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Journal articles on the topic 'Obesity and metabolic disfunction'

Author: Grafiati

Published: 9 March 2023

Last updated: 10 March 2023

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1

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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Ghatan, Sam, Fariba Ahmadizar, Ruolin Li, Carolina Medina-Gomez, Maria Carola Zillikens, Fernando Rivadeneira, Maryam Kavousi, and Ling Oei. "Type 2 Diabetes Clusters Indicate Diabetes Duration Key in Fracture Risk." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A280—A281. http://dx.doi.org/10.1210/jendso/bvab048.570.

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Abstract Introduction: Individuals with type 2 diabetes mellitus (T2DM) are at an increased risk of developing fractures, despite higher mean BMI and BMD. Recently, clinically-relevant sub-groups of T2DM have been characterised using biomarkers of glycemic metabolism. Aim: Characterise T2DM sub-groups in a population-based setting and test for differences in fracture risk. Methods: A total of 10019 Rotterdam Study participants were available with glycemic and (incident) fracture follow-up. Participants with T2DM (n=1678) were partitioned in subgroups using K-means clustering based on: HOMA-B, HOMA-IR, age of diabetes onset, BMI and waist circumference measurements. Non-vertebral fracture risk was estimated across T2D subgroups using Cox proportional hazard models, adjusted for sex, age, BMI, collection cohort and prevalent T2DM. Results: Four T2D clusters were defined each with relatively-unique clinical characteristics namely, 1) advanced age of onset; 2) decreased insulin sensitivity; 3) beta-cell disfunction; 4) Obesity/high BMI. Individuals with prevalent and incident T2DM (independent of cluster) had lower risk of fracture than non-diabetics (see Forest plot). In contrast, individuals with prevalent T2DM (n=1152) had increased risk of non-vertebral fracture (HR: 2.1, 95%CI: 1.65–2.76), than individuals without T2DM. Conclusion: Despite that partitioning the heterogeneity of T2DM in clinically-meaningful clusters opens the road to tailored prevention and care, our findings with prevalent T2DM indicate that disease duration (likely with inadequate glycemic control) is the main determinant of fracture risk. In line with this contention, the association between T2DM and fracture risk is not causal, as causality requires association with incident cases, as also confirmed by earlier Mendelian randomization studies. Future work, using genetically-determined disease definitions and biomarkers will help unveil clusters of individuals with T2DM at increased risk of fracture.

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Uluısık, Deniz, and Ercan Keskin. "Hepatoprotective Effects of Ginseng in Rats Fed Cholesterol Rich Diet." Acta Scientiae Veterinariae 44, no. 1 (March 19, 2018): 5. http://dx.doi.org/10.22456/1679-9216.80887.

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Background: Ginseng species having been used in various traditional herbal therapies for many years in worldwide. In recent years, hyperlipidemia, hypercholesterolemia and obesity have become serious health problems. These are considered risk factor for metabolic and organic diseases such as atherosclerosis, fatty liver, diabetes. Therefore, prevention and treatment of these disorders are significant for ensuring comfortable and healthy life. It has been also stated that ginseng saponin suppressed liver enzyme increments caused by feeding with high cholesterol or fatty diet. The present study was undertaken to evaluate the effect of ginseng on liver enzymes of rats fed cholesterol-rich diet.Materials, Methods & Results: In this study, 24 healthy adult male Wistar Albino rats were equally divided into three groups as control group (K), cholesterol group (C), and cholesterol + ginseng group (CG). The K group had ad libitum access to a standard rat diet for 40 days. The C and CG groups had ad libitum access to the same diet containing 5% cholesterol powder and 5% cholesterol + 1 g/kg Panax ginseng root powder, respectively, for 40 days. On the 40 th day of the study, blood samples were taken from 8 animals in each group. At the end of the study, plasma samples were analyzed for aspartase transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), and gamma-glutamyltransferase (GGT) levels. The data were analyzed using one-way ANOVA. Differences among the groups were determined by Duncan’s multiple range test. In this study, the results showed that AST, ALT, GGT levels in cholesterol group significantly increased compared to control group but these parameters in cholesterol + ginseng group significantly decreased with ginseng administration compared to cholesterol group (P < 0.05). There was no significant difference among the groups with regard to ALP level.Discussion: AST, ALT, GGT and ALP are considered to be the markers of organ disfunction, indicator of cellular damage, cell leakage and the loss of cell membrane integritiy in the liver, kidney, heart and other organs. It was investigated effect of ginseng on some hepatic enzymes in rats fed a high cholesterol diet. In this study, feeding with the diet for 40 days resulted in elevation AST, ALT, GGT compared control levels (P < 0.05). In some studies, using high cholesterol diet caused hepatic injury in animal and human models. The harmful effects of high cholesterol on liver have been attributed to hepatic fibrosis, lipid peroxidation, increased endogenous oxidative stress, inducing cellular damage and engendering hyperlipidemia. Increases in ALT, AST, GGT levels are thought to be due to oxidative stress related to hyperlipidemia in present study. In this study, treated with red Korean ginseng extract significantly prevented the elevations in AST, ALT, GGT levels (P < 0.05). The use of ginseng as an unconventional health treatment is gaining remarkable popularity among the people. It has been known that ginseng have assorted beneficial pharmacological effects and hypolipidemic, antidiabetic, antioxidative and immunostimulator effects have been stated among its pharmacological properties. These beneficial effects of ginseng on liver enzymes attributed to its active components known as ginsenosides. In the light of the findings, Panax ginseng root powder may be useful for hepatic damage and fibrosis associated with high cholesterol diet.

