scholarly journals Obesity is the basis of metabolic syndrome

2021 ◽  
Vol 18 (2) ◽  
pp. 142-149
Author(s):  
A. F. Verbovoy ◽  
N. I. Verbovaya ◽  
Yu. A. Dolgikh
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Subcutaneous Fat ◽  
Visceral Obesity ◽  
Cardiovascular Risks ◽  
The Metabolic Syndrome ◽  
Symptom Complex ◽  
Visceral Adipose ◽  
Positive Effect

Metabolic syndrome is a symptom complex that is based on visceral obesity and insulin resistance. Its prevalence is quite high, which is a big problem, since this condition increases the risk of developing cardiovascular diseases and mortality from them. Metabolic syndrome includes, in addition to abdominal obesity, arterial hypertension, disorders of carbohydrate, lipid and purine metabolism. Visceral adipose tissue plays a key role in the formation of insulin resistance and other components of the metabolic syndrome. This is due to the fact that abdominal fat, in contrast to subcutaneous fat, synthesizes pro-inflammatory cytokines, as well as adipokines — adipose tissue hormones that are involved in the formation of insulin resistance, affect carbohydrate and fat metabolism and the cardiovascular system. These include leptin, adiponectin, resistin, apelin and others. Some adipokines have an adverse effect on metabolism and increase cardiovascular risks, while others, on the contrary, have a positive effect. Taking into account their role in the development of the components of the metabolic syndrome, the possibilities of a therapeutic effect on the hormones of adipose tissue to improve metabolic processes and prevent complications associated with it are discussed.

scholarly journals Visceral obesity, metabolic syndrome, insulin resistance and cancer

2011 ◽  
Vol 71 (1) ◽  
pp. 181-189 ◽  
Author(s):  
Suzanne L. Doyle ◽  
Claire L. Donohoe ◽  
Joanne Lysaght ◽  
John V. Reynolds
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Systemic Inflammation ◽  
Visceral Adipose Tissue ◽  
Tumour Progression ◽  
Visceral Adiposity ◽  
Oesophageal Adenocarcinoma ◽  
The Metabolic Syndrome ◽  
Visceral Adipose

This paper presents emerging evidence linking visceral adiposity and the metabolic syndrome (MetSyn) with carcinogenesis. The link between obesity and cancer has been clearly identified in a multitude of robust epidemiological studies. Research is now focusing on the role of visceral adipose tissue in carcinogenesis; as it is recognised as an important metabolic tissue that secretes factors that systemically alter the immunological, metabolic and endocrine milieu. Excess visceral adipose tissue gives rise to a state of chronic systemic inflammation with associated insulin resistance and dysmetabolism, collectively known as the MetSyn. Prospective cohort studies have shown associations between visceral adiposity, the MetSyn and increased risk of breast cancer, colorectal cancer and oesophageal adenocarcinoma. Furthermore, visceral adiposity and the MetSyn have been associated with increased tumour progression and reduced survival. The mechanisms by which visceral adiposity and the MetSyn are thought to promote tumorigenesis are manifold. These include alterations in adipokine secretion and cell signalling pathways. In addition, hyperinsulinaemia, subsequent insulin resistance and stimulation of the insulin-like growth factor-1 axis have all been linked with visceral adiposity and promote tumour progression. Furthermore, the abundance of inflammatory cells in visceral adipose tissue, including macrophages and T-cells, create systemic inflammation and a pro-tumorigenic environment. It is clear from current research that excess visceral adiposity and associated dysmetabolism play a central role in the pathogenesis of certain cancer types. Further research is required to elucidate the exact mechanisms at play and identify potential targets for intervention.

scholarly journals Mediterranean diet, endothelial function and vascular inflammatory markers

2006 ◽  
Vol 9 (8A) ◽  
pp. 1073-1076 ◽  
Author(s):  
Katherine Esposito ◽  
Miryam Ciotola ◽  
Dario Giugliano
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Endothelial Dysfunction ◽  
Low Grade ◽  
The Metabolic Syndrome ◽  
Inflammatory State ◽  
Triggering Factor ◽  
Inflammatory Milieu ◽  
Visceral Adipose

