Epigenetics regulates gene expression and has been confirmed to play a critical role in a variety of metabolic diseases, such as diabetes, obesity, non-alcoholic fatty liver disease (NAFLD), osteoporosis, gout, hyperthyroidism, hypothyroidism and others. The term 'epigenetics' was firstly proposed in 1942 and with the development of technologies, the exploration of epigenetics has made great progresses. There are four main epigenetic mechanisms, including DNA methylation, histone modification, chromatin remodelling, and noncoding RNA (ncRNA), which exert different effects on metabolic diseases. Genetic and non-genetic factors, including ageing, diet, and exercise, interact with epigenetics and jointly affect the formation of a phenotype. Understanding epigenetics could be applied to diagnosing and treating metabolic diseases in the clinic, including epigenetic biomarkers, epigenetic drugs, and epigenetic editing. In this review, we introduce the brief history of epigenetics as well as the milestone events since the proposal of the term 'epigenetics'. Moreover, we summarise the research methods of epigenetics and introduce four main general mechanisms of epigenetic modulation. Furthermore, we summarise epigenetic mechanisms in metabolic diseases and introduce the interaction between epigenetics and genetic or non-genetic factors. Finally, we introduce the clinical trials and applications of epigenetics in metabolic diseases. 

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Epigenetic regulation in metabolic diseases: mechanisms and advances in clinical study

Ageing - Oxidative stress, PTMs and disease.

The French Society of Anesthesiology and Intensive Care Medicine [Société Française d'Anesthésie et de Réanimation (SFAR)] aimed at providing guidelines for the implementation of perioperative optimization programs.A consensus committee of 29 experts from the SFAR was convened. A formal conflict-of-interest policy was developed at the outset of the process and enforced throughout. The entire guidelines process was conducted independently of any industry funding. The authors were advised to follow the principles of the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system to guide assessment of quality of evidence.Four fields were defined: 1) Generalities on perioperative optimization programs; 2) Preoperative measures; 3) Intraoperative measures and; 4) Postoperative measures. For each field, the objective of the recommendations was to answer a number of questions formulated according to the PICO model (population, intervention, comparison, and outcomes). Based on these questions, an extensive bibliographic search was carried out using predefined keywords according to PRISMA guidelines and analyzed using the GRADE® methodology. The recommendations were formulated according to the GRADE® methodology and then voted on by all the experts according to the GRADE grid method. As the GRADE® methodology could have been fully applied for the vast majority of questions, the recommendations were formulated using a "formalized expert recommendations" format.The experts' work on synthesis and application of the GRADE® method resulted in 30 recommendations. Among the formalized recommendations, 19 were found to have a high level of evidence (GRADE 1±) and ten a low level of evidence (GRADE 2±). For one recommendation, the GRADE methodology could not be fully applied, resulting in an expert opinion. Two questions did not find any response in the literature. After two rounds of rating and several amendments, strong agreement was reached for all the recommendations.Strong agreement among the experts was obtained to provide 30 recommendations for the elaboration and/or implementation of perioperative optimization programs in the highest number of surgical fields. 

Perioperative optimization protocol for the adult patient 2023.

To provide an update of the recent evidence on the potential of perioperative nutritional interventions to benefit adult patients undergoing head and neck and digestive procedures.Perioperative nutrition within multimodal prehabilitation programs improve postoperative outcomes. Perioperative fasting time can be reduced with beverages containing carbohydrate alone or blended with a nitrogenous source such as whey protein; this approach seems to be safe and improve outcome. The choice of protein-containing formula, as well as diet composition to be recommended early during the postoperative refeeding, can be optimized to reduce complications. Sarcopenia is an important risk factor for surgical patients, as such, prehabilitation along with preoperative nutrition is strongly advised. Perioperative supplementation with β-hydroxy β-methylbutyrate to mitigate sarcopenia requires further investigation. Although perioperative nutritional interventions reduce healthcare costs, recent data suggest it has been scarcely prescribed.Nutritional intervention is key in multimodal programs of enhanced recovery after surgery to ensure better outcomes. Perioperative fasting should be shortened, and include clear fluids containing carbohydrates and protein, especially in the early postoperative period. Multimodal prehabilitation is key to mitigate sarcopenia. Action to improve knowledge on the cost-effectiveness of nutritional interventions in the perioperative setting are needed. 

