–7. http://dx.doi.org/10.1155/2019/9376768.

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Background. Metabolic syndrome (MS) and its components have been demonstrated to facilitate the prevalence of thyroid nodules (TNs). The underlying pathogenesis needs to be elucidated. Methods. A total of 2722 subjects, who underwent health checkup in our institute from December 2014 to November 2018, were retrospectively and randomly collected. After exclusion, 2068 subjects were chosen, and their anthropic and clinical data were collected. Results. After matching age, gender, uric acid (UA), and creatinine (Cr) by propensity score matching (PSM), subjects with MS had higher prevalence of TNs

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Dang, Thao Thi Phuong, Linh My Dao, Anh Man Huynh, and Dan Thi Hanh Vo. "Transgenic Drosophila melanogaster model of metabolic disorders." Science and Technology Development Journal - Natural Sciences 4, no. 4 (2020): 811–17. http://dx.doi.org/10.32508/stdjns.v4i4.929.

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Metabolic syndrome is a collection of disorders related to metabolisms such as obesity, lipid disorders, hyper/hypoglycemia, ... Metabolic syndrome can lead to cardiovascular diseases, strokes, and diabetes - the leading death causes in the world. In many cases, metabolic disorders are original by the redundant/ reduction of insulin- the most important hormone in metabolism regulation. Both of them are involved in beta-cells dysfunction. Many mechanisms related to this phenomenon has been approved, notably mitochondrial dysfunction and the Ubiquitin proteasome system impairment. UCH-L1 is a pr

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Yuenyong, Ittipon, Prapassorn Potue, Putcharawipa Maneesai, et al. "Tangeretin Unravels Metabolic Dysfunction-Associated Fatty Liver Disease in Rats by Enhancing the IRS/Akt Pathway." Life 15, no. 3 (2025): 491. https://doi.org/10.3390/life15030491.

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Excessive high-fat diet (HFD) intake can precipitate metabolic dysfunction-associated fatty liver disease (MAFLD). Tangeretin is a citrus flavonoid possessing many biological properties. We examined the impact of tangeretin on MAFLD and its underlying mechanism. Rats were given HFD plus 15% fructose solution for four months to produce metabolic syndrome. Metabolic syndrome rats were administered 100 mg/kg of metformin or 25 mg/kg of tangeretin for the last four weeks. HFD-induced increased body weight, liver weight, adipose tissue weight, fasting blood glucose, serum insulin, total triglycerid

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Kumar, Shashank, Sabyasachi Senapati, Neetu Bhattacharya, et al. "Mechanism and recent updates on insulin-related disorders." World Journal of Clinical Cases 11, no. 25 (2023): 5840–56. http://dx.doi.org/10.12998/wjcc.v11.i25.5840.

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Insulin, a small protein with 51 amino acids synthesized by pancreatic β-cells, is crucial to sustain glucose homeostasis at biochemical and molecular levels. Numerous metabolic dysfunctions are related to insulin-mediated altered glucose homeostasis. One of the significant pathophysiological conditions linked to the insulin associated disorder is diabetes mellitus (DM) (type 1, type 2, and gestational). Insulin resistance (IR) is one of the major underlying causes of metabolic disorders despite its association with several physiological conditions. Metabolic syndrome (MS) is another pathophys

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Boiko, Anastasiia S., Irina A. Mednova, Elena G. Kornetova, et al. "Metabolic Hormones in Schizophrenia Patients with Antipsychotic-Induced Metabolic Syndrome." Journal of Personalized Medicine 12, no. 10 (2022): 1655. http://dx.doi.org/10.3390/jpm12101655.

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Metabolic syndrome (MetS) is a common complication of schizophrenia that is quite exacerbated by long-term use of (atypical) antipsychotics. The mechanism of MetS has neuronal, neuroendocrine, and neuroimmunological components and shows some overlap with those of aspects of schizophrenia. We examined 195 patients with schizophrenia (90 with and 105 without MetS) for the association of serum levels of ghrelin, insulin, and leptin with metabolic abnormalities. Serum glucose levels and lipid profiles were routinely measured with colorimetric enzymatic methods and hormone levels with multiplex ana

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Kao, Ting-Wei, and Chin-Chou Huang. "Recent Progress in Metabolic Syndrome Research and Therapeutics." International Journal of Molecular Sciences 22, no. 13 (2021): 6862. http://dx.doi.org/10.3390/ijms22136862.

