scispace - formally typeset
Search or ask a question

How does epigenetic affects metabolic syndrome? 

Best insight from top research papers

Epigenetic modifications play a crucial role in the development and progression of metabolic syndrome. These modifications can regulate gene expression, chromatin compaction, and DNA repair, thereby impacting the function of adipose tissue (AT) and metabolic pathways involved in obesity and metabolic disorders . The prenatal environment, aging, and lifestyle factors such as diet and physical activity can induce long-lasting epigenetic alterations that influence the risk of metabolic diseases later in life . Epigenetic changes in AT can lead to disturbances in its function, contributing to the onset of obesity and related metabolic disorders . Additionally, dietary factors can significantly affect epigenetic modifications and gene-diet interactions, which are important in the initiation and progression of metabolic syndrome . Understanding the role of epigenetics in metabolic syndrome can provide insights into the underlying mechanisms and potentially lead to the development of targeted therapeutic interventions .

Answers from top 5 papers

More filters
Papers (5)Insight
Epigenetic modifications by dietary factors can significantly affect genome stability and the expression of mRNA and proteins involved in metabolic dysfunction, contributing to the development and progression of metabolic syndrome.
Open accessJournal ArticleDOI
Caryn Carson, Heather A. Lawson 
31 Citations
Epigenetic factors play a role in the development of metabolic syndrome, as evidenced by studies investigating epigenetic changes in obesity, Type II diabetes, and cardiovascular disease.
Epigenetic deregulation in metabolic pathways may explain disturbances in epigenetic marks of adipose tissue in obesity and metabolic syndrome. This could lead to new therapeutic approaches based on epigenetic strategies.
Epigenetic events, such as DNA methylation, histone modifications, and microRNAs, play a crucial role in regulating adipocyte differentiation and can influence the development of metabolic syndrome.
Book ChapterDOI
01 Jan 2023
Epigenetic alterations, influenced by factors such as aging, lifestyle, and prenatal environment, may serve as prognostic markers and influence the risk of metabolic diseases later in life. These alterations can also be passed on to future generations through transgenerational inheritance.

