Diet, Gut Microbiota, and Obesity: Links with Host Genetics and Epigenetics and Potential Applications - PubMed (original) (raw)

Review

Amanda Cuevas-Sierra et al. Adv Nutr. 2019.

Abstract

Diverse evidence suggests that the gut microbiota is involved in the development of obesity and associated comorbidities. It has been reported that the composition of the gut microbiota differs in obese and lean subjects, suggesting that microbiota dysbiosis can contribute to changes in body weight. However, the mechanisms by which the gut microbiota participates in energy homeostasis are unclear. Gut microbiota can be modulated positively or negatively by different lifestyle and dietary factors. Interestingly, complex interactions between genetic background, gut microbiota, and diet have also been reported concerning the risk of developing obesity and metabolic syndrome features. Moreover, microbial metabolites can induce epigenetic modifications (i.e., changes in DNA methylation and micro-RNA expression), with potential implications for health status and susceptibility to obesity. Also, microbial products, such as short-chain fatty acids or membrane proteins, may affect host metabolism by regulating appetite, lipogenesis, gluconeogenesis, inflammation, and other functions. Metabolomic approaches are being used to identify new postbiotics with biological activity in the host, allowing discovery of new targets and tools for incorporation into personalized therapies. This review summarizes the current understanding of the relations between the human gut microbiota and the onset and development of obesity. These scientific insights are paving the way to understanding the complex relation between obesity and microbiota. Among novel approaches, prebiotics, probiotics, postbiotics, and fecal microbiome transplantation could be useful to restore gut dysbiosis.

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Figures

FIGURE 1

FIGURE 1

Gut microbiota, genomic/epigenomic stability, and obesity. Diverse environmental factors may alter microbiota composition (dysbiosis). Microbially derived metabolites may induce a set of genetic and epigenetic modifications. Dysbiosis can increase the number of SCFA-producing bacteria, which can be used as an extra energy source. An increase in gram-negative bacteria can produce LPS translocation caused by an increase in gut permeability, which can trigger endotoxemia and low-grade systemic inflammation. These factors appear to increase susceptibility to obesity and metabolic disease.

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