AbstractObjectivesTo discuss present knowledge about the relation between adipose tissue, inflammation and the Mediterranean-style diet.DesignReview of the literature and personal perspectives.Setting and resultsRecent studies indicate that adipose tissue is an endocrine organ producing numerous proteins, collectively referred to as adipokines, with broad biological activity, which play an important autocrine role in obesity-associated complications. Adipose tissue in general and visceral fat in particular are thought to be key regulators of inflammation which is heavily involved in the onset and development of atherothrombotic disease. Moreover, chronic inflammation may also represent a triggering factor in the origin of the metabolic syndrome and type 2 diabetes mellitus. An increased release of proinflammatory adipokines from the visceral adipose tissue, associated with a reduced secretion of anti-inflammatory adipokines and cytokines, could determine a low-grade chronic inflammatory state which might play a role in the future development of the metabolic syndrome, diabetes and atherosclerosis through both insulin resistance and endothelial dysfunction. Interventions aimed at decreasing weight loss and improving adherence to a Mediterranean-style diet in people with obesity or metabolic syndrome decrease the inflammatory milieu and ameliorate both insulin resistance and endothelial dysfunction.ConclusionsAppropriate dietary patterns, as those associated with the eating model of Mediterranean-type diets, represent therapeutic strategies to reduce inflammation and the associated metabolic and cardiovascular risk.

Effect of voluntary exercise on peripheral tissue glucocorticoid receptor content and the expression and activity of 11β-HSD1 in the Syrian hamster

2006 ◽  
Vol 100 (5) ◽  
pp. 1483-1488 ◽  
Author(s):  
Agnes E. Coutinho ◽  
Jonathan E. Campbell ◽  
Sergiu Fediuc ◽  
Michael C. Riddell
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Metabolic Syndrome ◽  
Enzyme Activity ◽  
Adipose Tissue ◽  
Protein Expression ◽  
Aerobic Exercise ◽  
Visceral Adipose Tissue ◽  
The Metabolic Syndrome ◽  
Visceral Adipose

Recent findings indicate that elevated levels of glucocorticoids (GC), governed by the expression of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) and GC receptors (GR), in visceral adipose tissue and skeletal muscle lead to increased insulin resistance and the metabolic syndrome. Paradoxically, evidence indicates that aerobic exercise attenuates the development of the metabolic syndrome even though it stimulates acute increases in circulating GC levels. To investigate the hypothesis that training alters peripheral GC action to maintain insulin sensitivity, young male hamsters were randomly divided into sedentary (S) and trained (T) groups ( n = 8 in each). The T group had 24-h access to running wheels over 4 wk of study. In muscle, T hamsters had lower 11β-HSD1 protein expression (19.2 ± 1.40 vs. 22.2 ± 0.96 optical density, P < 0.05), similar 11β-HSD1 enzyme activity (0.9 ± 0.27% vs. 1.1 ± 0.26), and lower GR protein expression (9.7 ± 1.86 vs. 15.1 ± 1.78 optical density, P < 0.01) than S hamsters. In liver, 11β-HSD1 protein expression tended to be lower in T compared with S (19.2 ± 0.56 vs. 21.4 ± 1.05, P = 0.07), whereas both enzyme activity and GR protein expression were similar. In contrast, visceral adipose tissue contained ∼2.7-fold higher 11β-HSD1 enzyme activity in T compared with S (12.9 ± 3.3 vs. 4.8 ± 1.5% conversion, P < 0.05) but was considerably smaller in mass (0.24 ± 0.02 vs. 0.71 ± 0.06 g). Thus the intracellular adaptation of GC regulators to exercise is tissue specific, resulting in decreases in GC action in skeletal muscle and increases in GC action in visceral fat. These adaptations may have important implications in explaining the protective effects of aerobic exercise on insulin resistance and other symptoms of the metabolic syndrome.

scholarly journals The contribution of omental adipose tissue to adipokine concentrations in patients with the metabolic syndrome

