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Introduction Epigenetic regulation, which involves reversible and heritable changes in gene expression that occur in response to external stimuli without altering the DNA sequence ( 1 , 2 ), is fundamental to understanding the pathogenesis of
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patients with sporadic SI-NETs, the determinant of genetic or epigenetic alterations and the outcomes of prognosis, survival or progression. Synonyms of SI-NETs and (epi)genetic alterations with the outcome described as prognosis, survival and progression
International Center for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
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International Center for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
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International Center for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
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International Center for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
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epigenetic studies. We have previously published one of the first studies demonstrating changes in DNA methylation patterns with the onset of puberty in healthy children ( 12 ) and identified the promotor of the thyroid hormone receptor interactor 6 gene
School of Medicine, Universidad de los Andes, Bogotá, Colombia
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Endocrinology Section, Hospital Universitario Fundación Santa Fe de Bogotá, Bogotá, Colombia
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School of Medicine, Universidad de los Andes, Bogotá, Colombia
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School of Medicine, Universidad de los Andes, Bogotá, Colombia
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at the population level. This environmental influence can also be explained from an epigenetic perspective. For example, the fetus and neonate development conditions have a significant influence on the onset of T2DM and obesity without inducing
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Hepatic thyroid hormone signaling has an important role in the development and progression of nonalcoholic steatohepatitis (NASH). While the systemic levels of thyroid hormone might remain stable, there is evidence that the intracellular signaling machinery consisting of transporters, deiodinases and receptors could be altered in NASH. However, clinical material from human liver biopsies of individuals with NASH has not been studied to date. In a cross-sectional study, we analyzed 85 liver biopsies from patients with different stages of NASH that underwent bariatric surgery. Using qPCR, we analyzed gene expression of thyroid hormone transporters NTCP (SLC10A1), MCT8 (SLC16A2) and OATP1C1 (SLCO1C1), thyroid hormone receptor α and β (THRA and THRB) and deiodinase type I, II and III (DIO1, DIO2, DIO3). The expression was correlated with serum TSH, triglyceride, HbA1c and NASH score and corrected for age or gender if required. While DIO2, DIO3 and SLCO1C1 were not expressed in human liver, we observed a significant negative correlation of THRB and DIO1 with age, and SLC16A2 with gender. THRB expression was also negatively associated with serum triglyceride levels and HbA1c. More importantly, its expression was inversely correlated with NASH score and further declined with age. Our data provide unique insight into the mRNA expression of thyroid hormone transporters, deiodinases and receptors in the human liver. The findings allow important conclusions on the intrahepatic mechanisms governing thyroid hormone action, indicating a possible tissue resistance to the circulating hormone in NASH, which becomes more prominent in advanced age.
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University Hospital, Krakow, Poland
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University Hospital, Krakow, Poland
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University Hospital, Krakow, Poland
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University Hospital, Krakow, Poland
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standard therapy ( 9 ). In light of this prior evidence of differential expression of several genes between the two treatment methods ( 9 ), it seemed strongly justified to test whether these can also be seen at the epigenetic level of gene methylation, a
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obesity and T2DM ( 7 , 8 ). Long-term maternal risks include T2DM and cardiovascular disease ( 9 ). Currently, the GD diagnosis is made during the late second trimester, possibly exposing the infant to intrauterine metabolic alterations and epigenetic
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Center for Genomic Research, University of Modena and Reggio Emilia, Modena, Italy
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Center for Genomic Research, University of Modena and Reggio Emilia, Modena, Italy
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Department of Medical Specialties, Azienda Ospedaliero-Universitaria di Modena, Modena, Italy
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Center for Genomic Research, University of Modena and Reggio Emilia, Modena, Italy
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Center for Genomic Research, University of Modena and Reggio Emilia, Modena, Italy
Department of Medical Specialties, Azienda Ospedaliero-Universitaria di Modena, Modena, Italy
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and gut microbiota composition ( 28 ). A possible hypothesis for the persistent side effects may be epigenetic modifications occurring in PFS patients. Indeed, downregulation and hypermethylation of 5α-R were observed in the rodent nervous system and
epiWELL, LLC, Ithaca, New York, USA
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physiologically active and the concept of adiponectin insensitivity is well accepted ( 3 ). Adiponectin secretion has been suggested to be regulated by epigenetic mechanisms ( 4 ), and interventions that activate its physiological secretion levels hold promise for
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over the last few years. Hallmarks of gastrointestinal NET development have been defined ( 9 , 10 ) and our understanding of genetics ( 11 , 12 , 13 ), epigenetics ( 14 , 15 ), tumourigenesis ( 9 ), angiogenesis ( 9 ), novel biomarkers ( 10 ) and