scholarly journals Rhubarb Supplementation Prevents Diet-Induced Obesity and Diabetes in Association with Increased Akkermansia muciniphila in Mice

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 2932
Author(s):  
Marion Régnier ◽  
Marialetizia Rastelli ◽  
Arianne Morissette ◽  
Francesco Suriano ◽  
Tiphaine Le Roy ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Control Diet ◽  
Strongly Correlated ◽  
Akkermansia Muciniphila ◽  
Diet Induced Obesity ◽  
Triglyceride Accumulation ◽  
Obesity And Diabetes ◽  
Nutritional Compounds ◽  
Improve Health

Obesity and obesity-related disorders, such as type 2 diabetes have been progressively increasing worldwide and treatments have failed to counteract their progression. Growing evidence have demonstrated that gut microbiota is associated with the incidence of these pathologies. Hence, the identification of new nutritional compounds, able to improve health through a modulation of gut microbiota, is gaining interest. In this context, the aim of this study was to investigate the gut-driving effects of rhubarb extract in a context of diet-induced obesity and diabetes. Eight weeks old C57BL6/J male mice were fed a control diet (CTRL), a high fat and high sucrose diet (HFHS) or a HFHS diet supplemented with 0.3% (g/g) of rhubarb extract for eight weeks. Rhubarb supplementation fully prevented HFHS-induced obesity, diabetes, visceral adiposity, adipose tissue inflammation and liver triglyceride accumulation, without any modification in food intake. By combining sequencing and qPCR methods, we found that all these effects were associated with a blooming of Akkermansia muciniphila, which is strongly correlated with increased expression of Reg3γ in the colon. Our data showed that rhubarb supplementation is sufficient to protect against metabolic disorders induced by a diet rich in lipid and carbohydrates in association with a reciprocal interaction between Akkermansia muciniphila and Reg3γ.

scholarly journals High-Fat Diet and Age-Dependent Effects of IgA-Bearing Cell Populations in the Small Intestinal Lamina Propria in Mice

2021 ◽  
Vol 22 (3) ◽  
pp. 1165
Author(s):  
Yuta Sakamoto ◽  
Masatoshi Niwa ◽  
Ken Muramatsu ◽  
Satoshi Shimo
Keyword(s):  
Immune Function ◽  
Lamina Propria ◽  
High Fat Diet ◽  
Immunoglobulin A ◽  
Immune Functions ◽  
High Fat ◽  
Intestinal Villi ◽  
Diet Induced Obesity ◽  
Obesity And Diabetes

Several studies highlighted that obesity and diabetes reduce immune function. However, changes in the distribution of immunoglobins (Igs), including immunoglobulin-A (IgA), that have an important function in mucosal immunity in the intestinal tract, are unclear. This study aimed to investigate the impaired immune functions in the context of a diet-induced obese murine model via the assessment of the Igs in the intestinal villi. We used mice fed a high-fat diet (HFD) from four to 12 or 20 weeks of age. The distributions of IgA, IgM, and IgG1 were observed by immunohistochemistry. Interestingly, we observed that IgA was immunolocalized in many cells of the lamina propria and that immunopositive cells increased in mice aged 12 to 20 weeks. Notably, mice fed HFD showed a reduced number of IgA-immunopositive cells in the intestinal villi compared to those fed standard chow. Of note, the levels of IgM and IgG1 were also reduced in HFD fed mice. These results provide insights into the impaired mucosal immune function arising from diet-induced obesity and type 2 diabetes.

LDL receptor but not apolipoprotein E deficiency increases diet-induced obesity and diabetes in mice

2002 ◽  
Vol 282 (1) ◽  
pp. E207-E214 ◽  
Author(s):  
Sandra A. Schreyer ◽  
Cynthia Vick ◽  
Theodore C. Lystig ◽  
Paul Mystkowski ◽  
Renée C. LeBoeuf
Keyword(s):  
Apolipoprotein E ◽  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Wild Type ◽  
Glucose Levels ◽  
Diet Induced Obesity ◽  
Obesity And Diabetes ◽  
Glucose And Lipid Homeostasis

The aim of this study was to determine whether phenotypes associated with type 2 diabetes are altered in dyslipidemic obese mice. C57BL/6 wild-type, low-density lipoprotein (LDL) receptor-deficient (LDLR−/−), and apolipoprotein E-deficient (apoE−/−) mice were fed a high-fat, high-carbohydrate diet (diabetogenic diet), and the development of obesity, diabetes, and hypertriglyceridemia was examined. Wild-type mice became obese and developed hyperglycemia, but not hypertriglyceridemia, in response to this diet. LDLR−/− mice fed the diabetogenic diet became more obese than wild-type mice and developed severe hypertriglyceridemia and hyperleptinemia. Surprisingly, glucose levels were only modestly higher and insulin levels and insulin-to-glucose ratios were not strikingly different from those of wild-type mice. In contrast, diabetogenic diet-fed apoE−/− mice were resistant to changes in glucose and lipid homeostasis despite becoming obese. These data suggest that modifications in lipoprotein profiles associated with loss of the LDL receptor or apoE function have profound and unique consequences on susceptibility to diet-induced obesity and type 2 diabetic phenotypes.