2007 ◽  
Vol 30 (5) ◽  
pp. 192 ◽  
Author(s):  
Giovanni Tarantino ◽  
Roberto Lobello ◽  
Francesco Scopacasa ◽  
Franco Contaldo ◽  
Fabrizio Pasanisi ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Venous Blood ◽  
Visceral Obesity ◽  
Systemic Circulation ◽  
Central Adiposity ◽  
Omental Adipose Tissue ◽  
The Metabolic Syndrome ◽  
Visceral Adipose ◽  
Endothelial Growth Factor

Purpose: To examine differences in peripheral vascular endothelial growth factor (VEGF), interleukin-6 (IL6) and cortisol concentrations between patients with both visceral obesity and metabolic syndrome, and lean controls. In a subsample of metabolic patients underwent abdominal surgery, the adipokine concentrations were measured in venous blood from the omentum to determine information on some processes of synthesis. Methods: Forty-two healthy lean controls and 46 overweight-obese patients with central adiposity and stigmata of metabolic syndrome were studied. In a subsample of 11 metabolic patients undergoing non-bariatric surgery, blood samples from omental and peripheral veins were taken intraoperatively to determine VEGF, IL6 and cortisol concentrations. Results: Median levels (range) of peripheral VEGF and IL6 were higher in patients than in controls [31.5 (3-112) pg/mL vs 21.35 (9-41.9) pg/mL (P < 0.05) and 5.50 (1.40-13) pg/mL vs 1.15 (0.3-1) pg/mL (P < 0.0001)]. On the other hand, concentrations of VEGF and IL6 from the omental and peripheral veins were similar in the surgery sub-group. Peripheral cortisol concentrations were not higher in patients than in controls, nor were omental concentrations different from the peripheral. Omental and peripheral VEGF and cortisol values were correlated, whereas no association was found between omental and peripheral IL6. Conclusions: In the presence of abdominal obesity, VEGF and IL6 concentrations are increased in the systemic circulation. The contribution of visceral adipose tissue to circulating levels of VEGF and IL6 was modest.

scholarly journals Вплив інгібіторів ароматази третього покоління на окремі компоненти перебігу експериментального метаболічного синдрому

2018 ◽  
Author(s):  
A. L. Zagayko ◽  
D. V. Lytkin ◽  
A. V. Maloshtan
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Glucose Tolerance ◽  
Aromatase Inhibitors ◽  
Electrochemical Method ◽  
Visceral Obesity ◽  
Insulin Level ◽  
Third Generation ◽  
The Metabolic Syndrome

Introduction. Nowadays, about 86 % among patients with metabolic syndrome have serious disorder of glucose tolerance and about 60 % of them suffer from visceral obesity. Moreover in many worldwide studies it was shown that these pathogenetic manifestations of the metabolic syndrome had a significant correlation with the imbalance of sex hormones.The aim of the study – to learn the effect of third-generation aromatase inhibitors on the parameters of insulin resistance and visceral obesity in hamsters with the experimental metabolic syndrome.Research Methods. The insulin level in the hamster`s blood serum was measured by the enzyme immunoassay method, and the glucose level by the electrochemical method. The mass coefficients of anatomical fragments of adipose tissue were calculated to estimate visceral obesity. The results were processed by using the Mann-Whitney U-test and the 4Pl method.Results and Discussion. All studied drugs, in varying degrees, influenced on the pathogenetic components of the experimental metabolic syndrome. Exemestane was demonstrated the greatest effectiveness in reducing parameter of the insulin resistance by, butletrozole – in decreasing of visceral obesity ratio.Сonclusion. Romatase inhibitors can become promising drugs for correcting the pathogenetic components of the metabolic syndrome, in particular insulin resistance and visceral obesity.

scholarly journals Elevated serum uric acid is a facilitating mechanism for insulin resistance mediated accumulation of visceral adipose tissue

