A Review on epigenetics alternations in high fat diet induced diabetes

Abstract

T2DM is complicated, with irreversible risk factors such as age, genetic, race, and ethnicity, as well as reversible risk factors like as food, physical activity, and smoking, with eating habits and sedentary lifestyle being the key contributors for fast growing incidence. Chronic exposure to HFD promotes liver damage, poor glucose homeostasis, hyper insulinemia, late pancreatic β-cell failure to generate insulin due to cell fatigue and resultant hyperglycemia, which are the key hallmarks of T2DM. Metabolic diseases such as T2DM have been linked to epigenetic changes that occur without changes in the DNA sequence, such as cytosine methylation of DNA, histone posttranslational modifications, and microRNA, which provide links between genes and environmental factors such as diet, smoking, and other lifestyle factors. T2DM affects insulin gene expression and beta cell differentiation via both histone modifications and DNA methylation in diabetic islets, which plays a vital role in regulating mitochondrial genes and in diabetes regulation. As a result, we provide existing evidence on epigenetic changes in high fat diet-induced diabetes. Metabolic diseases such as T2DM have been linked to epigenetic changes that occur without changes in the DNA sequence, such as cytosine methylation of DNA, histone posttranslational modifications, and microRNA, which provide links between genes and environmental factors such as diet, smoking, and other lifestyle factors. T2DM affects insulin gene expression and beta cell differentiation via both histone modifications and DNA methylation in diabetic islets, which plays a vital role in regulating mitochondrial genes and in diabetes regulation. In this review, we provide existing evidence on epigenetic changes in high fat diet-induced diabetes.