Genes with epigenetic alterations in human pancreatic islets impact mitochondrial function, insulin secretion, and type 2 diabetes

Epigenetic dysregulation may influence disease progression. Here we explore whether epigenetic alterations in human pancreatic islets impact insulin secretion and type 2 diabetes (T2D). In islets, 5,584 DNA methylation sites exhibit alterations in T2D cases versus controls and are associated with Hb...

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Veröffentlicht in:	Nature communications Jg. 14; H. 1; S. 8040 - 21
Hauptverfasser:	Rönn, Tina, Ofori, Jones K., Perfilyev, Alexander, Hamilton, Alexander, Pircs, Karolina, Eichelmann, Fabian, Garcia-Calzon, Sonia, Karagiannopoulos, Alexandros, Stenlund, Hans, Wendt, Anna, Volkov, Petr, Schulze, Matthias B., Mulder, Hindrik, Eliasson, Lena, Ruhrmann, Sabrina, Bacos, Karl, Ling, Charlotte
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	London Nature Publishing Group UK 12.12.2023 Nature Publishing Group Nature Portfolio
Schlagworte:	13/109 14/63 45 45/41 45/43 45/91 49/39 631/208/176/1988 692/163/2743/137/773 82/58 Adenosine diphosphate Animals Beta cells Calcium (mitochondrial) Calcium ions Clinical Medicine Diabetes Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Type 2 - genetics Diabetes Mellitus, Type 2 - metabolism DNA Methylation Electron transport Endocrinology and Diabetes Endokrinologi och diabetes Enhancers Epigenesis, Genetic Epigenetics Forkhead Transcription Factors - metabolism Foxp1 protein Glycine Humanities and Social Sciences Humans Hyperglycemia Insulin Insulin - metabolism Insulin resistance Insulin Secretion Insulin-Secreting Cells - metabolism Islets of Langerhans - metabolism Klinisk medicin Medical and Health Sciences Medicin och hälsovetenskap Metabolites Mitochondria Mitochondria - genetics Mitochondria - metabolism multidisciplinary Pancreas Proline Rats Repressor Proteins - metabolism Science Science (multidisciplinary) Secretion Transcription factors Transcription Factors - metabolism γ-Aminobutyric acid
ISSN:	2041-1723, 2041-1723
Online-Zugang:	Volltext
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