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Rymashevskii, A. N., S. S. Tumanyan, E. M. Frantsiyants, and S. V. Tumanyan. "ENDOCRINE DISFUNCTION IN WOMEN WITH PRE-ECLAMPSIA AND ALIMENTARY OBESITY." Obstetrics, Gynecology and Reproduction 11, no. 1 (January 1, 2017): 14–18. http://dx.doi.org/10.17749/2313-7347.2017.11.1.014-018.

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Karra, Prasoona, Maci Winn, Svenja Pauleck, Alicja Bulsiewicz‐Jacobsen, Lacie Peterson, Adriana Coletta, Jennifer Doherty, et al. "Metabolic dysfunction and obesity‐related cancer: Beyond obesity and metabolic syndrome." Obesity 30, no. 7 (July 2022): 1323–34. http://dx.doi.org/10.1002/oby.23444.

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Liu, Zhao. "Obesity and Metabolic Syndrome." American Chinese Journal of Medicine and Science 2, no. 3 (2009): 88. http://dx.doi.org/10.7156/v2i3p088.

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Krishnaveni, A., Lakshmi ANR., and Paramjyothi P. "Obesity and metabolic syndrome." International Journal of Biomedical Research 4, no. 2 (March 1, 2013): 99. http://dx.doi.org/10.7439/ijbr.v4i2.234.

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LEIBEL, RUDOLPH L. "Metabolic Characterization of Obesity." Annals of Internal Medicine 103, no. 6_Part_2 (December 1, 1985): 1000. http://dx.doi.org/10.7326/0003-4819-103-6-1000.

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Koopman, Richelle J., Sarah J. Swofford, Mark N. Beard, and Susan E. Meadows. "Obesity and Metabolic Disease." Primary Care: Clinics in Office Practice 36, no. 2 (June 2009): 257–70. http://dx.doi.org/10.1016/j.pop.2009.01.006.

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Gunton, Jenny. "Obesity and metabolic rate." Obesity Research & Clinical Practice 7 (December 2013): e5. http://dx.doi.org/10.1016/j.orcp.2013.12.508.

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Sheehan, Michael T., and Michael D. Jensen. "METABOLIC COMPLICATIONS OF OBESITY." Medical Clinics of North America 84, no. 2 (March 2000): 363–85. http://dx.doi.org/10.1016/s0025-7125(05)70226-1.

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Ross, Stephanie Maxine. "Obesity and Metabolic Syndrome." Holistic Nursing Practice 31, no. 5 (2017): 348–52. http://dx.doi.org/10.1097/hnp.0000000000000232.

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Keith, Jeanette N. "Metabolic Basis of Obesity." Gastroenterology 142, no. 5 (May 2012): 1255–56. http://dx.doi.org/10.1053/j.gastro.2012.03.024.

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Grundy, Scott M. "Metabolic Complications of Obesity." Endocrine 13, no. 2 (2000): 155–65. http://dx.doi.org/10.1385/endo:13:2:155.

