Endocrine, genetic, and microbiome nexus of obesity and potential role of postbiotics: a narrative review

Abstract

Obesity is a public health crisis, presenting a huge burden on health care and the economic system in both developed and developing countries. According to the WHO's latest report on obesity, 39% of adults of age 18 and above are obese, with an increase of 18% compared to the last few decades. Metabolic energy imbalance due to contemporary lifestyle, changes in gut microbiota, hormonal imbalance, inherent genetics, and epigenetics is a major contributory factor to this crisis. Multiple studies have shown that probiotics and their metabolites (postbiotics) supplementation have an effect on obesity-related effects in vitro, in vivo, and in human clinical investigations. Postbiotics such as the SCFAs suppress obesity by regulating metabolic hormones such as GLP-1, and PPY thus reducing feed intake and suppressing appetite. Furthermore, muramyl di-peptides, bacteriocins, and LPS have been tested against obesity and yielded promising results in both human and mice studies. These insights provide an overview of targetable pharmacological sites and explore new opportunities for the safer use of postbiotics against obesity in the future.

Keywords: Bacteriocins; Energy metabolism; Gut microbiome; LPS; Muramyl di-peptides; Obesity; Postbiotics; SCFAs.

Fig. 1

Environment, genetics, and epigenetics contribute as the main factors causing obesity. Environmental factors such as a sedentary lifestyle, unhealthy food, stress, and abnormal sleep along with genetics and epigenetics are predisposing causes for obesity. Both these factors cause epigenetics alteration, which causes energy dysbiosis, tissue inflammation, decrease insulin resistance, and increase lipid accumulation. In turn, obesity is capable of causing severe health problems such as cancer, type-2 diabetes, ageing, and cardiovascular disease are the most common

Fig. 2

The molecular mechanism of SCFAs mitigating obesity through energy regulation. The intestinal wall absorbs acetate and butyrate in the intestine produced by the gut microbiota; regulate fatty acids, and insulin level through PPARα, GLP-1, and PPY signalling pathways