scispace - formally typeset
Search or ask a question

What is the role of epigenetics in the development of diabetes? 


Best insight from top research papers

Epigenetics 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 .

Answers from top 5 papers

More filters
Papers (5)Insight
Open accessBook ChapterDOI
31 Aug 2022
1 Citations
Epigenetic changes, such as DNA methylation, may contribute to the development of diabetes, particularly type 2 diabetes, by affecting the cells of the pancreatic islets of Langerhans.
Epigenetic modifications, such as DNA methylation and histone modifications, play a role in the development of type 2 diabetes and its long-term complications.
Epigenetics plays a role in the development of diabetes by explaining how environmental factors interact with an individual's genome to lead to diseases such as type 2 diabetes mellitus (T2DM).
Epigenetics plays an important role in the transmission of type 2 diabetes from one generation to another and is implicated in insulin resistance, impaired insulin secretion, and the development of complications.
Epigenetic modifications provide a potential association between environmental factors and altered gene expression that might cause diabetes phenotypes.

Related Questions

What is the role of DNA methylation in the development and progression of metabolic disorders?4 answersDNA methylation plays a crucial role in the development and progression of metabolic disorders. It is a mechanism of nutritional programming that regulates gene expression through the addition of a methyl group to DNA. Excessive nutrition in early life can lead to abnormal developmental planning of key metabolic organs, resulting in long-term obesity and metabolic disorders in offspring. Changes in DNA methylation have been strongly associated with the development of metabolic disorders such as diabetes and obesity. Methylation-induced silencing of diabetes/obesity-related genes may contribute to the pathogenesis of these diseases. Epigenetic alterations, including DNA methylation, can serve as prognostic markers and influence the risk of metabolic diseases later in life. They may also be passed on to future generations through transgenerational inheritance. Additionally, differential methylation within mitochondrial DNA has been linked to hepatic lipid accumulation and metabolic associated fatty liver disease (MAFLD), suggesting a role for DNA methylation in promoting mitochondrial dysfunction and impaired lipid metabolism.
What is the role of epigenetics in the development of cancer?4 answersEpigenetics plays a crucial role in the development of cancer. Mutations or abnormal expression of oncogenes and tumor suppressor genes are known to cause cancer, but recent studies have shown that epigenetic modifications are also key drivers of cancer development and progression. Epigenetic changes, such as DNA methylation and histone modifications, regulate gene expression without altering the primary DNA sequence. These changes can cooperate with genetic alterations to drive the cancer phenotype. The plasticity of cancer cell phenotypes is a result of stochastic changes in the epigenetic landscape, which can be quantitatively mapped onto phenotypic outcomes. Epigenetic dysregulation in the tumor microenvironment is also important, as it affects both cancer cells and non-cancer cells. Understanding the role of epigenetics in cancer development is crucial for the development of epigenetic drugs and the comprehensive treatment of cancer.
What is the role of epigenetics in neuroplasticity?5 answersEpigenetics plays a crucial role in neuroplasticity, which refers to the brain's ability to adapt and change in response to experiences and environmental stimuli. Epigenetic regulation involves modifications to the structure of DNA and its associated proteins, without altering the DNA sequence itself. These modifications can influence gene expression and ultimately impact neuronal plasticity. Epigenetic processes, such as DNA methylation, histone modifications, and chromatin remodeling, are involved in regulating the activity of genes related to plasticity and memory formation. Environmental factors and developmental cues can trigger changes in epigenetic marks, leading to the activation or silencing of specific gene programs in the brain. Dysregulation of epigenetic and transcriptional regulation has been implicated in various neuropsychiatric disorders, highlighting the importance of epigenetics in understanding the complex risk architecture of mental illness. Overall, epigenetics provides a mechanism through which the brain can dynamically adapt and respond to its environment, influencing neuroplasticity and potentially offering new therapeutic targets for brain disorders.
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.
Why is epigenetics important for health?5 answersEpigenetics is important for health because it influences gene expression without changing the DNA sequence, and altered epigenetic marks are common in cancer and developmental disorders. Epigenetic processes play a role in cardiovascular and metabolic diseases, and understanding them can lead to precision medicine and personalized healthcare. Epigenetic changes can occur throughout life and mediate cell differentiation and determination of cell fates. Epigenetic biomarkers are being used for early diagnosis, and drugs targeting epigenetic changes are being developed. Overall, epigenetics has the potential to revolutionize the approach to complex diseases, improve disease prevention and treatment strategies, and ultimately improve the lives of individuals affected by these conditions.
What isthe Role of epigenetics in diabetes?5 answersEpigenetics plays a significant role in diabetes. Epigenetic changes, such as DNA methylation and histone modifications, have been linked to the etiology of both type 1 diabetes (T1D) and type 2 diabetes (T2D). In T1D, epigenetic modifications have been associated with the pathogenesis of the disease, including the regulation of islet β cell death. In T2D, DNA methylation and histone modifications have been investigated in relation to glycemic traits and insulin resistance. However, consistent associations between epigenetic marks and diabetes have not been found, possibly due to challenges related to study design and tissue heterogeneity. Despite these challenges, epigenetics holds potential for predicting high-risk patients and disease prevention in diabetes. Further research is needed to better understand the interaction between genetic and non-genetic factors, including epigenetic effects, in the development and progression of diabetes.

