scholarly journals Effect of Exercise on Intestinal Microbium and Insulin Resistance in Person with Metabolic Syndrome

2020 ◽  
Vol 5 (5) ◽  
pp. 324-331
Author(s):  
O. O. Hurenko ◽  
◽  
S. B. Drozdovska

Metabolic syndrome is a cluster of cardiometabolic risk factors. They include obesity, dyslipidemia, hypertension, and insulin resistance. Central obesity and resistance to insulin, in particular, are recognized as causative factors, which form the development of metabolic syndrome. Metabolic syndrome is a progressive and genetically determined condition. The result of its progression is that carbohydrate, lipid and purine metabolism break down. The intestinal microbiome has a significant role in the pathogenesis of metabolic syndrome. One of the methods of influencing the micribiotic composition is the physical activity. The human intestinal microbiome is a complex ecosystem consisting not only of microorganisms, but also including bacteria, archaea, fungi and viruses. Biodiversity and the overall composition of the microbiota play a crucial role in maintaining normal homeostasis in the human body. With the recent advent of the possibility of studying the intestinal microbiome, the impact on its taxonomic composition and metabolism through exercise is the subject of scientific interest. Recent studies showed that the intestinal microbiota was directly involved in the formation of the metabolic syndrome. The function of the microbiome is just as important as the function of the "metabolic organs" that affect energy homeostasis and control body weight. In addition, changes in the intestinal microbiotic composition lead to increased intestinal permeability, endotoxemia, which plays a role in the development of chronic inflammation in the host, contributing to the development of metabolic syndrome and related chronic metabolic diseases. Intestinal microbiota in its own right is injected into the development of systemic inflammation in obesity, such a rank, inappropriate insertions in development or regression of insulin resistance, and hyperglycemia in metabolic syndrome. Physical activity can affect not only the composition of the microbial composition, but also the metabolic activity of the intestinal microbiome. The health-improving effect of physical exercises is connected with their ability to change the composition of an intestinal microbiota. Studies involving professional athletes and a specially selected control group indicated that athletes had a lower pro-inflammatory status and a high degree of bacterial diversity. Due to this, there is a positive dynamics of improving carbohydrate metabolism and the impact on the course of pathological processes associated with the metabolic syndrome, through the introduction of regular physical activity. Conclusion. The literature review presents data on the metabolic syndrome, its pathogenesis and components of the spectrum of development of metabolic disorders. We also analyzed material on influence of gut microbiota on development of metabolic disturbances and inreraction of structure of a microbiotic composition with physical exercises

2004 ◽  
Vol 29 (6) ◽  
pp. 808-829 ◽  
Author(s):  
Lindsay E. Robinson ◽  
Terry E. Graham

The metabolic syndrome comprises an array of cardiovascular disease (CVD) risk factors such as abdominal obesity, dyslipidemia, hypertension, and glucose intolerance. Insulin resistance and/or increased abdominal (visceral) obesity have been suggested as potential etiological factors. More recently, increasing evidence has associated insulin resistance and subclinical inflammation involving cytokines derived from adipose tissue, or adipocytokines. Despite the fact that precise mechanisms have yet to be established, there is a significant role for both diet and physical activity to improve the many factors associated with the metabolic syndrome, including modulation of various adipocytokines. Although both diet and physical activity have been studied for their ability to modify cytokines in more traditional inflammatory conditions, such as rheumatoid arthritis, they have been less studied in relation to inflammation as an underlying cause of the metabolic syndrome and/or CVD. A more thorough understanding of the clustering of metabolic abnormalities and their underlying etiology will help to define diet and physical activity guidelines for preventing and treating the metabolic syndrome, an important aspect of CVD prevention. This paper will address potential underlying causes of the metabolic syndrome, with a focus on the putative mechanistic role of adipocytokines, and will discuss the impact of diet and physical activity on the metabolic syndrome. Key words: insulin resistance syndrome, obesity, adipose tissue, skeletal muscle, cytokines, TNF-α, IL-6, PAI-1, inflammation, nutrition, exercise


Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1652 ◽  
Author(s):  
Jonathan Myers ◽  
Peter Kokkinos ◽  
Eric Nyelin

Both observational and interventional studies suggest an important role for physical activity and higher fitness in mitigating the metabolic syndrome. Each component of the metabolic syndrome is, to a certain extent, favorably influenced by interventions that include physical activity. Given that the prevalence of the metabolic syndrome and its individual components (particularly obesity and insulin resistance) has increased significantly in recent decades, guidelines from various professional organizations have called for greater efforts to reduce the incidence of this condition and its components. While physical activity interventions that lead to improved fitness cannot be expected to normalize insulin resistance, lipid disorders, or obesity, the combined effect of increasing activity on these risk markers, an improvement in fitness, or both, has been shown to have a major impact on health outcomes related to the metabolic syndrome. Exercise therapy is a cost-effective intervention to both prevent and mitigate the impact of the metabolic syndrome, but it remains underutilized. In the current article, an overview of the effects of physical activity and higher fitness on the metabolic syndrome is provided, along with a discussion of the mechanisms underlying the benefits of being more fit or more physically active in the prevention and treatment of the metabolic syndrome.


2014 ◽  
Vol 2014 ◽  
pp. 1-16 ◽  
Author(s):  
Saeid Golbidi ◽  
Ismail Laher

The lack of adequate physical activity and obesity created a worldwide pandemic. Obesity is characterized by the deposition of adipose tissue in various parts of the body; it is now evident that adipose tissue also acts as an endocrine organ capable of secreting many cytokines that are though to be involved in the pathophysiology of obesity, insulin resistance, and metabolic syndrome. Adipokines, or adipose tissue-derived proteins, play a pivotal role in this scenario. Increased secretion of proinflammatory adipokines leads to a chronic inflammatory state that is accompanied by insulin resistance and glucose intolerance. Lifestyle change in terms of increased physical activity and exercise is the best nonpharmacological treatment for obesity since these can reduce insulin resistance, counteract the inflammatory state, and improve the lipid profile. There is growing evidence that exercise exerts its beneficial effects partly through alterations in the adipokine profile; that is, exercise increases secretion of anti-inflammatory adipokines and reduces proinflammatory cytokines. In this paper we briefly describe the pathophysiologic role of four important adipokines (adiponectin, leptin, TNF-α, and IL-6) in the metabolic syndrome and review some of the clinical trials that monitored these adipokines as a clinical outcome before and after exercise.


Toxics ◽  
2020 ◽  
Vol 8 (4) ◽  
pp. 105
Author(s):  
Ilona Górna ◽  
Marta Napierala ◽  
Ewa Florek

The metabolic syndrome is a combination of several metabolic disorders, such as cardiovascular disease, atherosclerosis, and type 2 diabetes. Lifestyle modifications, including quitting smoking, are recommended to reduce the risk of metabolic syndrome and its associated complications. Not much research has been conducted in the field of e-cigarettes and the risk of metabolic syndrome. Furthermore, taking into account the influence of e-cigarettes vaping on the individual components of metabolic syndrome, i.e, abdominal obesity, insulin resistance, dyslipidemia and elevated arterial blood pressure, the results are also ambiguous. This article is a review and summary of existing reports on the impact of e-cigarettes on the development of metabolic syndrome as well as its individual components. A critical review for English language articles published until 30 June 2020 was made, using a PubMed (including MEDLINE), Cochrane, CINAHL Plus, and Web of Science data. The current research indicated that e-cigarettes use does not affect the development of insulin resistance, but could influence the level of glucose and pre-diabetic state development. The lipid of profile an increase in the TG level was reported, while the influence on the level of concentration of total cholesterol, LDL fraction, and HDL fraction differed. In most cases, e-cigarettes use increased the risk of developing abdominal obesity or higher arterial blood pressure. Further research is required to provide more evidence on this topic.


