Altered Gut Microbiota Profile in Lin28a Transgenic Mice Can Improve Glucose Tolerance

2021 ◽  
Author(s):  
J. Chen ◽  
W. Liu
Keyword(s):  
Glucose Tolerance ◽  
Gut Microbiota ◽  
Transgenic Mice ◽  
Improve Glucose Tolerance

scholarly journals Alterations in the Gut-Microbial-Inflammasome-Brain Axis in a Mouse Model of Alzheimer’s Disease

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 779
Author(s):  
Pradeep K. Shukla ◽  
David F. Delotterie ◽  
Jianfeng Xiao ◽  
Joseph F. Pierre ◽  
RadhaKrishna Rao ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Gut Microbiota ◽  
Transgenic Mice ◽  
Nlrp3 Inflammasome ◽  
Inflammasome Activation ◽  
Gut Barrier Function ◽  
Elevated Expression ◽  
5Xfad Mice

Alzheimer’s disease (AD), a progressive neurodegenerative disorder characterized by memory loss and cognitive decline, is a major cause of death and disability among the older population. Despite decades of scientific research, the underlying etiological triggers are unknown. Recent studies suggested that gut microbiota can influence AD progression; however, potential mechanisms linking the gut microbiota with AD pathogenesis remain obscure. In the present study, we provided a potential mechanistic link between dysbiotic gut microbiota and neuroinflammation associated with AD progression. Using a mouse model of AD, we discovered that unfavorable gut microbiota are correlated with abnormally elevated expression of gut NLRP3 and lead to peripheral inflammasome activation, which in turn exacerbates AD-associated neuroinflammation. To this end, we observe significantly altered gut microbiota compositions in young and old 5xFAD mice compared to age-matched non-transgenic mice. Moreover, 5xFAD mice demonstrated compromised gut barrier function as evident from the loss of tight junction and adherens junction proteins compared to non-transgenic mice. Concurrently, we observed increased expression of NLRP3 inflammasome and IL-1β production in the 5xFAD gut. Consistent with our hypothesis, increased gut–microbial–inflammasome activation is positively correlated with enhanced astrogliosis and microglial activation, along with higher expression of NLRP3 inflammasome and IL-1β production in the brains of 5xFAD mice. These data indicate that the elevated expression of gut–microbial–inflammasome components may be an important trigger for subsequent downstream activation of inflammatory and potentially cytotoxic mediators, and gastrointestinal NLRP3 may promote NLRP3 inflammasome-mediated neuroinflammation. Thus, modulation of the gut microbiota may be a potential strategy for the treatment of AD-related neurological disorders in genetically susceptible hosts.

scholarly journals Gut microbiota and diet in patients with various glucose tolerance

2016 ◽  
Author(s):  
Lilit Egshatyan ◽  
Daria Kashtanova ◽  
Anna Popenko ◽  
Olga Tkacheva ◽  
Alexander Tyakht ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Gut Microbiota

Inulin fiber dose-dependently modulates energy balance, glucose tolerance, gut microbiota, hormones and diet preference in high-fat-fed male rats

2018 ◽  
Vol 59 ◽  
pp. 142-152 ◽  
Author(s):  
Arashdeep Singh ◽  
Rizaldy C. Zapata ◽  
Adel Pezeshki ◽  
Roger D. Reidelberger ◽  
Prasanth K. Chelikani
Keyword(s):  
Energy Balance ◽  
Glucose Tolerance ◽  
Gut Microbiota ◽  
Male Rats ◽  
High Fat ◽  
Diet Preference

scholarly journals Can targeting ANGPTL proteins improve glucose tolerance?

Diabetologia ◽  
2018 ◽  
Vol 61 (6) ◽  
pp. 1277-1281 ◽  
Author(s):  
Brandon S. J. Davies
Keyword(s):  
Glucose Tolerance ◽  
Improve Glucose Tolerance

scholarly journals Characterization of the Gut Microbiota of Individuals at Different T2D Stages Reveals a Complex Relationship with the Host

2020 ◽  
Vol 8 (1) ◽  
pp. 94 ◽  
Author(s):  
Alejandra Chávez-Carbajal ◽  
María Luisa Pizano-Zárate ◽  
Fernando Hernández-Quiroz ◽  
Guillermo Federico Ortiz-Luna ◽  
Rosa María Morales-Hernández ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Metabolic Pathways ◽  
Dietary Intervention ◽  
Metabolic Characteristics ◽  
Significant Difference ◽  
Bacterial Richness ◽  
Microbiota Diversity ◽  
Improve Glucose Tolerance ◽  
M 14