Related Questions

What are the molecular pathways involved in the development of metabolic syndrome?5 answersThe development of metabolic syndrome involves intricate molecular pathways. Adipose tissue inflammation, triggered by factors like saturated fatty acids, plays a pivotal role in the pathogenesis of metabolic syndrome. Insulin resistance, a key component of metabolic syndrome, is linked to pro-inflammatory cytokines like TNF-α and IL-6, which disrupt insulin signaling and glucose transport. Additionally, the serotonin system and tryptophan hydroxylase-2 in the CNS are implicated in regulating feeding behavior and energy balance, contributing to metabolic syndrome development. Furthermore, dysregulation in post-transcriptional gene regulatory mechanisms involving noncoding RNAs and RNA-binding proteins can lead to metabolic syndrome by affecting glucose and lipid metabolic pathways. Understanding these molecular pathways is crucial for developing targeted therapies for metabolic syndrome.
What are the risk factors associated with metabolic syndrome?5 answersMetabolic syndrome is associated with various risk factors including obesity, high blood pressure, hyperglycemia, and dyslipidemia. These risk factors play a crucial role in the development and diagnosis of metabolic syndrome. Lifestyle factors such as smoking, sedentary behavior, poor dietary habits, and alcohol consumption can also increase the risk of metabolic syndrome. Additionally, factors like central obesity, elevated blood pressure, impaired glucose tolerance, and dyslipidemia are key components of metabolic syndrome. Studies have shown that high blood sugar, high blood pressure, high body mass index, and hypertriglyceridemia are common risk factors associated with metabolic syndrome, emphasizing the importance of preventive measures and public awareness programs. These findings highlight the significance of addressing these risk factors to reduce the prevalence and impact of metabolic syndrome.
Can epigenetic nutrition modify gene expression and improve health outcomes?5 answersEpigenetic nutrition can modify gene expression and improve health outcomes. Epigenetic modifications, such as DNA methylation and histone modifications, can be influenced by factors like diet and lifestyle habits. Nutritional intake during key developmental windows in early life, both from the maternal and paternal diet, can induce epigenetic changes in offspring that can persist throughout life and influence disease susceptibility. Nutrients in the diet can act as substrates for writing epigenetic marks and modulate the activity of epigenetic enzymes. Understanding the relationship between epigenetic interactions and diet is crucial for gene regulation and the prevention of diseases like obesity, diabetes, aging, and cancer. Nutrition can directly influence the chromatin landscape and gene expression through epigenetic regulation, even after the nutritional exposure has ended. Therefore, personalized nutrition strategies that target specific beneficial health effects through epigenetic modifications have the potential to improve long-term health outcomes.
What is the role of epigenetics in the development of diabetes?5 answersEpigenetics plays a crucial role in the development of diabetes. It is involved in the transmission of type 2 diabetes mellitus (T2DM) from one generation to another. Epigenetic changes are implicated in the two main pathogenic components of T2DM, namely insulin resistance and impaired insulin secretion. Hyperglycemia-induced permanent epigenetic modifications of DNA expression contribute to the phenomenon of metabolic memory in T2DM. Epigenetics also influences the development of micro- and macrovascular complications of T2DM and can be used as biomarkers for predicting these complications. Furthermore, epigenetic modifications have been observed in chronic complications of T2DM, such as diabetic nephropathy, retinopathy, and neuropathy. Understanding epigenetic changes in diabetes has led to the development of new therapeutic targets and drugs, such as apabetalone, which acts on epigenetic readers to prevent cardiovascular events in T2DM patients. Overall, epigenetics plays a significant role in the risks, pathogenesis, complications, and therapeutic evolution of diabetes.
How can epigenetic therapies be used to treat diseases?4 answersEpigenetic therapies can be used to treat diseases by targeting the chemical modifications of DNA and its associated proteins that influence gene expression. These therapies have the potential to reverse epigenetic modifications and provide new therapeutic avenues for various diseases, including cardiovascular disease, cancer, neurodevelopmental disorders, neurodegenerative disorders, and pulmonary hypertension. Epigenetic drugs, such as inhibitors of DNA methyltransferases, histone deacetylases, and histone methyltransferases, can modify aberrant DNA methylation and histone acetylation or methylation, which play important roles in gene regulation and various DNA processes. In the context of neurodegenerative diseases, epigenetic mechanisms have emerged as important factors, and targeting these mechanisms holds promise for the development of novel treatment strategies. However, it is important to conduct rigorous studies to minimize the risks associated with epigenetic therapies and ensure their safety and effectiveness in improving human health.
What is the pathophysiology behind metabolic syndrome?5 answersThe pathophysiology of metabolic syndrome involves a combination of factors such as insulin resistance, dyslipidemia, central obesity, and systemic hypertension. Metabolic syndrome is associated with a pro-inflammatory and pro-thrombotic state, characterized by increased activity of pro-thrombotic and inflammatory markers. Endothelial dysfunction, specifically related to endoplasmic reticulum stress and unfolded protein response development, plays a role in the emergence of metabolic syndrome. Sedentary lifestyles and unbalanced dietary patterns are also believed to contribute to the development of metabolic syndrome. Hypertension is a key component of metabolic syndrome, and the pathogenesis of hypertension in metabolic syndrome is not fully understood, but it may be influenced by increased caloric intake, decreased physical activity, and the consumption of sugars, particularly fructose and sucrose.