scholarly journals Modulation of gut microbiota dysbioses in type 2 diabetic patients by macrobiotic Ma-Pi 2 diet

2016 ◽  
Vol 116 (1) ◽  
pp. 80-93 ◽  
Author(s):  
Marco Candela ◽  
Elena Biagi ◽  
Matteo Soverini ◽  
Clarissa Consolandi ◽  
Sara Quercia ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Metabolic Control ◽  
Gut Microbiome ◽  
Control Diet ◽  
Normal Weight ◽  
Diabetic Patients ◽  
Open Label ◽  
Type 2 Diabetic Patients ◽  
Before And After

AbstractThe gut microbiota exerts a role in type 2 diabetes (T2D), and deviations from a mutualistic ecosystem layout are considered a key environmental factor contributing to the disease. Thus, the possibility of improving metabolic control in T2D by correcting gut microbiome dysbioses through diet has been evaluated. Here, we explore the potential of two different energy-restricted dietary approaches – the fibre-rich macrobiotic Ma-Pi 2 diet or a control diet recommended by Italian professional societies for T2D treatment – to correct gut microbiota dysbioses in T2D patients. In a previous 21-d open-label MADIAB trial, fifty-six overweight T2D patients were randomised to the Ma-Pi 2 or the control diet. For the present study, stools were collected before and after intervention from a subset of forty MADIAB participants, allowing us to characterise the gut microbiota by 16S rRNA sequencing and imputed metagenomics. To highlight microbiota dysbioses in T2D, the gut microbiota of thirteen normal-weight healthy controls were characterised. According to our findings, both diets were effective in modulating gut microbiome dysbioses in T2D, resulting in an increase of the ecosystem diversity and supporting the recovery of a balanced community of health-promoting SCFA producers, such asFaecalibacterium,Roseburia,Lachnospira,BacteroidesandAkkermansia. The Ma-Pi 2 diet, but not the control diet, was also effective in counteracting the increase of possible pro-inflammatory groups, such asCollinsellaandStreptococcus, in the gut ecosystem, showing the potential to reverse pro-inflammatory dysbioses in T2D, and possibly explaining the greater efficacy in improving the metabolic control.

scholarly journals EXERCISE-INDUCED BENEFITS ON GLUCOSE HANDLING IN A MODEL OF DIET-INDUCED OBESITY ARE REDUCED BY CONCURRENT NICOTINAMIDE MONONUCLEOTIDE

2020 ◽  
Author(s):  
Josephine Yu ◽  
D. Ross Laybutt ◽  
Lynn-Jee Kim ◽  
Lake-Ee Quek ◽  
Lindsay E. Wu ◽  
...  
Keyword(s):  
Treadmill Exercise ◽  
Control Diet ◽  
Redox Status ◽  
Metabolic Effects ◽  
Mitochondrial Activity ◽  
List Type ◽  
Diet Induced Obesity ◽  
Triglyceride Accumulation ◽  
Nicotinamide Mononucleotide ◽  
Exercise Induced

ABSTRACTObjectiveAlmost 40% of adults worldwide are classified as overweight or obese. Exercise is a beneficial intervention in obesity, partly due to increases in mitochondrial activity, with a potential role for the concomitant increase in nicotinamide adenine dinucleotide (NAD+). Recent studies have shown that increasing NAD+ levels through pharmacological supplementation with precursors such as nicotinamide mononucleotide (NMN) improved metabolic health in high fat diet (HFD) fed mice. We examined the combined effects of NMN and treadmill exercise on the metabolic dysregulation in HFD-induced obesity.MethodsFive-week old female C57BL/6J mice were exposed to control diet or HFD. Mice fed HFD were treated with NMN in drinking water (400mg/kg; HNMN), treadmill exercise (HEx) or combined NMN and exercise (HNEx).ResultsUnexpectedly, NMN administration impaired several aspects of exercise-induced benefits in HFD mice, including glucose tolerance, glucose stimulated insulin secretion from islets and reduced hepatic triglyceride accumulation. Mechanistically, HNEx mice displayed increased antioxidant and reduced prooxidant gene expression in both islets and muscle, suggesting that altered redox status is associated with the loss of exercise-induced health benefits with NMN co-treatment.ConclusionOur data show that NMN treatment blocks the beneficial metabolic effects of exercise in a mouse model of diet-induced obesity in association with disturbances in redox metabolism.HighlightsNMN dampened exercise-induced benefits on glucose handling in diet-induced obesity.NMN administration in exercise enhanced ratio of antioxidants to prooxidants.We suggest NMN administration may not be beneficial when NAD+ levels are replete.

