Epigenetic silencing of the ANKRD26 gene correlates to the pro-inflammatory profile and increased cardio-metabolic risk factors in human obesity.
Antonella DesiderioMichele LongoLuca ParrilloMichele CampitelliGiuseppe CacaceSonia de SimoneRosa SpinelliFederica ZatteraleSerena CabaroPasquale DolcePietro FormisanoMarco MiloneClaudia MieleFrancesco BeguinotGregory A RacitiPublished in: Clinical epigenetics (2019)
Downregulation of the ANKRD26 gene and hyper-methylation at specific CpGs of its promoter are common abnormalities in obese patients. These changes correlate to the pro-inflammatory profile and the cardio-metabolic risk factors of the obese individuals, indicating that, in humans, they mark adverse health outcomes.
Keyphrases
- obese patients
- risk factors
- bariatric surgery
- dna methylation
- genome wide
- weight loss
- roux en y gastric bypass
- gastric bypass
- metabolic syndrome
- copy number
- endothelial cells
- gene expression
- type diabetes
- insulin resistance
- genome wide identification
- adipose tissue
- signaling pathway
- cell proliferation
- transcription factor
- emergency department
- high fat diet induced
- body mass index
- genome wide analysis
- pluripotent stem cells