Influences of intestinal flora disorder, inflammation, stress and glycolipid metabolism on depression patients

2021 ◽  
Author(s):  
Fa Ye ◽  
Xiaofan Zhuang ◽  
Yiming Zhang ◽  
Linlin Hu
Keyword(s):  
Intestinal Flora ◽  
Glycolipid Metabolism

Enhancing bile tolerance of Lactobacilli is involved in the hypolipidemic effects of liraglutide

2021 ◽  
Author(s):  
Chang Wang ◽  
Hai-Jie Hu ◽  
Qing-Qing Dong ◽  
Rui Huang ◽  
Wei Zhao ◽  
...  
Keyword(s):  
Normal Saline ◽  
Intestinal Flora ◽  
Ldl Receptor ◽  
Basal Diet ◽  
Lipid Lowering ◽  
Bile Tolerance ◽  
Glycolipid Metabolism ◽  
Real Time Quantitative Pcr ◽  
Rdna Sequencing ◽  
Key Enzyme

Abstract Liraglutide is an analogue of human glucagon-like peptide-1 (GLP-1), an endogenous intestinal hormone which play essential roles in the regulation of glycolipid metabolism. To investigate the role of lactic acid bacteria (LAB) in the lipid-lowering effect of liraglutide, forty mice were divided into normal saline-treated basal diet (NFD), normal saline-treated high-fat food (HFD), 10.0 mg/kg/d simvastatin-treated HFD (SIM + HFD), 200 and 400 μg/kg/d liraglutide-treated HFD (LL + HFD and HL + HFD) groups for 5 weeks. 16S rDNA sequencing, real-time quantitative PCR and western blot were used to detected changes of intestinal flora, cholesterol 7α-hydroxylase (CYP7A1), LDL-receptor (LDLR) and 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR). Results showed that liraglutide could up-regulate CYP7A1 and LDLR, whereas down-regulate HMGCR. Besides, liraglutide enhance the abundance of lactobacillaceae in gut of hyperlipidemic mice and increase the bile tolerance ability of LAB by up-regulating bile salt hydrolases, and the lysate of liraglutide-sensitive LAB could also directly down-regulate HMGCR, the key enzyme in cholesterol synthesis, and inhibit hepatocyte steatosis. These findings might provide new theoretical guidance for clinical application of liraglutide and threw a light on research and development of anti-obesity, hypolipidemic and cholesterol-lowering drugs or functional foods.

scholarly journals Carbon Black Nanoparticles Exposure Induces Intestinal Flora Dysbiosis and Consequent Activation of Gut-Liver Axis Leading to Liver Lipid Accumulation in Zebrafish

2021 ◽  
Author(s):  
Qingqing Liu ◽  
Bing Wang ◽  
Shengchen Wang ◽  
Hongyuan Jing ◽  
Shiwen Xu
Keyword(s):  
Carbon Black ◽  
Lipid Accumulation ◽  
Glycogen Synthase ◽  
Liver Lipid ◽  
Intestinal Flora ◽  
Mucosal Barrier ◽  
Vacuolar Degeneration ◽  
Glycolipid Metabolism ◽  
Ppar Γ ◽  
Carbon Black Nanoparticles

Abstract Background:Carbon black nanoparticles (CBNPs) are a major carbonaceous nanomaterial, which have been widely left in the environment. The integrity of the gut-liver axis function is critical to the survival of animals. Therefore, we studied the effects of three concentrations of CBNPs (50, 100, 200 mg/L) on zebrafish intestines, liver and intestinal flora. Results:The results showed that CBNPs exposure could reduce the diversity of intestinal flora, change the structure of core microbial populations, enhance the permeability of the intestinal mucosal barrier, and cause changes in genes related to tight junctions in intestinal tissues. The H&E staining and Oil red O staining showed that CBNPs exposure would lead to vacuolar degeneration and lipid accumulation in zebrafish liver. Further detection of glycolipid metabolism related genes showed that CBNPs exposure induced the up-regulation of glycolysis related genes PFKFB3, LDHA, and LEPr, reduces the expression of glycogen synthase kinase GSK-3b, and increases lipid transport and production related genes PPAR-α, PPAR-γ, LIPC, apoa4, Fabp2 and Fabp11 expression. Conclusions:In brief, our data demonstrated that CBNPs exposure induced intestinal microflora disturbance in zebrafish can lead to liver lipid accumulation.

scholarly journals Carbon Black Nanoparticles Exposure Induces Intestinal Flora Dysbiosis and Consequent Activation of Gut-liver Axis Leading to Liver Lipid Accumulation in Zebrafish