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Pedersen, Sue D. "Metabolic complications of obesity." Best Practice & Research Clinical Endocrinology & Metabolism 27, no. 2 (April 2013): 179–93. http://dx.doi.org/10.1016/j.beem.2013.02.004.

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Xu, Haiyan. "Obesity and metabolic inflammation." Drug Discovery Today: Disease Mechanisms 10, no. 1-2 (June 2013): e21-e25. http://dx.doi.org/10.1016/j.ddmec.2013.03.006.

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Hoque, Nasimul, and Nabid Shahriar Sarker. "Obesity and Metabolic Health." Journal of Monno Medical College 8, no. 2 (February 26, 2023): 29–30. http://dx.doi.org/10.3329/jmomc.v8i2.64435.

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Rusdiana, Maya Savira, and Sry Suryani Widjaja. "Comparison Ghrehlin at Obesity Without Metabolic Sydrome With Obesity with Metabolic Syndrome." ABDIMAS TALENTA: Jurnal Pengabdian Kepada Masyarakat 6, no. 1 (March 15, 2021): 174–78. http://dx.doi.org/10.32734/abdimastalenta.v6i1.5864.

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Obesity is principal causative factor in the development of metabolic syndrome and Ghrelin as human natural hormones is involved in fundamental regulatory processof eating and energy balance.Obesity, which has become a global public health problem, is one of the major risk factors for development metabolic syndrome and type 2 diabetes mellitus.This study aimed to analyze the comparison of ghrelin hormone levels in obese with metabolic syndrome and obese non metabolic syndrome . The sample population is obese adults, then we examined the weight, height, waist size, blood pressure, laboratory tests such as blood sugar levels and lipid profile of sample population to separate obese with metabolic syndrome and obese non metabolic syndrome. After we determined each group we measured stress oxidative levels in blood in obese with metabolic syndrome and obese non metabolic syndrome by ELISA method.With statistical analysis using T test found that there was significant difference of ghrelin hormone levels between obese with metabolic syndrome and obese without metabolic syndrome (p<0.005).

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RADU DRĂGOI, Ștefana-Iuliana, Mihaela BAȘA, Adina PETCU, Alina LUPU ȘURLEA, and Natalia ROȘOIU. "Type I Diabetes – Metabolic Disfunction and Change Induced by Sars-Cov 2 Infection." Annals of the Academy of Romanian Scientists Series on Biological Sciences 11, no. 1 (2022): 53–64. http://dx.doi.org/10.56082/annalsarscibio.2022.1.53.

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Diabetes mellitus is a chronic metabolic disease characterized by a deficiency in insulin production and its action or both which leads to prolonged hyperglycaemia with disturbances in most metabolic processes inside the human body. In the case of infection with the new coronavirus SARS-COV-2 (COVID19) these patients have a higher risk of having a severe prognosis. Some studies suggest that diabetes may increase the risk of infection by two to three times, regardless of the presence of other conditions. The role of ferritin in correlation with the severity of COVID-19 patients is unknown. Research hypothesis. The level of blood ferritin. Serum ferritin levels appear to correlate with the severity of COVID-19 patients, which may make them a candidate for the role of biomarker. In this paper I want to show whether ferritin can be a marker of poor prognosis in patients with type I diabetes infected with SARS-COV 2 virus.

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Yu, Yi-Hao. "Making sense of metabolic obesity and hedonic obesity." Journal of Diabetes 9, no. 7 (February 28, 2017): 656–66. http://dx.doi.org/10.1111/1753-0407.12529.

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Bayliak, Maria. "Metabolic Syndrome, Obesity, and Drosophila." Journal of Vasyl Stefanyk Precarpathian National University 7, no. 4 (December 30, 2020): 7–18. http://dx.doi.org/10.15330/jpnu.7.4.7-18.

