Glucose metabolism: Focus on gut microbiota, the endocannabinoid system and beyond

2014 ◽  
Vol 40 (4) ◽  
pp. 246-257 ◽  
Author(s):  
P.D. Cani ◽  
L. Geurts ◽  
S. Matamoros ◽  
H. Plovier ◽  
T. Duparc
Keyword(s):  
Glucose Metabolism ◽  
Gut Microbiota ◽  
Endocannabinoid System

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

2014 ◽  
Vol 5 (1) ◽  
pp. 3-17 ◽  
Author(s):  
L. Geurts ◽  
A.M. Neyrinck ◽  
N.M. Delzenne ◽  
C. Knauf ◽  
P.D. Cani
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Glucose Metabolism ◽  
Gut Microbiota ◽  
Endocannabinoid System ◽  
Gut Permeability ◽  
Gut Barrier ◽  
Glucagon Like Peptide

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.

scholarly journals Effects of chronic noise on glucose metabolism and gut microbiota–host inflammatory homeostasis in rats

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Bo Cui ◽  
Zhihui Gai ◽  
Xiaojun She ◽  
Rui Wang ◽  
Zhuge Xi
Keyword(s):  
Glucose Metabolism ◽  
Gut Microbiota

scholarly journals Effects of a ready‐to‐eat cereal formula powder on glucose metabolism, inflammation, and gut microbiota in diabetic db/db mice

2020 ◽  
Vol 8 (8) ◽  
pp. 4523-4533
Author(s):  
Caina Li ◽  
Xing Wang ◽  
Sujuan Sun ◽  
Shuainan Liu ◽  
Yi Huan ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Gut Microbiota

Chitosan oligosaccharides improve the disturbance in glucose metabolism and reverse the dysbiosis of gut microbiota in diabetic mice

2018 ◽  
Vol 190 ◽  
pp. 77-86 ◽  
Author(s):  
Junping Zheng ◽  
Xubing Yuan ◽  
Gong Cheng ◽  
Siming Jiao ◽  
Cui Feng ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Gut Microbiota ◽  
Diabetic Mice ◽  
Chitosan Oligosaccharides

scholarly journals Endocannabinoid System in Hepatic Glucose Metabolism, Fatty Liver Disease, and Cirrhosis

2019 ◽  
Vol 20 (10) ◽  
pp. 2516 ◽  
Author(s):  
Ivonne Bazwinsky-Wutschke ◽  
Alexander Zipprich ◽  
Faramarz Dehghani
Keyword(s):  
Insulin Resistance ◽  
Portal Hypertension ◽  
Liver Disease ◽  
Glucose Metabolism ◽  
Cannabinoid Receptors ◽  
Cannabinoid Receptor ◽  
Expression Patterns ◽  
Endocannabinoid System ◽  
Hepatic Glucose Metabolism ◽  
Hepatic Glucose

There is growing evidence that glucose metabolism in the liver is in part under the control of the endocannabinoid system (ECS) which is also supported by its presence in this organ. The ECS consists of its cannabinoid receptors (CBRs) and enzymes that are responsible for endocannabinoid production and metabolism. ECS is known to be differentially influenced by the hepatic glucose metabolism and insulin resistance, e.g., cannabinoid receptor type 1(CB1) antagonist can improve the glucose tolerance and insulin resistance. Interestingly, our own study shows that expression patterns of CBRs are influenced by the light/dark cycle, which is of significant physiological and clinical interest. The ECS system is highly upregulated during chronic liver disease and a growing number of studies suggest a mechanistic and therapeutic impact of ECS on the development of liver fibrosis, especially putting its receptors into focus. An opposing effect of the CBRs was exerted via the CB1 or CB2 receptor stimulation. An activation of CB1 promoted fibrogenesis, while CB2 activation improved antifibrogenic responses. However, underlying mechanisms are not yet clear. In the context of liver diseases, the ECS is considered as a possible mediator, which seems to be involved in the synthesis of fibrotic tissue, increase of intrahepatic vascular resistance and subsequently development of portal hypertension. Portal hypertension is the main event that leads to complications of the disease. The main complication is the development of variceal bleeding and ascites, which have prognostic relevance for the patients. The present review summarizes the current understanding and impact of the ECS on glucose metabolism in the liver, in association with the development of liver cirrhosis and hemodynamics in cirrhosis and its complication, to give perspectives for development of new therapeutic strategies.

scholarly journals TRIM31 Deficiency Is Associated with Impaired Glucose Metabolism and Disrupted Gut Microbiota in Mice

2018 ◽  
Vol 9 ◽  
Author(s):  
Jing Cheng ◽  
Fei Xue ◽  
Meng Zhang ◽  
Cheng Cheng ◽  
Lei Qiao ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Gut Microbiota ◽  
Impaired Glucose Metabolism

scholarly journals Ramulus Mori (Sangzhi) Alkaloids (SZ-A) Ameliorate Glucose Metabolism Accompanied by the Modulation of Gut Microbiota and Ileal Inflammatory Damage in Type 2 Diabetic KKAy Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Quan Liu ◽  
Shuainan Liu ◽  
Hui Cao ◽  
Wenming Ji ◽  
Caina Li ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Glucose Metabolism ◽  
Gut Microbiota ◽  
Gut Microbiome ◽  
Insulin Response ◽  
Mucosal Barrier ◽  
Inflammatory Damage ◽  
Kkay Mice ◽  
Mucosal Barrier Function

The novel Traditional Chinese Medicine Ramulus Mori (Sangzhi) alkaloid tablets (SZ-A) are approved by The China National Medical Products Administration for the treatment of type 2 diabetes mellitus (T2DM). However, the extensive pharmacological characteristics and the underlying mechanism are unknown. This study investigated the mechanisms by which SZ-A ameliorates glucose metabolism in KKAy mice, an animal model of T2DM. Diabetic KKAy mice were treated intragastrically with SZ-A once daily for 8 weeks, after which glucose levels, lipid metabolism, gut microbiome, systemic inflammatory factors, luminal concentrations of short-chain fatty acids (fecal samples), and ileal proteomic changes were evaluated. The ileum tissues were collected, and the effects of SZ-A on pathological inflammatory damage were evaluated by hematoxylin and eosin staining, immunofluorescence, and immunohistochemistry. The mRNA and protein expression levels of various inflammatory markers, including monocyte chemoattractant protein-1 and phosphorylated nuclear factor kappa B p65, were detected in the ileum tissues. SZ-A improved glucose metabolism with enhanced insulin response and elevated glucagon-like peptide 1 (GLP-1) nearly 2.7-fold during the glucose tolerance test in diabetic KKAy mice. Gut microbiota analysis demonstrated that SZ-A administration elevated the abundance of Bacteroidaceae and Verrucomicrobia, reduced the levels of Rikenellaceae and Desulfovibrionaceae; and increased the concentrations of fecal acetic and propionic acids compared to the diabetic model group. Additionally, SZ-A markedly improved ileal inflammatory injury and pro-inflammatory macrophage infiltration and improved intestinal mucosal barrier function in diabetic KKAy mice. SZ-A also attenuated the levels of circulating endotoxin, pro-inflammatory cytokines, and chemokines in the mice sera. Collectively, SZ-A ameliorated the overall metabolic profile including glucose and lipid metabolism in KKAy mice, which may be associated with an improvement in GLP-1 and insulin secretion, at least in part by modulating the gut microbiome and relieving the degree of ileal and systemic inflammation.

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