2021 ◽  
Author(s):  
Qingqing Liu ◽  
Bing Wang ◽  
Shengchen Wang ◽  
Hongyuan Jing ◽  
Shiwen Xu
Keyword(s):  
Lipid Accumulation ◽  
Glycogen Synthase ◽  
Liver Lipid ◽  
Intestinal Flora ◽  
Mucosal Barrier ◽  
Vacuolar Degeneration ◽  
Glycolipid Metabolism ◽  
Ppar Γ ◽  
Carbon Black Nanoparticles ◽  
Carbonaceous Nanomaterial

Abstract BackgroundCarbon black nanoparticles (CBNPs) are a major carbonaceous nanomaterial, which have been widely left in the environment. The integrity of the gut-liver axis function is critical to the survival of animals. Therefore, we studied the effects of three concentrations of CBNPs (50, 100, 200 mg/L) on zebrafish intestines, liver and intestinal flora. ResultsThe results showed that CBNPs exposure could reduce the diversity of intestinal flora, change the structure of core microbial populations, enhance the permeability of the intestinal mucosal barrier, and cause changes in genes related to tight junctions in intestinal tissues. The H&E staining and Oil red O staining showed that CBNPs exposure would lead to vacuolar degeneration and lipid accumulation in zebrafish liver. Further detection of glycolipid metabolism related genes showed that CBNPs exposure induced the up-regulation of glycolysis related genes PFKFB3, LDHA, and LEPr, reduces the expression of glycogen synthase kinase GSK-3b, and increases lipid transport and production related genes PPAR-α, PPAR-γ, LIPC, apoa4, Fabp2 and Fabp11 expression. ConclusionsIn brief, our data demonstrated that CBNPs exposure induced intestinal microflora disturbance in zebrafish can lead to liver lipid accumulation.

Effect of Dapagliflozin on Intestinal Flora in MafA-deficient Mice

2018 ◽  
Vol 24 (27) ◽  
pp. 3223-3231 ◽  
Author(s):  
Luyao Li ◽  
Shiyao Xu ◽  
Tingting Guo ◽  
Shouliang Gong ◽  
Chuan Zhang
Keyword(s):  
Blood Glucose ◽  
High Throughput Sequencing ◽  
Fatty Acid Content ◽  
Fasting Blood Glucose ◽  
Intestinal Flora ◽  
Short Chain Fatty Acids ◽  
The Body ◽  
Short Chain ◽  
Control Group ◽  
Deficient Mice

Objective: To investigate the effect of dapagliflozin on intestinal microflora in MafA-deficient mice using an animal model of diabetes. Methods: Male MafA-deficient mice were administered dapagliflozin (1.0 mg/kg/d) intragastrically for 6 weeks. Mouse body weights and fasting blood glucose levels were measured, and intestinal short-chain fatty acids were measured by gas chromatography. A series of methods was used to analyse the number of primary harmful bacteria in the faeces, and high-throughput sequencing was used to sequence the changes in intestinal flora. Results: The weight of the mice decreased after dapagliflozin gavage, and fasting blood glucose was significantly lower than that in the control group (P < 0.001). Acetic acid and butyric acid contents in the intestinal tracts of the mice increased, and the growth of harmful microorganisms, such as Clostridium perfringens, enterococci, Enterobacteriaceae, and intestinal enterococci, was inhibited. Blautia is a species found in the experimental group and was significantly different from the control and blank groups as determined by the LDA score from highthroughput sequencing. Conclusion: Dapagliflozin can reduce fasting blood glucose, decrease body weight, increase short-chain fatty acid content, regulate the intestinal microecological balance of the body and promote blood glucose and energy homeostasis.

Berberine in the treatment of diabetes mellitus: a review

2020 ◽  
Vol 20 ◽  
Author(s):  
Aleksandra Baska ◽  
Kamil Leis ◽  
Przemysław Gałązka
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Intestinal Flora ◽  
Glucose Absorption ◽  
Hepatocyte Nuclear Factor ◽  
Peripheral Tissues ◽  
Macrophages Polarization ◽  
Treatment Of Diabetes ◽  
Hepatocyte Nuclear Factor 4

: Berberine is an alkaloid found in plants. It has e.g. neuroprotective, anti-inflammatory and hypolipidemic activity. The research proves that it also strongly impacts the carbohydrate metabolism. The compound also protects pancreatic βcells and increases sensitivity to insulin in peripheral tissues via the induction of GLUT-1, GLUT-4 and insulin type 1 (Ins1) receptors activity. It also stimulates glycolysis and leads to a decrease in insulin resistance by macrophages polarization, lipolytic processes induction and energy expenditure enhancement (by reducing body mass and limiting insulin resistance caused by obesity). In liver berberine inhibits FOX01, SREBP1 and ChREBP pathways, and HNF-4α (hepatocyte nuclear factor 4 alpha) mRNA that hinder gluconeogenesis processes. In intestines it blocks α-glucosidase contributing to glucose absorption decrease. Its interference in intestinal flora reduces levels of monosaccharides and suppresses diabetes mellitus complications development.

Sign in / Sign up

Export Citation Format

Share Document