The diet-induced metabolic syndrome is accompanied by whole-genome epigenetic changes

Abstract

Consuming a high-fat/high-fructose diet (HFD) starting at a young age leads to the development of obesity and to the progression of metabolic syndrome (MS). We are interested in the relationship between MS and DNA methylation as a mediator of the metabolic memory and the early appearance of these diseases in the progeny. To this end, Wistar rats were fed a HFD for 1 year, and every 12 weeks, biochemical analyses were performed. After 24 weeks, animals fed the HFD showed alterations related to MS such as elevated blood levels of fasting glucose, triglycerides, and insulin compared with their littermate controls. During the experimental period, the control females exhibited a 40 % lower 5-methylcytosine (5-mC) level compared to the control males. The HFD affected the 5-mC levels in males and females differently. The HFD induced a 20 % decrease in the 5-mC levels in males and a 15 % increase in females. We found that the HFD induces an early presentation of MS in the progeny of treated animals and that the DNA methylation was altered in the F1 generation. The presentation of MS is positively associated with changes in the global percentage of 5-mC in the DNA.

Fig. 1

Percentage of animals with metabolic syndrome. The percentage of animals fed with high-fat/high-fructose diet (HFD) or control diet (CON) that developing MS a F₀ and b F₁ generation. The black bars represent males and white bars females

Fig. 2

Linear regression of 5-mC. a Male and b female of F₀ generation. The black represents high-fat/high-fructose diet (HFD) and white control diet (CON). Male F₀ CON: y = 0.0081x + 2.054 R ² = 0.95316 HFD: y = 0.0067x + 1.6083, R ² = 0.99705