THE ROLE OF EPIGENOME AND MICROBIOME IN ENDOCRINOID-MEDIATED INFLAMMATION REGULATION IN DIET-INDUCED OBESITY

Abstract

New evidence suggests that microbiomes, often called epigenomes, contribute to metabolic health and the inflammation associated with diet-induced obesity (DIO). Within the context of endocannabinoid-mediated inflammatory regulation in a mouse model, this study investigates the interplay of DIO, the epigenomic landscape, and the composition of the microbes in the digestive tract. Inducing obesity in C57BL/6J mice and then tracking their weight allowed the researchers to analyze the consequences of a high-fat diet (HFD). The goal was to identify any changes in metabolic parameters, inflammatory markers, or both. By combining genomic sequencing with epigenetic profiling, researchers were able to identify alterations in DNA methylation patterns associated with obesity. The genes that regulate inflammation and lipid metabolism showed the most significant modifications. Simultaneously, researchers performed gut microbiota analyses using 16S rRNA sequencing; their findings showed that the HFD was linked to significant changes in microbial diversity and composition. Notably, researchers observed an increase in inflammatory-promoting microbial taxa, which is associated with elevated levels of endogenous cannabinoids. To find the pathways, researchers modified endocannabinoid signaling using pharmaceutical therapy and evaluated the effect on inflammatory responses and metabolic consequences. The microbiota and the epigenome work together to influence inflammation in DIO, according to the findings. This, in turn, impacts endocannabinoid signaling. More research is needed to determine the exact mechanisms involved and their implications for the treatment and prevention of obesity, but this work highlights the complex interplay between nutrition, microbiome, and epigenetic pathways in metabolic health and the potential of targeting these pathways as treatment approaches for inflammation associated with obesity.