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

  title={Gut microbiota controls adipose tissue expansion, gut barrier and glucose metabolism: novel insights into molecular targets and interventions using prebiotics.},
  author={Lucie Geurts and Audrey M. Neyrinck and N. M. Delzenne and Claude Knauf and Patrice D Cani},
  journal={Beneficial microbes},
  volume={5 1},
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… 

Figures from this paper

Adipose tissue NAPE-PLD controls fat mass development by altering the browning process and gut microbiota

It is reported that Napepld-deleted mice present an altered browning programme and are less responsive to cold-induced browning, highlighting the essential role of NAPE-PLD in regulating energy homeostasis and metabolism in the physiological state.

Inflammation and Gut-Brain Axis During Type 2 Diabetes: Focus on the Crosstalk Between Intestinal Immune Cells and Enteric Nervous System

The role of the crosstalk between intestinal immune cells and ENS neurons in the control of glycemia is focused on and its potential contribution and role on the immune and neuronal systems are discussed.

Intestinal Barrier Function and Immune Homeostasis Are Missing Links in Obesity and Type 2 Diabetes Development

Intestinal epithelial cells emerged as critical modulators of obesity and glucose homeostasis through their effect on lipopolysaccharide (LPS) signaling and decontamination and create a link between microbial metabolites and whole-body metabolic function.

Talking microbes: When gut bacteria interact with diet and host organs

Obesity and diabetes have reached epidemic proportions. Evidence suggests that besides dietary habits and physical activity, other environmental factors, such as gut microbes, are recognized as

Obesity and Metabolic Syndrome

Insulin resistance in obesity: an overview of fundamental alterations

An overview of concepts and their potential inter-relationships in the development of insulin resistance, with particular regard to changes in adipose organ and skeletal muscle is provided.



Involvement of gut microbiota in the development of low-grade inflammation and type 2 diabetes associated with obesity

Obesity is associated with metabolic alterations related to glucose homeostasis and cardiovascular risk factors. These metabolic alterations are associated with low-grade inflammation that

The role of the gut microbiota in energy metabolism and metabolic disease.

Data obtained in experimental models and human subjects are in favour of the fact that changing the gut microbiota (with prebiotics and/or probiotics) may participate in the control of the development of metabolic diseases associated with obesity.

Altered Gut Microbiota and Endocannabinoid System Tone in Obese and Diabetic Leptin-Resistant Mice: Impact on Apelin Regulation in Adipose Tissue

Deep-gut microbiota profiling revealed that the gut microbial community of type 2 diabetic mice is significantly different from that of their lean counterparts, which indicates specific relationships between the gut microbiota and the regulation of the apelinergic system.

Targeting gut microbiota in obesity: effects of prebiotics and probiotics

The gut microbiota is a potential nutritional and pharmacological target in the management of obesity and obesity-related disorders and suggests that specific phyla, classes or species of bacteria, or bacterial metabolic activities could be beneficial or detrimental to patients with obesity.

Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fat Diet–Induced Obesity and Diabetes in Mice

It is found that changes of gut microbiota induced by an antibiotic treatment reduced metabolic endotoxemia and the cecal content of LPS in both high-fat–fed and ob/ob mice, demonstrating that changes in gut microbiota controls metabolic endotoxinemia, inflammation, and associated disorders by a mechanism that could increase intestinal permeability.

Changes in gut microbiota control inflammation in obese mice through a mechanism involving GLP-2-driven improvement of gut permeability

It is found that a selective gut microbiota change controls and increases endogenous GLP-2 production, and consequently improves gut barrier functions by a GLP1-2-dependent mechanism, contributing to the improvement of Gut barrier functions during obesity and diabetes.

The endocannabinoid system links gut microbiota to adipogenesis

It is reported that gut microbiota modulate the intestinal eCB system tone, which in turn regulates gut permeability and plasma lipopolysaccharide (LPS) levels, and shows that LPS acts as a master switch to control adipose tissue metabolism both in vivo and ex vivo by blocking cannabinoid‐driven adipogenesis.

The gut microbiota as an environmental factor that regulates fat storage.

It is found that conventionalization of adult germ-free (GF) C57BL/6 mice with a normal microbiota harvested from the distal intestine of conventionally raised animals produces a 60% increase in body fat content and insulin resistance within 14 days despite reduced food intake.

Metabolic adaptation to a high-fat diet is associated with a change in the gut microbiota

The HFD-D gut microbial profile was associated with increased gut permeability linked to increased endotoxaemia and to a dramatic increase in cell number in the stroma vascular fraction from visceral white adipose tissue.

Mechanisms underlying the resistance to diet-induced obesity in germ-free mice

GF animals are protected from diet-induced obesity by two complementary but independent mechanisms that result in increased fatty acid metabolism: elevated levels of Fiaf, which induces Pgc-1α; and increased AMPK activity.