See what other people are reading

What are the changes in histone H3.3 content with age in terminally differentiated tissues?
4 answers
The histone variant H3.3 plays a crucial role in the maintenance and regulation of chromatin structure in terminally differentiated tissues, with its content and modification patterns undergoing significant changes with age. Studies have shown that H3.3 accumulates to near saturation levels in the chromatin of various mouse somatic tissues by late adulthood, indicating a profound shift in the chromatin landscape that is associated with aging. This accumulation is not uniform across all tissues or cell types; for instance, in the epidermis, distinct chromatin states correlated with cellular differentiation are maintained into adulthood, but aging is accompanied by alterations in histone modification patterns, such as reduced levels of H4K16ac in aged basal epidermis. The dynamics of H3.3 deposition and its impact on chromatin accessibility and gene expression are complex. While H3.3 is traditionally associated with active chromatin, its accumulation in slowly replicating cells over time could potentially lead to aberrant effects on heterochromatin, suggesting a nuanced role in the regulation of gene expression and chromatin structure that may contribute to the aging process. Furthermore, the specific methylation patterns on H3.3, such as H3.3K27me3, have been shown to play distinct roles in regulating gene expression during differentiation and aging, highlighting the importance of understanding the effects of post-translational modifications not only on canonical histones but also on histone variants like H3.3. Interestingly, the expression of H3.3 and its ratio to other histone variants, such as in oral squamous cell carcinoma and oral leukoplakia, suggests that changes in H3.3 content and its modification landscape could be indicative of broader chromatin and epigenetic alterations associated with aging and disease. These findings underscore the critical role of H3.3 in maintaining chromatin integrity and function in terminally differentiated tissues and highlight the complex interplay between histone variants, chromatin modifications, and aging.
Amyloid Cascade Hypothesis as the primary model of Alzheimer's disease pathogenesis.
4 answers
The Amyloid Cascade Hypothesis (ACH) has been a prominent model in Alzheimer's disease (AD) pathogenesis, suggesting that abnormal protein aggregation, particularly of β-amyloid (Aβ), initiates a cascade leading to neurodegeneration. However, recent studies propose a more complex etiology, indicating that Aβ and amyloid might play a minor role in AD development, with multiple pathogenic factors contributing to the disease. While the ACH remains widely studied, other hypotheses like Tau hyperphosphorylation, neuroinflammation, oxidative stress, and vascular factors are gaining support. Clinical trials targeting Aβ have shown uncertain cognitive effects, prompting a shift towards multi-factor disease models for more effective treatment strategies. The ACH, although significant, may not fully encompass the intricate mechanisms underlying AD pathogenesis.
What are the most effective treatments for leptine resistance?
5 answers
Effective treatments for leptin resistance include the internal administration of leptin sensitizers or their derivatives. Various natural treatments, leptin replacement therapy, testosterone replacement therapy, and insulin-sensitizing drugs are utilized, albeit with limited success. Recent research suggests that reducing circulating leptin levels through approaches like CRISPR-Cas9-based leptin depletion, partial leptin deficiency, or neutralizing leptin-specific antibodies can sensitize the body to leptin, leading to improved metabolic parameters and resistance to weight gain induced by a high-fat diet. Additionally, compounds like those of formula (I) have been developed to improve leptin resistance, potentially treating metabolic disorders, obesity, hyperphagia, steatosis, diabetes, and dyslipidemia. Further studies are needed to determine the full effectiveness of these treatments in combating leptin resistance.
What are the current research studies exploring the potential causes of cervical cancer?
5 answers
Current research studies on cervical cancer explore various potential causes. Human papillomavirus (HPV) infection is a major contributor to cervical cancer development. Additionally, epigenetic modifications, including DNA methylation, histone modification, noncoding RNA regulation, and chromatin regulation, play a crucial role in the occurrence and progression of cervical cancer. Factors such as long-term use of oral contraceptives, age of marriage, parity, and exposure to cigarette smoke have also been linked to an increased risk of cervical cancer. Furthermore, genetics, smoking, and HPV infection are highlighted as key factors influencing the etiology of cervical cancer, emphasizing the importance of prevention measures like HPV vaccination and early screening methods such as Pap smears. Ultrasound-based quantitative analysis of cervical tissues shows promise as a non-invasive diagnostic tool for cervical cancer.