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Metabolic syndrome (MetS) is a well-defined yet difficult-to-manage disease entity. Both the precipitous rise in its incidence due to contemporary lifestyles and the growing heterogeneity among affected populations present unprecedented challenges. Moreover, the predisposed risk for developing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in populations with MetS, and the viral impacts on host metabolic parameters, underscores the need to investigate this mechanism thoroughly. Recent investigations of metabolomics and proteomics have revealed not only differentially ex

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Shobatake, Ryogo, Hiroyo Ota, Nobuyuki Takahashi, Satoshi Ueno, Kazuma Sugie, and Shin Takasawa. "The Impact of Intermittent Hypoxia on Metabolism and Cognition." International Journal of Molecular Sciences 23, no. 21 (2022): 12957. http://dx.doi.org/10.3390/ijms232112957.

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Intermittent hypoxia (IH), one of the primary pathologies of sleep apnea syndrome (SAS), exposes cells throughout the body to repeated cycles of hypoxia/normoxia that result in oxidative stress and systemic inflammation. Since SAS is epidemiologically strongly correlated with type 2 diabetes/insulin resistance, obesity, hypertension, and dyslipidemia included in metabolic syndrome, the effects of IH on gene expression in the corresponding cells of each organ have been studied intensively to clarify the molecular mechanism of the association between SAS and metabolic syndrome. Dementia has rece

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Guo, Shaodong. "Insulin signaling, resistance, and metabolic syndrome: insights from mouse models into disease mechanisms." Journal of Endocrinology 220, no. 2 (2013): T1—T23. http://dx.doi.org/10.1530/joe-13-0327.

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Insulin resistance is a major underlying mechanism responsible for the ‘metabolic syndrome’, which is also known as insulin resistance syndrome. The incidence of metabolic syndrome is increasing at an alarming rate, becoming a major public and clinical problem worldwide. Metabolic syndrome is represented by a group of interrelated disorders, including obesity, hyperglycemia, hyperlipidemia, and hypertension. It is also a significant risk factor for cardiovascular disease and increased morbidity and mortality. Animal studies have demonstrated that insulin and its signaling cascade normally cont

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Hsu, Chien-Ning, Chih-Yao Hou, Wei-Hsuan Hsu, and You-Lin Tain. "Early-Life Origins of Metabolic Syndrome: Mechanisms and Preventive Aspects." International Journal of Molecular Sciences 22, no. 21 (2021): 11872. http://dx.doi.org/10.3390/ijms222111872.

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One of the leading global public-health burdens is metabolic syndrome (MetS), despite the many advances in pharmacotherapies. MetS, now known as “developmental origins of health and disease” (DOHaD), can have its origins in early life. Offspring MetS can be programmed by various adverse early-life conditions, such as nutrition imbalance, maternal conditions or diseases, maternal chemical exposure, and medication use. Conversely, early interventions have shown potential to revoke programming processes to prevent MetS of developmental origins, namely reprogramming. In this review, we summarize w

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Dharmalingam, Mala, and Sara Rani Marcus. "Pathogenetic Mechanism of Type 2 Diabetes Mellitus and its Clinical Implications." Annals of the National Academy of Medical Sciences (India) 55, no. 03 (2019): 132–34. http://dx.doi.org/10.1055/s-0039-1698544.

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AbstractOxidative stress is an important pathogenetic mechanism for the development of type 2 diabetes mellitus (T2DM) and its complications. Oxidative stress is an imbalance of the generation of free radicals (reactive oxygen species [ROS] and reactive nitrogen species [RNS]) and their neutralization by the antioxidant mechanisms. Increased levels of ROS and RNS lead to damage of lipids, proteins, and DNA, ultimately causing the destruction of the islet cells of pancreas through apoptosis. Another important factor in the development of diabetes mellitus and metabolic syndrome is inflammation.

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