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Metabolic syndrome (MetS) is a cluster of metabolic disturbances increasing a risk of cardiovascular diseases and diabetes 2 types. The main features of MetS include atherogenic dyslipidemia, elevated blood pressure, insulin resistance and elevated glucose levels, a pro-thrombotic state, pro-oxidant and pro-inflammatory states. Excessive consumption of high caloric food and sedentary lifestyle followed by overweight and obesity, as well as aging and stresses are major contributing factors to the MetS development. MeS affects between 10 and 84% of adults depending on the used MetS criteria and increases significantly a risk of cardiovascular diseases, diabetes 2 type and kidney diseases. Patients with metabolic disorders like obesity, diabetes, cardiovascular, and liver disease may have a higher risk of infection of COVID-19 with significantly worse prognosis and outcomes in these patients. In recent years, the fruit fly, Drosophila melanogaster, has been actively used to study human metabolic disorders as a cost-effective and expedient model. Drosophila belongs to insects with full metamorphosis and its life cycle includes four developmental stages: embryo, larva, pupa, and adult flies. Each developmental stage has its own specific advantages and can be used to study metabolic homeostasis. Studies of metabolic disturbances in Drosophila and mammalian models along with humans have demonstrated that flies and small mammalian models have many similarities with humans in basic metabolic functions and share many molecular mechanisms which regulate these metabolic processes. In this paper, we describe the advantages and limitations of Drosophila models of metabolic syndrome and obesity in light of physiological and biochemical similarities and differences between insects and mammals.

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Gade, Wayne, and Jean Gade. "Obesity and Metabolic Syndrome Overview." American Society for Clinical Laboratory Science 23, no. 1 (January 2010): 37–38. http://dx.doi.org/10.29074/ascls.23.1.37.

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Yokaichiya, D. K., D. R. Araujo, J. A. Silva, B. B. Torres, and E. Galembeck. "Obesity: the new metabolic frontier." Revista de Ensino de Bioquímica 2, no. 2 (May 15, 2004): 10. http://dx.doi.org/10.16923/reb.v2i2.142.

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Working on active learning strategies for web based courses, the Biochemical Education Research groupfrom USP and Unicamp;s departments of Biochemistry has developed the educational software Obesity:the new metabolic frontier. The software was designed to be used as a major reference to study thissubject on 2003 Biochemistry of Nutrition course, and was based on the most recent publications aboutobesity, specially concerning the leptin role in this metabolic disturb. The most relevant characteristicof this software is the use of animated models to represent the cellular response and the presentationof many other mechanisms involved in obesity. We also intended to focus the relationship betweenleptin and other mechanisms that lead to obesity. The teaching strategy consisted in providing thestudents with the software and a text about Obesity. After few days, they should discuss the topic ina two-hour synchronous discussions chat-rooms (specially designed for this purpose), with a TeachingAssistant;s (TA) help. After the discussion, the students were asked to answer an evaluation surveyabout the activity and the software ecience to the learning process. The TAs were asked to evaluatethe software as a tool to help in teaching process. In the following week the students had to go backto the chat-rooms for an online synchronous test. The results of this experience (students and TAssatisfaction) were very clear and stimulated us to go on with software development and to improvethe use of this kind of educational tool in Biochemistry classes.

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Repina, М. A. "Menopausal metabolic syndrome and obesity." Journal of obstetrics and women's diseases 52, no. 3 (August 14, 2003): 75–84. http://dx.doi.org/10.17816/jowd88987.

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In this review, it is presented the importance for metabolic processes of decreasing estradiol concentration in connection with prolapsus of ovary function in women. Here, influence of different modes of substitute hormonal therapy, of different progestagenic components included in preparations is discussed.

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Yadav, Jaivinder, Jeyaraj Munusamy, Rakesh Kumar, Anil Bhalla, and Devi Dayal. "Metabolic complications of childhood obesity." Journal of Family Medicine and Primary Care 10, no. 6 (2021): 2325. http://dx.doi.org/10.4103/jfmpc.jfmpc_975_20z.

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Dzugkoev, S. G., F. S. Dzugkoeva, I. V. Mozhaeva, and O. I. Margieva. "ADIPOKINES, OBESITY AND METABOLIC DISORDERS." Современные проблемы науки и образования (Modern Problems of Science and Education), no. 6 2020 (2020): 82. http://dx.doi.org/10.17513/spno.30321.

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36

Lee, Sang Yeoup. "Smoking, Obesity and Metabolic Syndrome." Korean Journal of Obesity 23, no. 3 (2014): 162. http://dx.doi.org/10.7570/kjo.2014.23.3.162.

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Dodson, M. V., P. S. Mir, G. J. Hausman, L. L. Guan, Min Du, Z. Jiang, M. E. Fernyhough, and W. G. Bergen. "Obesity, Metabolic Syndrome, and Adipocytes." Journal of Lipids 2011 (2011): 1–5. http://dx.doi.org/10.1155/2011/721686.

