Epigenetic modifications in obesity-associated diseases.
Yiqian LongChao MaoShuang LiuKonstantin M J SparrerDesheng XiaoPublished in: MedComm (2024)
The global prevalence of obesity has reached epidemic levels, significantly elevating the susceptibility to various cardiometabolic conditions and certain types of cancer. In addition to causing metabolic abnormalities such as insulin resistance (IR), elevated blood glucose and lipids, and ectopic fat deposition, obesity can also damage pancreatic islet cells, endothelial cells, and cardiomyocytes through chronic inflammation, and even promote the development of a microenvironment conducive to cancer initiation. Improper dietary habits and lack of physical exercise are important behavioral factors that increase the risk of obesity, which can affect gene expression through epigenetic modifications. Epigenetic alterations can occur in early stage of obesity, some of which are reversible, while others persist over time and lead to obesity-related complications. Therefore, the dynamic adjustability of epigenetic modifications can be leveraged to reverse the development of obesity-associated diseases through behavioral interventions, drugs, and bariatric surgery. This review provides a comprehensive summary of the impact of epigenetic regulation on the initiation and development of obesity-associated cancers, type 2 diabetes, and cardiovascular diseases, establishing a theoretical basis for prevention, diagnosis, and treatment of these conditions.
Keyphrases
- insulin resistance
- type diabetes
- weight loss
- metabolic syndrome
- high fat diet induced
- gene expression
- bariatric surgery
- adipose tissue
- weight gain
- dna methylation
- high fat diet
- early stage
- endothelial cells
- blood glucose
- cardiovascular disease
- stem cells
- risk factors
- oxidative stress
- blood pressure
- cardiovascular events
- lymph node
- physical activity
- obese patients
- signaling pathway
- vascular endothelial growth factor