Gut microbiome: Microflora association with obesity and obesity-related comorbidities
Introduction
The potential role of gut microbiota in the development of obesity and obesity-related comorbidities has attracted much attention from the public and academics. Excess energy intake and sedentary lifestyle with reduced physical activity are the most popular factors which could contribute to obesity and its related comorbidities. Its development is a complex process and the contributing factors including environmental factors and genetic susceptibility are often shrouded in mystery [1]. Lately, several scientific reports suggest that the altered diversity of the gut microbiome may play a role in the development of obesity, and other metabolic, and inflammatory disorders [[2], [3], [4], [5], [6], [7], [8], [9], [10]].
The host and gut microbiota concomitantly evolve through symbiotic interactions influenced by genetics, background, age, sex, immune system and gut motility [11,12]. Furthermore, gut microbiota in individuals predisposing to obesity could be altered by changes in the diet, prebiotic and probiotic use (Fig. 1). Some of the key factors that affect maintaining a balanced healthy gut microbiota are; however, not limited to nutritional imbalance, harmful microbial infections, diseases, alteration in intestinal barrier, and gut microenvironment [13,14]. Many research findings indicate that the imbalance in gut microbiota may pose a threat for host metabolism and energy homeostasis that triggers the development of conditions like insulin resistance, diabetes mellitus, and obesity [2,3,7,[15], [16], [17]]. For instance, the microbial imbalance is characterized by altered secretion of blood glucose, lowering metabolic hormones known as incretins, misregulated production of short-chain fatty acids known as butyrate, enhanced proportions of gut microbiota lipopolysaccharide (LPS). Translocation of host microbiota-derived LPS to the bloodstream beyond its threshold results in metabolic endotoxemia, which could activate a Toll-like receptor-mediated inflammatory response, and in severe cases could cause organ damage and cardiovascular disease [18]. As previously indicated, modifications in the gut microbiota have been linked to obesity and its related-comorbidities. This review provides a general overview of the potential role of gut microbiota in the development of adverse metabolic state as well as the respective prevention and treatment strategies.
Section snippets
Transformed gut microbiota and obesity
The microbial organ is a term coined to represent human microbiota as gut that harbors various types of microorganisms [3,19]. The bacterial component of the microbiota has been studied much by large-scale projects such as the Human Microbiome Project and MetaHIT [19]. Studies from Human Microbiome Project (HMP) and Metagenome of Human Intestinal Tract (MetaHIT) revealed that human microbiome could at least encode for 10 million genes [19]. The combined genome content of the microbial organ
Gut microbiota and metabolic syndrome
Metabolic syndrome is a term coined to define the integration of physiological, metabolic, and biochemical factors that have a role to play in pathologies such as cardiovascular disease and type 2 diabetes mellitus [33]. The primary cardiovascular risk factors associated with metabolic syndrome are hypertension, obesity, dyslipidemia, hypertriglyceridemia, and insulin resistance [34]. The International Diabetes Federation defines raised blood pressure, raised fasting glucose, and obesity,
Gut permeability and metabolic endotoxemia
Deterioration of the harmony between microbial organ and host immune system could result in the intestinal translocation of antigens of bacterial origin culminating in ‘metabolic endotoxemia’, that has been related to systemic inflammation and insulin resistance [41]. As previously mentioned, high-fat diet increases the proportion of gram-negative bacterial species in microbiota [42]. High-fat diet resulted in the increased levels of Deltaproteobacteria, Gammaproteobacteria, and pathobionts (
Gut microbiota modulation by probiotics and prebiotics
Improving host and microbial interaction through probiotics and prebiotics in obese subjects has extensively been explored and revealed to be a pharmaco-nutritional management strategy to reverse the dysbiosis-linked host metabolic alterations [53]. Probiotics are the living microorganisms present in the food supplements, being widely reported in changing the composition of colon microbiota by shifting the microbial balance towards the positive end [54]. Probiotics must be able to remain viable
Gut microbiota modulation by fecal microbial transplantation
Fecal microbial transplantation (FMT) although only just starting to develop, is emerging as an effective tool for manipulation of gut microbial ecology in order to ameliorate obesity and other metabolic disorders [64,65]. Cândido et al. [42], pointed out that fecal or gut microbiome transfer could rapidly modify an unhealthy gut microbiota in order to extenuate various metabolic disorders, namely obesity and type 2 diabetes mellitus. Various reports suggest that FMT in persons having metabolic
Gut microbiota modulation by dietary interventions
The control of changes in gut microbial ecology could protect the host from gut and tissue microbiota dysbiosis [69]. In this regard, dietary habits play a vital role in modulating the gut microbiota composition [70]. Obese subjects were shown to be associated with an increased ratio of Firmicutes to Bacteroidetes in comparison to lean subjects [71]. For instance, a report suggested that unsaturated fatty acids and fiber-enriched diet could increase beneficial bacteria level [72]. Furthermore,
Conclusion
In conclusion, gut microbiota has crucial therapeutic potential in curbing the epidemic of obesity which poses a great challenge to disease or illness prevention and promotion of good health through the course of life around the world. Experiments in animal models have presented evidence for a recurrent role of gut microbiota in the etiology of obesity and obesity-related comorbidities. Unfortunately, animal causation studies do not necessarily equate or replicate human causation regarding gut
Author's contribution
IAR & ATJ conceived the idea. IAR, JBL, WKP & WYK contributed to writing of the manuscript. HAP & WKP contributed in designing the paper and literature survey. JL, IAR and ATJ critically reviewed, edited, and finalized the manuscript for submission.
Funding
No funding was availed to carry out the study.
Conflicts of interest
The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Acknowledgement
Author Arif Tasleem Jan acknowledge University Grants Commision (UGC), India for startup grant. Authors extends thanks to colleagues Drs. Safikur Rahman and Mudsser Azam for criticism that helped to improve the quality of contents in the perspective of broader audience.
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Both author contributed equally.