Dietary induction of obesity and insulin resistance is associated with changes in Fgf21 DNA methylation in liver of mice.

DNA methylation is dynamically regulated in metabolic diseases, but it remains unclear whether the changes are causal or consequential. Therefore, we used a longitudinal approach to refine the onset of metabolic and DNA methylation changes at high temporal resolution. Male C57BL/6N mice were fed with 60 % high-fat diet (HFD) for up to 12 weeks and metabolically characterized weekly.

Epigenetic Downregulation of FASN in Visceral Adipose Tissue of Insulin Resistant Subjects.

Objective: The risk to develop type 2 diabetes increases with the amount of visceral adiposity presumably due to increased lipolysis and subsequent lipid accumulation in visceral organs. However, data describing the molecular regulation of these pathways in humans are rare. We tested if genes of the lipogenic and lipolytic pathways are associated with glucose intolerance independently of obesity in visceral adipose tissue (VAT) of obese subjects.

Critical evaluation of the DNA-methylation markers ABCG1 and SREBF1 for Type 2 diabetes stratification.

Validation of epigenome-wide association studies is sparse. Therefore, we evaluated the methylation markers cg06500161 () and cg11024682 () as classifiers for diabetes stratification. DNA methylation was measured in blood (n = 167), liver (n = 99) and visceral adipose tissue (n = 99) of nondiabetic or Type 2 diabetic subjects by bisulfite pyrosequencing.

Reduced expression of thyroid hormone receptor β in human nonalcoholic steatohepatitis.

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.