2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Eduardo Spinedi ◽  
Daniel P. Cardinali

Polycystic ovary syndrome is a highly frequent reproductive-endocrine disorder affecting up to 8–10% of women worldwide at reproductive age. Although its etiology is not fully understood, evidence suggests that insulin resistance, with or without compensatory hyperinsulinemia, and hyperandrogenism are very common features of the polycystic ovary syndrome phenotype. Dysfunctional white adipose tissue has been identified as a major contributing factor for insulin resistance in polycystic ovary syndrome. Environmental (e.g., chronodisruption) and genetic/epigenetic factors may also play relevant roles in syndrome development. Overweight and/or obesity are very common in women with polycystic ovary syndrome, thus suggesting that some polycystic ovary syndrome and metabolic syndrome female phenotypes share common characteristics. Sleep disturbances have been reported to double in women with PCOS and obstructive sleep apnea is a common feature in polycystic ovary syndrome patients. Maturation of the luteinizing hormone-releasing hormone secretion pattern in girls in puberty is closely related to changes in the sleep-wake cycle and could have relevance in the pathogenesis of polycystic ovary syndrome. This review article focuses on two main issues in the polycystic ovary syndrome-metabolic syndrome phenotype development: (a) the impact of androgen excess on white adipose tissue function and (b) the possible efficacy of adjuvant melatonin therapy to improve the chronobiologic profile in polycystic ovary syndrome-metabolic syndrome individuals. Genetic variants in melatonin receptor have been linked to increased risk of developing polycystic ovary syndrome, to impairments in insulin secretion, and to increased fasting glucose levels. Melatonin therapy may protect against several metabolic syndrome comorbidities in polycystic ovary syndrome and could be applied from the initial phases of patients’ treatment.


2005 ◽  
Vol 64 (1) ◽  
pp. 23-29 ◽  
Author(s):  
Helen M. Roche

The metabolic syndrome is a very common condition, characterised by insulin resistance, dyslipidaemia, abdominal obesity and hypertension, that is associated with a high risk of type 2 diabetes mellitus (T2DM) and CVD. Obesity is a key aetiological factor in the development of the metabolic syndrome. In light of the increasing prevalence of obesity, there is a high requirement to reduce the impact of the adverse health effects associated with the metabolic syndrome. The aetiological role of nutrient-derived metabolic stressors, in particular fatty acids, in the development of obesity and the metabolic syndrome is explored. Also, the evidence that pro-inflammatory stressors may predispose to obesity-induced insulin resistance is reviewed. The present paper explores the concept that reducing the impact of metabolic and inflammatory stressors may reduce the adverse health effects of obesity and slow the progression towards the metabolic syndrome and T2DM. Evidence from human dietary intervention studies that have investigated the potential therapeutic effects of dietary fatty acid modification is explored. The present review highlights the requirement to take account of genetic background, within the context of nutrient regulation of gene expression and individual responsiveness to dietary therapy. This approach will further the understanding of the interaction between fatty acids in the pathogenesis and progression of the metabolic syndrome.


2014 ◽  
Vol 112 (11) ◽  
pp. 1826-1836 ◽  
Author(s):  
Camilla T. Damsgaard ◽  
Stine-Mathilde Dalskov ◽  
Rikke P. Laursen ◽  
Christian Ritz ◽  
Mads F. Hjorth ◽  
...  

