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Leht 1 alates 651 tulemused
Fidarestat improves cardiomyocyte contractile function in db/db diabetic obese mice through a histone deacetylase Sir2-dependent mechanism.
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BACKGROUND
Fidarestat, an aldose reductase (AR) inhibitor, displays promise for the treatment of diabetic neuropathy, although the underlying mechanism of action remains unclear. Histone modification, especially histone acetylation, has been implicated in the pathogenesis of diabetes and its
Acute Strenuous Exercise Induces an Imbalance on Histone H4 Acetylation/Histone Deacetylase 2 and Increases the Proinflammatory Profile of PBMC of Obese Individuals.
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This study evaluated the response of global histone H4 acetylation (H4ac), histone deacetylase 2 (HDAC2) activity, as well as the production of proinflammatory cytokines and monocyte phenotypes of lean and obese males after exercise. Ten lean and ten obese sedentary men were submitted to one session
Role of histone methylation and demethylation in adipogenesis and obesity.
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Adipocyte differentiation is a complex developmental process that involves the coordinated interplay of numerous transcription factors. PPARγ has emerged as a master regulator of adipogenesis and recent global target gene analysis demonstrated that PPARγ targets many genes encoding chromatin
Global differences in specific histone H3 methylation are associated with overweight and type 2 diabetes.
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BACKGROUND
Epidemiological evidence indicates yet unknown epigenetic mechanisms underlying a propensity for overweight and type 2 diabetes. We analyzed the extent of methylation at lysine 4 and lysine 9 of histone H3 in primary human adipocytes from 43 subjects using modification-specific
The Landscape of Histone Modifications in a High-Fat Diet-Induced Obese (DIO) Mouse Model.
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Type 2 diabetes (T2D) is a major chronic healthcare concern worldwide. Emerging evidence suggests that a histone-modification-mediated epigenetic mechanism underlies T2D. Nevertheless, the dynamics of histone marks in T2D have not yet been carefully analyzed. Using a mass spectrometry-based
Impaired histone deacetylases 5 and 6 expression mimics the effects of obesity and hypoxia on adipocyte function.
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The goal of the study was to investigate the role of histone deacetylases (HDACs) in adipocyte function associated with obesity and hypoxia.
Total proteins and RNA were prepared from human visceral adipose tissues (VAT) of human obese and normal weight subjects and from white adipose tissue (WAT) of
Schisandra chinensis berry extract protects against steatosis by inhibiting histone acetylation in oleic acid-treated HepG2 cells and in the livers of diet-induced obese mice.
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We hypothesized that hepatic steatosis could be mitigated by the hypolipidemic activity of Schisandra chinensis berry ethanol extract (SCE) via the inhibition of histone acetyltransferase (HAT) activity. HepG2 cells treated with oleic acid (OA) in the presence of SCE exhibited reduced OA-induced
Butyrate stimulates adipose lipolysis and mitochondrial oxidative phosphorylation through histone hyperacetylation-associated β3 -adrenergic receptor activation in high-fat diet-induced obese mice.
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What is the central question of this study? Butyrate can prevent diet-induced obesity through increasing energy expenditure. However, it is unclear whether β3 -adrenergic receptors (ARβ3) mediate butyrate-induced adipose lipolysis. What is the main finding and its importance? Short-term oral
Obesity and metabolic syndrome in histone demethylase JHDM2a-deficient mice.
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Histone H3 lysine 9 (H3K9) methylation is a crucial epigenetic mark of heterochromatin formation and transcriptional silencing. Recent studies demonstrated that most covalent histone lysine modifications are reversible and the jumonji C (JmjC)-domain-containing proteins have been shown to possess
Hepatic cellular senescence pathway genes are induced through histone modifications in a diet-induced obese rat model.
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Overnutrition, such as a high-fat (HF) diet, is a feature followed by some in developed nations that leads to obesity and fatty liver disease. In rats, when fed a fat-high diet, some develop obesity (obesity prone, OP) while others display an obesity-resistant (OR) phenotype. The present study
ALDH2 protects against high fat diet-induced obesity cardiomyopathy and defective autophagy: role of CaM kinase II, histone H3K9 methyltransferase SUV39H, Sirt1, and PGC-1α deacetylation.
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OBJECTIVE
Uncorrected obesity contributes to cardiac remodeling and contractile dysfunction although the underlying mechanism remains poorly understood. Mitochondrial aldehyde dehydrogenase (ALDH2) is a mitochondrial enzyme with some promises in a number of cardiovascular diseases. This study was
Attenuation of diet-induced obesity and induction of white fat browning with a chemical inhibitor of histone deacetylases.
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In the last decade, a strict link between epigenetics and metabolism has been demonstrated. Histone deacetylases (HDACs) have emerged as key epigenetic regulators involved in metabolic homeostasis in normal and pathologic conditions. Here we investigated the effect of the class I HDAC inhibitor
DNA CpG Methylation (5-Methylcytosine) and Its Derivative (5-Hydroxymethylcytosine) Alter Histone Posttranslational Modifications at the Pomc Promoter, Affecting the Impact of Perinatal Diet on Leanness and Obesity of the Offspring.
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A maternal high-fat diet (HFD) alters the offspring's feeding regulation, leading to obesity. This phenomenon is partially mediated by aberrant expression of the hypothalamic anorexigenic neuropeptide proopiomelanocortin (POMC). Nevertheless, although some individual offspring suffer from morbid
Genome-wide profiling of histone H3K27 acetylation featured fatty acid signalling in pancreatic beta cells in diet-induced obesity in mice.
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Epigenetic regulation of gene expression has been implicated in the pathogenesis of obesity and type 2 diabetes. However, detailed information, such as key transcription factors in pancreatic beta cells that mediate environmental effects, is not yet available.
To analyse genome-wide cis-regulatory
The histone demethylase Phf2 acts as a molecular checkpoint to prevent NAFLD progression during obesity.
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Aberrant histone methylation profile is reported to correlate with the development and progression of NAFLD during obesity. However, the identification of specific epigenetic modifiers involved in this process remains poorly understood. Here, we identify the histone demethylase Plant Homeodomain
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