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Obesity and metabolic syndromes are examples whereby excess energy consumption and energy flux disruptions are causative agents of increased fatness. Because other, as yet elucidated, cellular factors may be involved and because potential treatments of these metabolic problems involve systemic agents that are not adipose depot-specific in their actions, should we be thinking of adipose depot-specific (cellular) treatments for these problems? For sure, whether treating obesity or metabolic syndrome, the characteristics of all adipose depot-specific adipocytes and stromal vascular cells should be considered. The focus of this paper is to begin to align metabolic dysfunctions with specific characteristics of adipocytes.

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Tilg, Herbert. "Obesity, Metabolic Syndrome, and Microbiota." Journal of Clinical Gastroenterology 44 (September 2010): S16—S18. http://dx.doi.org/10.1097/mcg.0b013e3181dd8b64.

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39

Olvera, Rene L., Douglas E. Williamson, Susan P. Fisher-Hoch, Kristina P. Vatcheva, and Joseph B. McCormick. "Depression, Obesity, and Metabolic Syndrome." Journal of Clinical Psychiatry 76, no. 10 (October 21, 2015): e1300-e1305. http://dx.doi.org/10.4088/jcp.14m09118.

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McGinley, Brian, and Naresh M. Punjabi. "Obesity, Metabolic Abnormalities, and Asthma." American Journal of Respiratory and Critical Care Medicine 183, no. 4 (February 15, 2011): 424–25. http://dx.doi.org/10.1164/rccm.201009-1525ed.

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Keller, Kathryn Buchanan, and Louis Lemberg. "Obesity and the Metabolic Syndrome." American Journal of Critical Care 12, no. 2 (March 1, 2003): 167–70. http://dx.doi.org/10.4037/ajcc2003.12.2.167.

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Khromylev, Khromylev A. V., and Makatsaria A. D. Makatsaria. "Obesity, metabolic syndrome, and thrombophilia." Akusherstvo i ginekologiia 10_2017 (November 2, 2017): 27–33. http://dx.doi.org/10.18565/aig.2017.10.27-33.

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Ghada, Welwel. "Obesity, Diabetes, and Metabolic Syndrome." Global Journal of Obesity, Diabetes and Metabolic Syndrome 7, no. 2 (June 30, 2020): 034–35. http://dx.doi.org/10.17352/2455-8583.000045.

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44

Després, Jean-Pierre, and Isabelle Lemieux. "Abdominal obesity and metabolic syndrome." Nature 444, no. 7121 (December 2006): 881–87. http://dx.doi.org/10.1038/nature05488.

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Cunningham, M., and K. K. G. Alberti. "Metabolic Syndrome and Obesity Update." MD Conference Express 6, no. 2 (August 1, 2006): 25–28. http://dx.doi.org/10.1177/155989770600600213.

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Hlubik, P., H. Stritecka, and J. Hlubik. "116 OBESITY AND METABOLIC SYNDROME." Atherosclerosis Supplements 12, no. 1 (June 2011): 27. http://dx.doi.org/10.1016/s1567-5688(11)70117-9.

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Shuval, Kerem, Carolyn E. Barlow, Carrie E. Finley, Kelley Pettee Gabriel, Michael D. Schmidt, and Laura F. DeFina. "Standing, Obesity, and Metabolic Syndrome." Mayo Clinic Proceedings 90, no. 11 (November 2015): 1524–32. http://dx.doi.org/10.1016/j.mayocp.2015.07.022.

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Wollin, Daniel A., Andreas Skolarikos, and Glenn M. Preminger. "Obesity and metabolic stone disease." Current Opinion in Urology 27, no. 5 (September 2017): 422–27. http://dx.doi.org/10.1097/mou.0000000000000427.

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Erusan, R. Raskin. "Obesity, inflammation and metabolic disorders." Indian Journal of Science and Technology 1, no. 4 (September 30, 2008): 1–5. http://dx.doi.org/10.17485/ijst/2008/v1i4.8.

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Bosello, O., and M. Zamboni. "Visceral obesity and metabolic syndrome." Obesity Reviews 1, no. 1 (May 2000): 47–56. http://dx.doi.org/10.1046/j.1467-789x.2000.00008.x.

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