An increasing number of children are exhibiting features of the metabolic syndrome (MetS) including abdominal fatness, hypertension, adverse lipid profile and insulin resistance. Healthy eating practices during school hours may improve the cardiometabolic profile, but there is a lack of evidence. In the present study, the effect of provision of school meals rich in fish, vegetables and fibre on a MetS score (primary outcome) and on individual cardiometabolic markers and body composition (secondary outcomes) was investigated in 834 Danish school children. The study was carried out as a cluster-randomised, controlled, non-blinded, cross-over trial at nine schools. Children aged 8–11 years received freshly prepared school lunch and snacks or usual packed lunch from home (control) each for 3 months. Dietary intake, physical activity, cardiometabolic markers and body composition were measured at baseline and after each dietary period. The school meals did not affect the MetS score (P= 1·00). However, it was found that mean arterial pressure was reduced by 0·4 (95 % CI 0·0, 0·8) mmHg (P= 0·04), fasting total cholesterol concentrations by 0·05 (95 % CI 0·02, 0·08) mmol/l (P= 0·001), HDL-cholesterol concentrations by 0·02 (95 % CI 0·00, 0·03) mmol/l, TAG concentrations by 0·02 (95 % CI 0·00, 0·04) mmol/l (bothP< 0·05), and homeostasis model of assessment-insulin resistance by 0·10 (95 % CI 0·04, 0·16) points (P= 0·001) compared with the control diet in the intention-to-treat analyses. Waist circumference increased 0·5 (95 % CI 0·3, 0·7) cm (P< 0·001), but BMIz-score remained unaffected. Complete-case analyses and analyses adjusted for household educational level, pubertal status and physical activity confirmed the results. In conclusion, the school meals did not affect the MetS score in 8–11-year-olds, as small improvements in blood pressure, TAG concentrations and insulin resistance were counterbalanced by slight undesired effects on waist circumference and HDL-cholesterol concentrations.


2021 ◽  
Author(s):  
Ranyao Yang ◽  
Yue Hu ◽  
Chi Ho Lee ◽  
Yan Liu ◽  
Candela Diaz-Canestro ◽  
...  

Objective: Peptidase M20 domain containing 1 (PM20D1), a secreted enzyme catalysing condensation of fatty acids and amino acids into the bioactive lipids N-acyl amino acids (NAAA), induces uncoupling protein 1 (UCP1)-independent adaptive thermogenesis in brown/beige adipocytes in mice. This study aimed to explore the associations of the circulating levels of PM20D1 and major NAAA with obesity-related metabolic complications in humans. Design and Methods: Serum concentrations of PM20D1 and NAAA (C18:1-Leu and C18:1-Phe) in 256 Chinese subjects, including 78 lean and 178 overweight/obese individuals with or without diabetes, were measured with immunoassays and liquid chromatography-mass spectrometry respectively. The impact of sulfonylurea and rosiglitazone on their circulating levels was examined in 62 patients with type 2 diabetes. Results: Serum PM20D1 level was significantly elevated in overweight/obese individuals, and was closely associated with circulating levels of C18:1-Leu and C18:1-Phe. Furthermore, serum PM20D1, C18:1-Leu and C18:1-Phe concentrations correlated positively with several parameters of adiposity as well as fasting and 2-h postprandial glucose, HbA1c, fasting insulin, and HOMA-IR independent of BMI and age. Moreover, a significant elevation in PM20D1, C18:1-Leu and C18:1-Phe concentrations corresponding with increases in the number of components of the metabolic syndrome (MetS) was observed. Treatment with sulfonylurea significantly decreased circulating PM20D1, C18:1-Leu and C18:1-Phe in patients with type 2 diabetes. Conclusions: Increased serum levels of PM20D1 and its catalytic products NAAA are closely associated with obesity-related glucose dysregulation, insulin resistance and MetS, and can be potentially used as clinical biomarkers for diagnosing and monitoring these disorders.


2021 ◽  
Vol 74 (10) ◽  
pp. 2510-2515
Author(s):  
Inna Diemieszczyk ◽  
Paulina Głuszyńska ◽  
Pawel Andrzej Wojciak ◽  
Jerzy Robert Ładny ◽  
Hady Razak Hady

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 attributed to disorders of the hypothalamic-pituitary-adrenal axis in the form of increased cortisol control, which may initiate the development of abdominal obesity, insulin resistance, hypertension and dyslipidemia. Aforementioned factors (environmental, hormonal and genetic) lead to excessive fat tissue gathering. The excess of abdominal fat tissue – abdominal obesity – leads to insulin resistance, the concentration of which causes body mass gain. Such mechanism is dangerous for our health and may lead to the occurrence of type 2 diabetes and premature development of atherosclerosis with all its consequences such as atherosclerotic cardiovascular diseases including coronary artery disease.


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