Involvement of the gut microbiota in the development of low grade inflammation associated with obesity: Focus on this neglected partner

Université catholique de Louvain, Louvain Drug Research Institute, Metabolism and Nutrition Research Group, Brussels, Belgium.
Acta gastro-enterologica Belgica (Impact Factor: 0.91). 04/2010; 73(2):267-9.
Source: PubMed


Nowadays, the literature provides evidence that obesity, type 2 diabetes and insulin resistance are characterized by a low grade inflammation. Among the environmental factors involved in such diseases, the gut microbiota has been proposed as a key player. This neglected "organ" has been found to be different between healthy and or obese and type 2 diabetic patients. For example, recent data have proposed that dysbiosis of gut microbiota (at phyla, genus, or species level) affects host metabolism and energy storage. Among the mechanisms, metabolic endotoxemia (higher plasma LPS levels), gut permeability and the modulation of gut peptides (GLP-1 and GLP-2) have been proposed as putative targets. Here we discuss 1 degrees the specific modulation of the gut microbiota composition by using prebiotics and 2 degrees the novel findings that may explain how gut microbiota can be involved in the development or in the control of obesity and associated low-grade inflammation.

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    • "Even the lung tumors of smokers has considerable association with microbes as well (Cummins and Tangney, 2013). The microbiome has also been shown to secrete metabolites that promote liver cancer through the senescence secretome (Cani and Delzenne, 2010; DiBaise et al., 2008; Kadooka et al., 2010; Pischon et al., 2008; Wang et al., 2014; Yoshimoto et al., 2013). Turnbaugh performed an interesting study where he was able to demonstrate significant effects of diet on the microbiome by transplanting fresh or frozen adult fecal microbial communities into germ-free c57BL/6 J mice (Turnbaugh et al., 2009b). "
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    • "The consumption of prebiotics able to favor the proliferation of a given microbiota has also been suggested as a potential strategy to improve obesity. In fact, Cani et al. (2012) demonstrated that prebiotic treatment decreases gut permeability and metabolic endotoxemia and improves insulin sensitivity, steatosis, and lowgrade inflammation via several mechanisms including the following: (i) an increased L cell number and endogenous GLP-1 and GLP-2 production and (ii) an increased leptin sensitivity, which controls energy homeostasis and GLP-1 production [19]. "
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    ABSTRACT: Gut microbiota, its evolutive dynamics and influence on host through its protective, trophic and metabolic actions, has a key role in health and opens unique opportunities for the identification of new markers of the physiopathological state of each individual. Alterations in gut microbiota composition have been associated with plenty disorders. Of interest, the vast number of studies demonstrates the role of microbiota in obesity, a serious public health problem that has reached epidemic proportions in many developed and middle-income countries. The economic and health costs of this condition and its comorbidities such as fatty liver, insulin resistance/diabetes, or cardiovascular events are considerable. Therefore, every strategy designed to reduce obesity would imply important savings. Targeting microbiota, in order to restore/modulate the microbiota composition with antibiotics, probiotics, prebiotics, or even fecal transplants, is considered as a promising strategy for the development of new solutions for the treatment of obesity. However, there is still lot to do in this field in order to identify the exact composition of microbiota in "health" and the specific mechanisms that regulate the host-microbiotal crosstalk. In addition, it is important to note that changes not only in the gut microbiota profile (abundance) but also in its metabolism and functions need to be taken into account in the context of contribution in the physiopathology of obesity and related disorders.
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    • "Also, resveratrol up-regulated SIRT1 expression in the mucosa and mitigated the increase in the number of mucosal CD4+ T cells suggesting that resveratrol may exert its anti-inflammatory effects by modulating activated immune cells [123]. Thus, activation of SIRT1 maintains gut barrier function, which is compromised in obesity [125] and through its regulation of gut inflammation controls colitis and colon cancer, which are also more prevalent in obese individuals [126]. "
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    ABSTRACT: Obesity is a chronic disease characterized by persistent low-grade inflammation with alterations in gut motility. Motor abnormalities suggest that obesity has effects on the enteric nervous system (ENS), which controls virtually all gut functions. Recent studies have revealed that the gut microbiota can affect obesity and increase inflammatory tone by modulating mucosal barrier function. Furthermore, the observation that inflammatory conditions influence the excitability of enteric neurons may add to the gut dysfunction in obesity. In this article, we discuss recent advances in understanding the role of gut microbiota and inflammation in the pathogenesis of obesity and obesity-related gastrointestinal dysfunction. The potential contribution of sirtuins in protecting or regulating the circuitry of the ENS under inflamed states is also considered.
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