Extending the benefit of nutrition intervention beyond the operative setting

Abstract The interplay between genetic alterations and metabolic dysregulation is increasingly recognized as a pivotal axis in cancer pathogenesis. Both elements are mutually reinforcing, thereby expediting the ontogeny and progression of malignant neoplasms. Intriguingly, recent findings have highlighted the translocation of metabolites and metabolic enzymes from the cytoplasm into the nuclear compartment, where they appear to be intimately associated with tumor cell proliferation. Despite these advancements, significant gaps persist in our understanding of their specific roles within the nuclear milieu, their modulatory effects on gene transcription and cellular proliferation, and the intricacies of their coordination with the genomic landscape. In this comprehensive review, we endeavor to elucidate the regulatory landscape of metabolic signaling within the nuclear domain, namely nuclear metabolic signaling involving metabolites and metabolic enzymes. We explore the roles and molecular mechanisms through which metabolic flux and enzymatic activity impact critical nuclear processes, including epigenetic modulation, DNA damage repair, and gene expression regulation. In conclusion, we underscore the paramount significance of nuclear metabolic signaling in cancer biology and enumerate potential therapeutic targets, associated pharmacological interventions, and implications for clinical applications. Importantly, these emergent findings not only augment our conceptual understanding of tumoral metabolism but also herald the potential for innovative therapeutic paradigms targeting the metabolism–genome transcriptional axis. 

Potential therapies targeting nuclear metabolic regulation in cancer

Background and purpose Obesity is becoming a major global health issue and is mainly induced by the accumulation of adipose tissues mediated by adipogenesis, which is reported to be regulated by peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT enhancer-binding protein α (C/EBPα). Trichostatin A (TSA) is a novel histone deacetylase inhibitor (HDACI) that was recently reported to exert multiple pharmacological functions. The present study will investigate the inhibitory effect of TSA on adipogenesis, as well as the underlying mechanism. Methods The adipogenesis of 3T3-L1 cells was induced by stimulation with a differentiation cocktail (DMI) medium for 8 days. MTT assay was used to measure the cell viability and Oil Red O staining was used to evaluate the adipogenesis of 3T3-L1 cells. The total level of triglyceride and released glycerol were detected to evaluate the lipolysis during 3T3-L1 adipogenesis. The expression levels of Leptin, fatty acid-binding protein 4 (FABP4), and sterol regulatory element-binding protein (SREBP1C) were determined by qRT-PCR. qRT-PCR assay was utilized to detect the expression levels of PPARγ and C/EBPα in 3T3-L1 cells. A high-fat diet (HFD) was used to construct an obese mice model, followed by the treatment with TSA. HE staining was conducted to evaluate the pathological state of adipose tissues. Body weights and the weights of adipose tissues were recorded to evaluate the anti-obesity property of TSA. Results Firstly, the promoted lipid accumulation induced by DMI incubation was significantly reversed by the treatment with TSA in a dose-dependent manner. The elevated expression levels of Leptin, FABP4, SREBP1C, PPARγ, and C/EBPα induced by the stimulation with DMI incubation were dramatically inhibited by the introduction of TSA, accompanied by the upregulation of phosphorylated AMP-activated protein kinase (p-AMPK). Secondly, the inhibitory effect of TSA against the expression level of PPARγ and lipid accumulation was greatly abolished by an AMPK inhibitor. Lastly, the increased body weights and visceral adipocyte tissue weight, as well as the enlarged size of adipocytes induced by HFD were pronouncedly reversed by the administration of TSA. Conclusion TSA inhibited adipogenesis in 3T3-L1 preadipocytes by activating the AMPK pathway. Background and purpose Obesity is becoming a major global health issue and is mainly induced by the accumulation of adipose tissues mediated by adipogenesis, which is reported to be regulated by peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT enhancer-binding protein α (C/EBPα). Trichostatin A (TSA) is a novel histone deacetylase inhibitor (HDACI) that was recently reported to exert multiple pharmacological functions. The present study will investigate the inhibitory effect of TSA on adipogenesis, as well as the underlying mechanism. Methods The adipogenesis of 3T3-L1 cells was induced by stimulation with a differentiation cocktail (DMI) medium for 8 days. MTT assay was used to measure the cell viability and Oil Red O staining was used to evaluate the adipogenesis of 3T3-L1 cells. The total level of triglyceride and released glycerol were detected to evaluate the lipolysis during 3T3-L1 adipogenesis. The expression levels of Leptin, fatty acid-binding protein 4 (FABP4), and sterol regulatory element-binding protein (SREBP1C) were determined by qRT-PCR. qRT-PCR assay were utilized to detect the expression levels of PPARγ and C/EBPα in 3T3-L1 cells. A high-fat diet (HFD) was used to construct an obese mice model, followed by the treatment with TSA. HE staining was conducted to evaluate the pathological state of adipose tissues. Body weights and the weights of adipose tissues were recorded to evaluate the anti-obesity property of TSA. Results Firstly, the promoted lipid accumulation induced by DMI incubation was significantly reversed by the treatment with TSA in a dose-dependent manner. The elevated expression levels of Leptin, FABP4, SREBP1C, PPARγ, and C/EBPα induced by the stimulation with DMI incubation were dramatically inhibited by the introduction of TSA, accompanied by the upregulation of phosphorylated AMP-activated protein kinase (p-AMPK). Secondly, the inhibitory effect of TSA against the expression level of PPARγ and lipid accumulation was greatly abolished by an AMPK inhibitor. Lastly, the increased body weights and visceral adipocyte tissue weight, as well as the enlarged size of adipocytes induced by HFD were pronouncedly reversed by the administration of TSA. Conclusion TSA inhibited adipogenesis in 3T3-L1 preadipocytes by activating the AMPK pathway.