Pathogenesis of epilepsy?
5 answers
The pathogenesis of epilepsy involves various factors such as abnormal ion channels, neurotransmitters, genetic mutations like PCDH-19, and environmental triggers like brain injuries. Imbalances between inhibition and excitation at the molecular level, leading to changes in cell excitability, are considered key mechanisms in epilepsy. The abnormal discharge of brain neurons due to genetic or environmental factors can result in recurrent seizures, characterizing epilepsy. The Wnt/β‐catenin signaling pathway is highlighted as a potential target for epilepsy treatment. The International League Against Epilepsy (ILAE) has classified epilepsy into six etiologic categories, emphasizing the complexity and heterogeneity of the disorder. Understanding these diverse factors is crucial for effective diagnosis and treatment of epilepsy.
What is known about the G34W mutation of histone H3?
10 answers
The G34W mutation of histone H3, specifically in the context of Giant Cell Tumor of Bone (GCTB), has been identified as a significant marker for diagnosing GCTB, distinguishing it from other bone tumors. This mutation is expressed in the nuclei of mononuclear stromal cells but not in osteoclast-like giant cells, with a specificity of 100% and a sensitivity of 77.8% for GCTB, indicating its potential as a diagnostic tool. The mutation acts as a mutated driver gene in GCTB within the Indonesian population, suggesting its utility in differentiating GCTB from mimics. Research has shown that G34W and other G34 mutations in histone H3.3, such as G34R/V, have distinct effects on the epigenome and genomic stability. These mutations differentially affect H3K36 modifications, subtelomeric silencing, and DNA repair, demonstrating the complexity of their impact even at a single residue level. Specifically, G34W mutations in giant cell tumors of bone alter the enhancer chromatin landscape of mesenchymal stem cells, impeding methylation at lysine 36 on histone H3 (H3K36) and promoting an aberrant gain of PRC2-mediated H3K27me2/3 at active enhancers. Furthermore, G34 mutations, including G34W, disrupt the epigenome by altering H3K36 modifications, potentially leading to genomic instability and dysregulated gene expression patterns. These mutations are associated with massive epigenetic alterations, affecting DNA methylation, chromatin accessibility, and histone modification levels, which can influence genomic instability and the osteolytic phenotype of GCTB. Additionally, G34W-mutated bone tumors exhibit specific methylomic effects, suggesting that these mutations exert characteristic epigenomic roles regardless of the tumor tissue-of-origin. In summary, the G34W mutation of histone H3 plays a critical role in the pathogenesis and diagnosis of GCTB, with significant implications for understanding its molecular mechanisms and developing targeted therapies.
How do healthcare professionals diagnose polycystic ovary syndrome (PCOS) and type 2 diabetes simultaneously?
6 answers
Healthcare professionals diagnose polycystic ovary syndrome (PCOS) and type 2 diabetes (T2D) simultaneously through a combination of clinical assessments, laboratory tests, and consideration of diagnostic criteria, while also navigating the complexities and uncertainties inherent in diagnosing these conditions. For PCOS, the diagnosis is often based on the Rotterdam criteria, which require two out of three of the following: irregular menstrual cycles, hyperandrogenism, and polycystic ovary morphology, as identified through electronic medical records and natural language processing to capture a more specific cohort of PCOS subjects. However, the diagnosis of PCOS is complicated by its heterogeneous presentation and the need for differential diagnosis of androgen excess, requiring careful clinical judgment and possibly additional blood testing or imaging techniques. Type 2 diabetes diagnosis in PCOS patients involves assessing glycemic status, with the oral glucose tolerance test (OGTT) being the gold standard for diagnosing T2D. This is particularly important in PCOS due to the high risk of insulin resistance and T2D in these patients. The OGTT is more effective than fasting plasma glucose (FPG) alone in detecting dysglycemia in women with PCOS, as relying solely on FPG can miss a significant proportion of dysglycemia cases. Clinicians face challenges in diagnosing these conditions due to the variability in diagnostic criteria used, the limitations of current evidence, and the risk of both under- and overdiagnosis. Despite these challenges, early diagnosis is crucial for managing both PCOS and T2D effectively, allowing for earlier intervention and potentially better outcomes. Moreover, recent advancements in biosensing technologies for disease detection highlight the potential for simultaneous sensing of multiple biomarkers, which could improve the diagnosis and management of complex conditions like PCOS and T2D. Additionally, miRNA profiling has emerged as a promising tool for the accurate diagnosis of PCOS, potentially distinguishing it from conditions with overlapping clinical presentations like obesity. However, the application of diagnostic criteria varies significantly among healthcare professionals, underscoring the need for standardized diagnostic approaches and training to improve care quality for patients with PCOS.
