Epigenetic modulations after weight-loss
Epigenetic modulations after weight-loss
Bariatric surgery is the most effective treatment for severe obesity, significantly improving insulin sensitivity and reversing type 2 diabetes (T2DM) in up to 77% of patients within two years. Additionally, it lowers chronic inflammation, reduces cancer risk, and enhances cardiovascular health, though the molecular mechanisms behind these benefits remain unclear. Obesity typically leads to harmful changes in white adipose tissue (WAT), including hypertrophy, ectopic fat deposition, and chronic inflammation, all of which increase T2DM risk. Bariatric surgery has been shown to enhance WAT function for up to five years, even with some weight regain, potentially by downregulating inflammation-related gene expression in WAT - a key pathway for metabolic improvements post-surgery.
Intervention studies have shown that DNA methylation patterns can respond to environmental changes, with some marks reversible following weight loss. Studies on bariatric surgery suggest that epigenetic changes may contribute to the surgery's beneficial effects, but these changes have mostly been analyzed in blood, limiting insights into tissue-specific responses. A few studies indicate that obesity-related methylation marks in blood may be comparable to those in adipose tissue (AT), suggesting AT-focused analysis could provide further insights into the epigenetic consequences of weight loss.
By investigating how DNA methylation patterns in blood, subcutaneous and visceral WAT in parallel respond to bariatric surgery and weight loss, this research could uncover mechanisms driving metabolic health improvements and identify blood- as well as tissue-specific epigenetic markers.