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Review
, 2019, 3291367
eCollection

A Review on Role of Microbiome in Obesity and Antiobesity Properties of Probiotic Supplements

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Review

A Review on Role of Microbiome in Obesity and Antiobesity Properties of Probiotic Supplements

Bhagavathi Sundaram Sivamaruthi et al. Biomed Res Int.

Abstract

Probiotics are now recognized for several health benefits and they have been recommended as a complementary therapeutic agent for metabolic disorders. Obesity is an altered health condition, which is a resultant of irregular energy intake and energy balance, changes in gut microbiota, and improper diet with the influence of genetic makeup and environmental factors. Several studies revealed the influence of probiotic supplementation on obesity-associated consequences in vitro, in vivo, and in human clinical studies. The current manuscript discussed the factors influencing the occurrence of obesity, the interplay between microbiome and obesity, the effect of the probiotic intervention on the health status of obese people, and possible mechanism of antiobesity activity of probiotics. The literature survey revealed that the antiobese activity of probiotics might be associated with their ability to alter the intestinal microbiota, remodeling of energy metabolism, alter the expression of genes related to thermogenesis, glucose metabolism, and lipid metabolism, and change the parasympathetic nerve activity. Further intense research is necessary to figure out the best probiotic or synbiotic mixture and optimum dosage and duration of the intervention to reduce obesity and prevent the recurring of obese condition.

Figures

Figure 1
Figure 1
The factors influencing the incidence and development of obesity.
Figure 2
Figure 2
The major consequences of obesity.
Figure 3
Figure 3
Gut microbial communication with immune cells and cells of target organs, pathways leading to obesity. Microbiota adipose tissue axis: metabolites of gut microbiota promote adipogenesis by triggering LPS based inflammation and SCF induced adipocyte differentiation. Gut-liver axis: microbiota dysbiosis alters the gut permeability enhancing the release of bacteria derived bioactive molecules in the liver. LPS interacts with TLR4 of the Kupffer cells enhancing the recruitment of MyD88 protein, IRAK, TRAF6, and NIK which promotes activation of MAPK, JNK, p38, and NF-κB signaling pathways leading to inflammation and insulin resistance ultimately causing nonalcohol fatty liver (NAFLD). Metabolites like bile acid, SCF, and choline play a vital role in causing NAFLD. Gut-brain axis: neuroactive peptides, lactate, SCF, and LPS of gut microbiota activate vagal afferent neurons and gut hormones leading to alteration in appetite and neuroinflammation.
Figure 4
Figure 4
The possible mechanism behind the antiobesity property of probiotics.

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