See what other people are reading

Which are the most important changes in plants as a result of climate change?
5 answers
Climate change induces various significant changes in plants, impacting their physiology and productivity. The elevated CO2 levels, water stress, extreme temperatures, and stress combinations negatively affect plant growth. These changes lead to alterations in plant physiology, reduced photosynthetic capacity, and metabolic responses to mitigate stress effects. Additionally, climate change affects the quality and yield of vegetable crops, leading to crop failures, low yields, and increased pest and disease issues. Furthermore, plants experience genome-wide epigenetic alterations in response to environmental stresses, influencing gene expression and phenotypic plasticity. High temperatures impact xylem and phloem formation, root growth, and nutrient uptake, affecting crop yield and quality. Overall, climate change poses a serious threat to plant health, productivity, and food supply, necessitating the development of stress-resilient crops.
What is the dominant species and carbon of triglyceride in mouse model?
5 answers
The dominant species of triglyceride in mouse models varies based on the study. In the FLS (fatty liver Shionogi) mouse model, preα-lipoprotein was the predominant lipoprotein class, indicating a unique hypertriglyceridemia phenotype. In another study using C57BL/6J mice, a structured lipid with medium- and long-chain triacylglycerols (MLCTs) was synthesized, showing changes in major triacylglyceride species after enzymatic interesterification. Additionally, in a study on homocysteinemia/homocystinuria mouse models, hepatic levels of various triacylglycerol species were analyzed, showing significant differences in lipid components between fatty and non-fatty livers. These findings highlight the diversity of triglyceride species in different mouse models, emphasizing the importance of understanding lipid metabolism in various physiological conditions.
How does metabolism affect the expression of microRNAs in macrophages?
5 answers
Metabolism significantly influences the expression of microRNAs in macrophages. Studies have shown that macrophages adjust their metabolic programs to regulate gene expression and inflammatory responses, with microRNAs playing a crucial role in this process. In conditions like obesity, oxidative stress triggers dysregulation of signaling pathways, altering the expression of various microRNAs in organs involved in glucose and lipid metabolism regulation. Specifically, miR-210 induction in activated macrophages supports a switch towards a proinflammatory state by modulating metabolism, favoring glycolysis over mitochondrial respiration, partly through downregulating the ISCU enzyme. Additionally, obesity influences adipose tissue miRNAs in a cell-specific manner, with macrophage miR-155 potentially impacting neighboring adipocytes, showcasing the intricate relationship between metabolism, microRNAs, and macrophages.
Cancer biomaker and toxicogenomics
5 answers
Cancer biomarkers play a crucial role in cancer pharmacogenomics, aiding in the identification of genetic alterations that influence drug response and toxicity. Toxicogenomics, on the other hand, focuses on genetic-environmental interactions in carcinogenesis and the detection of genetic aberrations in cancer genomes. Advances in genomics have revolutionized cancer research, enabling the development of high-throughput technologies for gene expression profiling and genotyping. These technologies help elucidate how genetic variations and cellular responses to various factors contribute to complex diseases like cancer. By integrating genomics into medical practice, the era of cancer therapy has shifted towards precision medicine, allowing for tailored treatments based on individual genetic profiles. This integration also aids in predicting toxicity, disease outcomes, and identifying genetically susceptible individuals.
What are the effects of FoxO3 proteins in adipocytes?
5 answers
FoxO3 proteins play crucial roles in adipocytes by regulating lipid accumulation, inflammation, and autophagy. In adipocytes, FoxO3a promotes lipid accumulation and inflammation by targeting autophagy, as evidenced by studies on obese mouse models and 3T3-L1 adipocytes. Additionally, FoxO3 is involved in adipogenic differentiation of human adipose-derived stem cells, where it interacts with reactive oxygen species (ROS) to promote adipogenesis while maintaining redox homeostasis. Furthermore, FoxO3 is linked to longevity and is a key regulator of protein turnover in skeletal muscle, impacting cell survival and death processes. The transcriptional regulation of FoxO3 is complex, involving glucocorticoid receptor activation and AMP-activated protein kinase stimulation, highlighting its role as a metabolic stress sensor in coordinating gene expression based on cellular energy status.
Can oxytocin administration increase inflammation?
5 answers
Oxytocin administration has shown anti-inflammatory effects in various studies. Research indicates that oxytocin can reduce inflammation by decreasing cytokine levels, inhibiting leukocyte accumulation, and diminishing markers of systemic inflammation. In murine models of obesity, chronic oxytocin treatment led to a reduction in adipose tissue inflammation and systemic inflammation markers. Additionally, in an air pouch model of inflammation, oxytocin significantly decreased exudate volume, leukocyte accumulation, and angiogenesis, showcasing its anti-inflammatory properties. Moreover, in adult male rats, oxytocin administration decreased proinflammatory responses, oxidative stress, and atherosclerosis progression by upregulating oxytocin receptors and reducing inflammatory markers. These findings collectively suggest that oxytocin administration can actually decrease inflammation through various mechanisms.
