A5018837080- Pancreatic function and diabetes
- Liver Disease Diagnosis and Treatment
- Epigenetics and DNA Methylation
- Diet, Metabolism, and Disease
- Diabetes Treatment and Management
- Peptidase Inhibition and Analysis
- Metabolism, Diabetes, and Cancer
- Birth, Development, and Health
- Diet and metabolism studies
- Cancer-related molecular mechanisms research
- MicroRNA in disease regulation
- Nuclear Receptors and Signaling
- Pancreatitis Pathology and Treatment
- Cancer-related gene regulation
- Genetics and Neurodevelopmental Disorders
- Diabetes and associated disorders
- RNA modifications and cancer
- Adipokines, Inflammation, and Metabolic Diseases
- Cardiovascular Disease and Adiposity
- Genetic Syndromes and Imprinting
- GDF15 and Related Biomarkers
- Adipose Tissue and Metabolism
- Neuropeptides and Animal Physiology
German Institute of Human Nutrition
2016-2023
German Center for Diabetes Research
2016-2023
Heinrich Heine University Düsseldorf
2016-2023
Deutsches Diabetes-Zentrum e.V.
2016-2023
Increased hepatic expression of dipeptidyl peptidase 4 (DPP4) is associated with non-alcoholic fatty liver disease (NAFLD). Whether this causative for the development NAFLD not yet clarified. Here we investigate effect DPP4 overexpression on steatosis in a mouse model diet-induced obesity.
In type 2 diabetes (T2D), hepatic insulin resistance is strongly associated with nonalcoholic fatty liver disease (NAFLD). this study, we hypothesized that the DNA methylome of livers from patients T2D compared individuals normal plasma glucose levels can unveil some mechanism could link to NAFLD. Using and transcriptome analyses obese individuals, found hypomethylation at a CpG site in PDGFA (encoding platelet-derived growth factor α) overexpression are both increased risk,...
Hepatic DPP4 expression is elevated in subjects with ectopic fat accumulation the liver. However, whether increased dipeptidyl peptidase 4 (DPP4) involved pathogenesis or rather a consequence of metabolic disease not known. We therefore studied transcriptional regulation hepatic Dpp4 young mice prone to diet-induced obesity. Already at 6 weeks age, was high weight gain, independent liver content. In same animals, methylation four intronic CpG sites decreased, amplifying glucose-induced...
Obesity and type 2 diabetes (T2D) arise from the interplay between genetic, epigenetic, environmental factors. The aim of this study was to combine bioinformatics functional studies identify miRNAs that contribute obesity T2D.
Obesity and ectopic fat disposition are risk factors for metabolic disease. Recent data indicate that IGFBP2 expression in liver is epigenetically inhibited during hepatic steatosis. The aim of this study was to investigate if epigenetic de-regulation Igfbp2 occurs already early life associated with increased diet-induced obesity (DIO) adolescence. Male C57BL/6J mice received a high-fat diet. After 3 weeks on diet (age 6 weeks), DIO-susceptible (responder, Resp) DIO-resistant (non-responder,...
The identification of individuals with a high risk developing type 2 diabetes (T2D) is fundamental for prevention. Here, we used translational approach and prediction criteria to identify changes in DNA methylation visible before the development T2D. Islets Langerhans were isolated from genetically identical 10-week-old female New Zealand Obese mice, which differ their degree hyperglycemia liver fat content. application semiexplorative identified 497 differentially expressed methylated genes...
Better disease management can be achieved with earlier detection through robust, sensitive, and easily accessible biomarkers. The aim of the current study was to identify novel epigenetic biomarkers determining risk type 2 diabetes (T2D). Livers 10-week-old female New Zealand Obese (NZO) mice, slightly differing in their degree hyperglycemia liver fat content thereby susceptibility were used for expression methylation profiling. We screened differences hepatic DNA diabetes-prone -resistant...
The identification of individuals with a high risk developing type 2 diabetes (T2D) is fundamental for prevention. Here, we used translational approach and prediction criteria to identify changes in DNA methylation visible before the development T2D. <p>Islets Langerhans were isolated from genetically identical 10-week-old female New Zealand Obese mice which differ their degree hyperglycemia liver fat content. application semi-explorative identified 497 differentially expressed...
Recent data indicate that hepatic expression of dipeptidyl peptidase 4 (DPP4) is associated with the development non-alcoholic fatty liver disease (NAFLD). Here, we investigated effect specific Dpp4 overexpression on hepatosteatosis and insulin resistance, tested if NAFLD patients show a systemic increase DPP4.
Background: NAFLD patients exhibit decreased hepatic Insulin-like growth factor binding protein-2 (IGFBP2) expression associated with DNA methylation1. Transcriptome analysis of livers from adiposity-susceptible (responder) C57BL/6J mice showed also levels Igfbp2 compared to adiposity-resistant (non-responder) mice. The aim this study was test if methylation and is altered before onset hepatosteatosis.
Dipeptidyl peptidase 4 (DPP4) has recently been described as novel adipokine upregulated in obesity. Furthermore, patients suffering from non-alcoholic fatty liver disease exhibit elevated hepatic DPP4 expression. We analyzed the capacity of livers to release compared with that adipose tissue and investigated epigenetic regulation
Deregulation of microRNA (miRNA) has been associated with different stages non-alcoholic fatty liver disease (NAFLD) or type 2 diabetes (T2D), while their biological role in the pathogenesis is unknown. Our study aims to characterize epigenetic signature a diabetic mouse model and identify new functional biomarkers predicting onset T2D.
Type 2 diabetes (T2D) is closely linked with non-alcoholic fatty liver disease (NAFLD) and hepatic insulin resistance, but the involved mechanisms are still elusive. Using DNA methylome transcriptome analyses of livers from obese individuals, we found that both hypomethylation at a CpG site in PDGFA (encoding platelet derived growth factor alpha) overexpression associated increased T2D risk, hyperinsulinemia, resistance steatohepatitis risk. Both genetic risk score studies human cell...
The development of type 2 diabetes (T2D) is driven by genetic as well environmental factors. However, even genetically identical mice show a broad variation in T2D onset upon high-fat feeding. aim this study was to investigate if differential DNA methylation can be linked the observed variations gene expression and thereby predicting T2D.
Obesity and T2D arise from the interplay between genetic, epigenetic, environmental factors. In recent studies we generated a backcross population of lean B6 obese NZO mice to determine quantitative trait loci (QTL) for obesity diabetes. parallel, detected high number differently expressed genes (DEG) by micro array analysis mouse strains. As most DEGs were located outside QTL hypothesized that other regulatory elements such as miRNAs must be responsible these effects.
Zusammenfassung Vor dem Hintergrund der steigenden Prävalenz von Adipositas und den damit einhergehenden Begleiterkrankungen (Nicht-alkoholische Fettleber, Typ-2-Diabetes u.a.) wird es immer wichtiger, neue Präventions- Behandlungsmöglichkeiten aufzuzeigen, die eine personalisierte Therapie ermöglichen. Die Entdeckung Veränderungen in bestimmten Signalwegen, durch ausgelöst werden, verbessern nicht nur unsere Kenntnisse über Pathophysiologie, sie können zudem auf pharmakologische...
The identification of individuals with a high risk developing type 2 diabetes (T2D) is fundamental for prevention. Here, we used translational approach and prediction criteria to identify changes in DNA methylation visible before the development T2D. <p>Islets Langerhans were isolated from genetically identical 10-week-old female New Zealand Obese mice which differ their degree hyperglycemia liver fat content. application semi-explorative identified 497 differentially expressed...