What is the role of tau protein in diabetes associated neurodegeneration?
5 answers
The tau protein plays a crucial role in diabetes-associated neurodegeneration by being hyperphosphorylated, leading to cognitive impairment and neurofibrillary tangle formation. In conditions like diabetes mellitus (DM), dysfunction of insulin signaling can enhance tau phosphorylation, contributing to the accumulation of neurofibrillary tangles, a hallmark of Alzheimer's disease (AD) pathology. Hyperphosphorylated tau protein, particularly at specific phosphosites, exacerbates behavioral deficits in AD under diabetic conditions like obesity and hyperinsulinemia. Tau protein abnormalities are central to neurodegeneration, with the accumulation of pathogenic forms like cis phosphorylated tau being implicated in neuronal loss during DM. Understanding the link between tau protein and diabetes is crucial for developing potential therapeutic strategies to mitigate neurodegenerative processes in diabetic conditions.
How APOE4 influence the development of atherosclerosis?
10 answers
The influence of Apolipoprotein E4 (APOE4) on the development of atherosclerosis is multifaceted, involving genetic predispositions, lipid metabolism alterations, and inflammatory processes. APOE4 is an established risk factor for atherosclerosis, with its structural components, particularly domain interaction, mediating proatherogenic effects partly by modulating lipoprotein metabolism and macrophage biology. This is further supported by studies showing that APOE4 carriers have significantly elevated ApoB and ApoB/ApoA ratios and decreased ApoE levels compared to ε2 carriers among Carotid Atherosclerosis (CAS) patients, indicating a direct link between APOE4 and lipid profile alterations conducive to atherosclerosis development. Moreover, the interaction between metabolic profiles and APOE4 genotype significantly impacts subclinical atherosclerosis, particularly in postmenopausal women. APOE4 carriers with a poor metabolic phenotype exhibit the highest common carotid intima-media thickness (CIMT), a marker of atherosclerosis, compared to those without the poor metabolic profile and non-APOE4 carriers. This suggests that APOE4's influence on atherosclerosis is exacerbated by adverse metabolic conditions. Additionally, computational and structural studies have revealed that the cysteine/arginine change at position 112 in APOE isoforms results in structural differences that affect ligand binding affinities, which could influence APOE4's role in cholesterol metabolism and its contribution to coronary artery disease (CAD) pathogenesis. This indicates a molecular basis for APOE4's involvement in atherosclerosis through altered lipid transport and metabolism. In summary, APOE4 contributes to the development of atherosclerosis through its influence on lipid metabolism, inflammatory processes, and genetic predispositions. Its interaction with metabolic factors and structural properties underscores the complex role APOE4 plays in atherogenesis, highlighting the importance of considering genetic and metabolic profiles in the management and treatment of atherosclerosis.
Is the fatty acid metabolism modified in IBD? iS IT UPREGULTAED OR DOWNREGULATED?
5 answers
Fatty acid metabolism in inflammatory bowel disease (IBD) shows alterations, with both upregulated and downregulated aspects. Research indicates that patients with Crohn's disease (CD) exhibit decreased levels of various polyunsaturated fatty acids (PUFAs). Conversely, in ulcerative colitis (UC), some PUFAs like arachidonic acid (AA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) are downregulated. Moreover, induction therapies like prednisone and tofacitinib can lead to significant increases in serum lipid levels, including total cholesterol, high-density lipoprotein cholesterol (HDL-c), and low-density lipoprotein cholesterol (LDL-c). These findings suggest a complex interplay of fatty acid metabolism in IBD, with variations depending on the specific type of IBD, disease activity, and treatment regimens.
What is the effect of purslane powder on human health and well-being?
4 answers
Purslane powder has shown various beneficial effects on human health. Studies have indicated that purslane supplementation can lead to reductions in triglycerides, total cholesterol, and LDL cholesterol levels. Additionally, it has been found to significantly decrease fasting blood sugar levels and oxidative stress markers while increasing total antioxidant capacity. Purslane powder is rich in proteins, fats, vitamins, minerals, and dietary fiber, making it a valuable component for functional bakery products. Furthermore, purslane supplementation has been linked to a decrease in C-reactive protein levels, indicating anti-inflammatory properties. Overall, incorporating purslane powder into the diet may contribute positively to human health by improving lipid profiles, glycemic control, antioxidant status, and inflammatory markers.