How does seabuckthorn help hair care?
5 answers
Sea buckthorn, rich in bioactive compounds like vitamins, amino acids, and fatty acids, offers significant benefits for hair care. Sea buckthorn oil, derived from its berries, is particularly valuable for cosmeceutical formulations due to its wound healing properties and balanced content of fatty acids, carotenoids, and vitamins. The plant's various parts contain essential nutrients like flavonoids, terpenoids, and phenolic acids, which contribute to its antimicrobial properties and potential in managing dermatological conditions. These components make sea buckthorn beneficial for promoting hair health by nourishing the scalp, improving hair texture, and potentially aiding in conditions like dandruff or scalp irritation. Incorporating sea buckthorn oil or extracts in hair care products can enhance overall hair quality and scalp health.
How is multiomics technique actionable in precirin medicine?
5 answers
Multiomics techniques play a crucial role in advancing precision medicine by integrating various omics levels like genomics, transcriptomics, epigenomics, proteomics, and metabolomics to understand the complex phenotypic heterogeneity of cardiovascular diseases (CVD). These techniques enable the linkage of an individual's unique omics profile with phenotypic data, aiding in disease diagnosis, subtyping, and prediction. By leveraging machine learning and deep learning-based approaches, multiomics data can be harmonized with phenotype data to extract valuable biological insights and develop personalized therapeutic strategies for diverse populations. This integration of multiomics data with clinical information enhances the ability to predict predisposition, diagnostic markers, prognostic indicators, and personalized treatment paths, ultimately driving the implementation of precision medicine in routine medical practice.
What are the potential benefits of integrating multiomics data in clinical decision-making processes for precision medicine?
4 answers
Integrating multiomics data in clinical decision-making processes for precision medicine offers numerous benefits. It enables a comprehensive understanding of diseases by analyzing various omics levels, linking an individual's unique omics profile with phenotypic data for precise diagnosis, personalized treatment, and disease prediction. This integration allows for the identification of key components, interactions, and emerging patterns using advanced analytical models and computational tools, enhancing the accuracy of patient care pathways in complex diseases like cancer or diabetes. By leveraging multiomics technologies and network medicine approaches, healthcare professionals can uncover associations between genetic variations, environmental factors, and disease outcomes, leading to improved patient outcomes, reduced costs, and accelerated drug discovery.
What is the elimination time of roflumilast in mice?
10 answers
The elimination time of roflumilast in mice, or its half-life, is not directly provided in the contexts of the research papers summarized above. However, insights into roflumilast's pharmacokinetics, effects, and mechanisms of action in various models can be gleaned from the provided abstracts, which indirectly inform about its metabolism and potential elimination characteristics in mice or other studied organisms. Roflumilast, a phosphodiesterase-4 (PDE4) inhibitor, has been extensively studied for its effects on cognitive functions, metabolic effects, and potential therapeutic applications in conditions such as Alzheimer's disease, sleep deprivation-induced cognitive dysfunction, obesity, alcohol use disorders, tuberculosis, cystic fibrosis, and chronic obstructive pulmonary disease (COPD). These studies have demonstrated roflumilast's ability to enhance cAMP signaling, improve memory and cognitive functions, reduce body weight and adipogenesis, decrease ethanol intake and preference, and exhibit anti-inflammatory properties. While the specific elimination time in mice is not mentioned, the pharmacokinetics of roflumilast in humans, including its peak plasma concentration, volume of distribution, and elimination half-life, have been characterized. In humans, roflumilast shows a mean elimination half-life of approximately 15.70 hours, with its active metabolite, roflumilast N-oxide, having a slightly longer half-life. Although these parameters are specific to humans, they provide a basis for understanding roflumilast's metabolic processing and potential elimination timeline in mammals. Given the absence of direct data on the elimination time of roflumilast in mice within the provided contexts, one can infer that its pharmacokinetic profile would need to be extrapolated from human data or directly studied in mice to obtain accurate elimination times. The research underscores roflumilast's broad therapeutic potential and its complex metabolic and pharmacokinetic profile across different species and conditions.
Does lecithin induce differentiation?
4 answers
Lecithin has been found to induce differentiation in various contexts. In adipogenesis and lipogenesis studies, lecithin was shown to promote adipocyte differentiation, increase triglycerides, and induce lipid accumulation in cells. Additionally, low concentrations of lecithin were found to upregulate genes associated with osteogenesis in mesenchymal stem cells, indicating a potential role in bone tissue engineering. Moreover, lecithin supplementation in diabetic rats led to morphological changes and enhanced macrophage functions, suggesting an immunomodulatory effect through modified production of lipid mediators. These findings collectively support the notion that lecithin can indeed induce differentiation processes in various cell types, highlighting its potential impact on cellular functions and tissue development.