In this work, we studied 217 Mexican subjects divided into six groups with different stages of glucose intolerance: 76 Controls (CO), 54 prediabetes (PRE), 14 T2D no medication (T2D−No−M), 14 T2D with Metformin (T2D−M), 22 T2D with polypharmacy (T2D−P), and 37 T2D with polypharmacy and insulin (T2D−P+I). We aimed to determine differences in the gut microbiota diversity for each condition. At the phylum level, we found that Firmicutes and Bacteroidetes outline major changes in the gut microbiota. The gut bacterial richness and diversity of individuals in the T2D−No−M group were lesser than other groups. Interestingly, we found a significant difference in the beta diversity of the gut microbiota among all groups. Higher abundance was found for Comamonadaceae in PRE, and Sutterella spp. in T2D−No−M. In addition, we found associations of specific microbial taxa with clinical parameters. Finally, we report predicted metabolic pathways of gut microbiota linked to T2D−M and PRE conditions. Collectively, these results indicate that each group has specific predicted metabolic characteristics and gut bacteria populations for each phenotype. The results of this study could be used to define strategies to modulate gut microbiota through noninvasive treatments, such as dietary intervention, probiotics or prebiotics, and to improve glucose tolerance of individuals with prediabetes or T2D.

scholarly journals Effects of whole-grain wheat, rye, and lignan supplementation on cardiometabolic risk factors in men with metabolic syndrome: a randomized crossover trial

2020 ◽  
Vol 111 (4) ◽  
pp. 864-876
Author(s):  
Anne K Eriksen ◽  
Carl Brunius ◽  
Mohsen Mazidi ◽  
Per M Hellström ◽  
Ulf Risérus ◽  
...  
Keyword(s):  
Risk Factors ◽  
Metabolic Syndrome ◽  
Glucose Tolerance ◽  
Gut Microbiota ◽  
Ldl Cholesterol ◽  
Oral Glucose ◽  
Microbiota Composition ◽  
Whole Grain ◽  
The Metabolic Syndrome

ABSTRACT Background A whole-grain (WG)–rich diet has shown to have potential for both prevention and treatment of the metabolic syndrome (MetS), which is a cluster of risk factors that increase the risk of type 2 diabetes and cardiovascular disease. Different WGs may have different health effects. WG rye, in particular, may improve glucose homeostasis and blood lipids, possibly mediated through fermentable dietary fiber and lignans. Recent studies have also suggested a crucial role of the gut microbiota in response to WG. Objectives The aim was to investigate WG rye, alone and with lignan supplements [secoisolariciresinol diglucoside (SDG)], and WG wheat diets on glucose tolerance [oral-glucose-tolerance test (OGTT)], other cardiometabolic outcomes, enterolignans, and microbiota composition. Moreover, we exploratively evaluated the role of gut microbiota enterotypes in response to intervention diets. Methods Forty men with MetS risk profile were randomly assigned to WG diets in an 8-wk crossover study. The rye diet was supplemented with 280 mg SDG at weeks 4–8. Effects of treatment were evaluated by mixed-effects modeling, and effects on microbiota composition and the role of gut microbiota as a predictor of response to treatment were analyzed by random forest plots. Results The WG rye diet (± SDG supplements) did not affect the OGTT compared with WG wheat. Total and LDL cholesterol were lowered (−0.06 and −0.09 mmol/L, respectively; P < 0.05) after WG rye compared with WG wheat after 4 wk but not after 8 wk. WG rye resulted in higher abundance of Bifidobacterium [fold-change (FC) = 2.58, P < 0.001] compared with baseline and lower abundance of Clostridium genus compared with WG wheat (FC = 0.54, P = 0.02). The explorative analyses suggest that baseline enterotype is associated with total and LDL-cholesterol response to diet. Conclusions WG rye, alone or with SDG supplementation, compared with WG wheat did not affect glucose metabolism but caused transient LDL-cholesterol reduction. The effect of WG diets appeared to differ according to enterotype. This trial was registered at www.clinicaltrials.gov as NCT02987595.

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