Gut microbiota controls adipose tissue expansion, gut barrier and glucose metabolism: novel insights into molecular targets and interventions using prebiotics

Jul 27, 2013Beneficial microbes

Gut bacteria influence fat tissue growth, gut lining health, and blood sugar control, with new findings on targets and prebiotic treatments

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Abstract

Inter-organ communication is crucial for controlling homeostatic systems like energy balance and glucose metabolism.

Pathological conditions such as obesity and type 2 diabetes may result from impaired inter-organ communication.
Metabolic endotoxaemia, characterized by increased plasma lipopolysaccharide levels, is linked to metabolic inflammation and insulin resistance.
Gut microbes may contribute to low-grade inflammation associated with metabolic disorders through gut barrier dysfunction.
Enteroendocrine cells and the endocannabinoid system regulate gut permeability and metabolic endotoxaemia.
Specific metabolic dysregulations across organs may arise from modifications in gut microbiota.
Non-digestible nutrients such as inulin-type fructans and polyphenols could influence gut microbiota composition and activity in the context of obesity and type 2 diabetes.

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Crosstalk between organs is crucial for controlling numerous homeostatic systems (e.g. energy balance, glucose metabolism and immunity). Several pathological conditions, such as obesity and type 2 diabetes, are characterised by a loss of or excessive inter-organ communication that contributes to the development of disease. Recently, we and others have identified several mechanisms linking the gut microbiota with the development of obesity and associated disorders (e.g. insulin resistance, type 2 diabetes, hepatic steatosis). Among these, we described the concept of metabolic endotoxaemia (increase in plasma lipopolysaccharide levels) as one of the triggering factors leading to the development of metabolic inflammation and insulin resistance. Growing evidence suggests that gut microbes contribute to the onset of low-grade inflammation characterising these metabolic disorders via mechanisms associated with gut barrier dysfunctions. We have demonstrated that enteroendocrine cells (producing glucagon-like peptide-1, peptide YY and glucagon-like peptide-2) and the endocannabinoid system control gut permeability and metabolic endotoxaemia. Recently, we hypothesised that specific metabolic dysregulations occurring at the level of numerous organs (e.g. gut, adipose tissue, muscles, liver and brain) rely from gut microbiota modifications. In this review, we discuss the mechanisms linking gut permeability, adipose tissue metabolism, and glucose homeostasis, and recent findings that show interactions between the gut microbiota, the endocannabinoid system and the apelinergic system. These specific systems are discussed in the context of the gut-to-peripheral organ axis (intestine, adipose tissue and brain) and impacts on metabolic regulation. In the present review, we also briefly describe the impact of a variety of non-digestible nutrients (i.e. inulin-type fructans, arabinoxylans, chitin glucans and polyphenols). Their effects on the composition of the gut microbiota and activity are discussed in the context of obesity and type 2 diabetes.

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Gut microbiota controls adipose tissue expansion, gut barrier and glucose metabolism: novel insights into molecular targets and interventions using prebiotics

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