HDAC inhibitor Trichostatin A suppresses adipogenesis in 3T3-L1 preadipocytes

The activation of glial cells may cause inflammatory responses to brain, leading to cognitive dysfunction. Green tea polyphenols have been reported to be neuroprotective. This study used the method of intracerebroventricular injection of A1-42 to establish an Alzheimer's disease (AD) model, and then treated with tea polyphenols. We aimed to investigate the effects and molecular mechanism of tea polyphenols on antagonizing the neurotoxicity induced by A1-42. Three-month-old male C57BL/6J mice were injected with A1-42 into the lateral ventricle and tea polyphenols were administered immediately after modeling. Morris water maze test was conducted to detect the cognitive function, Western blot assay was used to detect protein expressions of related signaling pathways in hippocampus tissue, and immunofluorescence assay was used to label microglia and astrocyte. Compared with AD model mice without tea polyphenols treatment, the latency to find the hidden platform of AD model mice with tea polyphenols treatment was significantly reduced, and the proportion of time spent in the quadrant was significantly increased. The expressions of BDNF and TrkB were significantly increased. In addition, microglia/astrocyte cell proliferation was significantly reduced and the activation of pro-inflammatory signaling pathway factors was down-regulated, while anti-inflammatory signaling pathway factors was up-regulated. This study indicates that tea polyphenols attenuate A1-42-induced cognition dysfunction and the effects may be related to hippocampal neurogenesis and glial cell-related inflammatory response.

Early-stage protective effects of tea polyphenols on hippocampal neurogenesis and cognitive dysfunction in alzheimer's disease model

Efficacy and safety of early oral feeding in postoperative patients with upper gastrointestinal tumor: A systematic review and meta-analysis

Efficacy and safety of early oral feeding in postoperative patients with upper gastrointestinal tumor: A systematic review and meta-analysis.

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HDAC inhibitor Trichostatin A suppresses adipogenesis in 3T3-L1 preadipocytes

Early-stage protective effects of tea polyphenols on hippocampal neurogenesis and cognitive dysfunction in alzheimer's disease model

Efficacy and safety of early oral feeding in postoperative patients with upper gastrointestinal tumor: A systematic review and meta-analysis.