2020 ◽  
Author(s):  
Luisa Fernández-Chirino ◽  
Neftali Eduardo Antonio-Villa ◽  
Arsenio Vargas-Vázquez ◽  
Paloma Almeda-Valdés ◽  
Donají Gómez-Velasco ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Uric Acid ◽  
Serum Uric Acid ◽  
Visceral Adipose Tissue ◽  
Visceral Obesity ◽  
Causal Mechanism ◽  
Mediation Analyses ◽  
Bidirectional Relationship ◽  
Visceral Adipose

BACKGROUND: Serum uric acid (SUA) has a relationship with cardiometabolic conditions such as insulin resistance (IR) and visceral adipose tissue (VAT) accumulation. Here, we aimed to clarify the nature of this relationship and the underlying causality mechanism. METHODS: We conducted a population-based cross-sectional study comprising 8,504 subjects joining both NHANES 2003-2004 and 2011-2012 cycles and ENSANUT Medio Camino 2016. We performed mixed effects linear regression models using HOMA2-IR, adipoIR, and METS-VF as indicators of IR and VAT accumulation. Furthermore, we performed mediation analyses to assess a potential causal mechanism and ROC curves to establish cut-off points for identification of IR and visceral obesity using SUA. Finally, with an additional dataset comprised of 226 subjects with both euglycemic hyperinsulinemic clamp (EHC) and dual X-ray absorptiometry (DXA) measurements for IR and VAT accumulation, we performed a network of confirmatory mediation analyses. RESULTS:We found that SUA has a mediating role inside the bidirectional relationship between IR and visceral obesity, and it is part of an underlying causality mechanism which includes adiponectin. The proportion of the mechanism mediated by SUA is greater when stated that IR (in either peripheral or adipose tissue) leads to VAT accumulation (14.90%[13.20%-17.00%] and 15.54%[13.61% - 18.00%] to 4.88%[3.06%-7.00%] and 8.13%[5.91% - 10.00%]) instead of the opposite direction. This result was confirmed by mediation analyses using gold-standard measurements. CONCLUSIONS:Elevated SUA acts as mediator inside the bidirectional relationship between IR andVAT accumulation. Its role appears to be larger when considering adipose tissue IR as the promoter for VAT accumulation.

scholarly journals The Relationship between Epicardial Adipose Tissue Thickness and Serum Interleukin-17a Level in Patients with Isolated Metabolic Syndrome

Biomolecules ◽  
2019 ◽  
Vol 9 (3) ◽  
pp. 97 ◽  
Author(s):  
Esra Demir ◽  
Nazmiye Harmankaya ◽  
İrem Kıraç Utku ◽  
Gönül Açıksarı ◽  
Turgut Uygun ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Epicardial Adipose Tissue ◽  
Control Group ◽  
Model Assessment ◽  
Tissue Thickness ◽  
The Metabolic Syndrome ◽  
Epicardial Adipose Tissue Thickness ◽  
The Relationship

In this study, it was aimed to investigate the relationship between the epicardial adipose tissue thickness (EATT) and serum IL-17A level insulin resistance in metabolic syndrome patients. This study enrolled a total of 160 subjects, of whom 80 were consecutive patients who applied to our outpatient clinic and were diagnosed with metabolic syndrome, and the other 80 were consecutive patients who were part of the control group with similar age and demographics in whom the metabolic syndrome was excluded. The metabolic syndrome diagnosis was made according to International Diabetes Federation (IDF)-2005 criteria. EATT was measured with transthoracic echocardiography (TTE) in the subjects. IL-17A serum levels were determined using the ELISA method. Fasting blood glucose, HDL, triglyceride, and fasting insulin levels were significantly higher in the metabolic syndrome group compared to the control group. In addition, the metabolic syndrome group had significantly higher high-sensitivity C-reactive protein (hs-CRP) and Homeostatic Model Assessment Insulin Resistance (HOMA-IR) levels than the control group. Similarly, serum IL-17A levels were significantly elevated in the metabolic syndrome group compared to the control group statistically (p < 0.001). As well, EATT was higher in the metabolic syndrome than the control group. Conclusion: By virtue of their proinflammatory properties, EATT and IL-17 may play an important role in the pathogenesis of the metabolic syndrome.

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