scholarly journals Exercise-induced benefits on glucose handling in a model of diet-induced obesity are reduced by concurrent nicotinamide mononucleotide

2021 ◽  
Author(s):  
Josephine Yu ◽  
David Ross Laybutt ◽  
Lynn-Jee Kim ◽  
Lake-Ee Quek ◽  
Lindsay E Wu ◽  
...  
Keyword(s):  
Treadmill Exercise ◽  
Control Diet ◽  
Redox Status ◽  
Metabolic Effects ◽  
Mitochondrial Activity ◽  
Diet Induced Obesity ◽  
Triglyceride Accumulation ◽  
Nicotinamide Mononucleotide ◽  
Glucose Stimulated Insulin Secretion ◽  
Exercise Induced

Almost 40% of adults worldwide are classified as overweight or obese. Exercise is a beneficial intervention in obesity, partly due to increases in mitochondrial activity, and subsequent increases in nicotinamide adenine dinucleotide (NAD+), an important metabolic cofactor. Recent studies have shown that increasing NAD+ levels through pharmacological supplementation with precursors such as nicotinamide mononucleotide (NMN) improved metabolic health in high fat diet (HFD) fed mice. However, the effects of combined exercise and NMN supplementation are unknown. Thus here we examined the combined effects of NMN and treadmill exercise in female mice with established obesity after 10 weeks of diet. Five-week old female C57BL/6J mice were exposed to control diet (n=16) or HFD. Sedentary mice fed HFD were either untreated (HFD; n=16), received NMN in drinking water (400mg/kg; HNMN; n=16), were exposed to treadmill exercise 6 days/week (HEx; n=16) or exercise combined with NMN (HNEx; n=16). Whilst some metabolic benefits of NMN have been described, at this dose, NMN administration impaired several aspects of exercise-induced benefits in obese mice, including glucose tolerance, glucose stimulated insulin secretion from islets and reduced hepatic triglyceride accumulation. HNEx mice also exhibited increased antioxidant and reduced prooxidant gene expression in both islets and muscle, suggesting that altered redox status is associated with the loss of exercise-induced health benefits with NMN co-treatment. Our data show that NMN treatment impedes the beneficial metabolic effects of exercise in a mouse model of diet-induced obesity in association with disturbances in redox metabolism.

scholarly journals The new views on the state of the gut microbiota in obesity and diabetes mellitus type 2

2019 ◽  
Vol 22 (3) ◽  
pp. 253-262
Author(s):  
Elena V. Pokrovskaya ◽  
Minara S. Shamkhalova ◽  
Marina V. Shestakova
Keyword(s):  
Diabetes Mellitus ◽  
Gut Microbiota ◽  
Human Body ◽  
Diabetes Mellitus Type 2 ◽  
Metabolic Disorders ◽  
Developed Countries ◽  
Diabetes Mellitus Type ◽  
Obesity And Diabetes

Obesity is a worldwide problem of the last century, the prevalence of which has reached pandemic proportions in developed countries. Over the past few years, a considerable amount of data has been gathered, reporting a direct link between changes in gut microbiota and the development of obesity, as well as related diseases, primarily, diabetes mellitus type 2. The elaboration of optimal methods of prevention and treatment regimens of these diseases needs to structure the existing knowledge about the mechanisms of development of metabolic disorders, the role of intestinal microbiota in the latter and possible therapeutic targets. This review examines the role of microorganisms in the human body, with the main focus on the developmental origins of metabolic disorders using animal models and accumulated experience of research on their effects on the human body, and also discusses possible treatment options, including bariatric surgery, fecal microbiota transplantation, the use of pre- and probiotics and certain particular groups of glucose-lowering drugs.

scholarly journals Host response to cholestyramine can be mediated by the gut microbiota

2020 ◽  
Author(s):  
Nolan K. Newman ◽  
Philip M. Monnier ◽  
Richard R. Rodrigues ◽  
Manoj Gurung ◽  
Stephany Vasquez-Perez ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Gut Microbiome ◽  
Metabolic Diseases ◽  
Control Diet ◽  
Alpha Diversity ◽  
Mammalian Host ◽  
Beneficial Effects ◽  
Glucose Levels ◽  
Diet Induced Obesity ◽  
Expression Of Genes

AbstractThe gut microbiome has been implicated as a major factor contributing to metabolic diseases as well as being contributors to the response to drugs used for the treatment of such diseases. In this study, using a diet-induced obesity mouse model, we tested the effect of cholestyramine, a bile acid sequestrant, on the murine gut microbiome and mammalian metabolism. We also explored the hypothesis that some beneficial effects of this drug on systemic metabolism can be attributed to alterations in gut microbiota. First, we demonstrated that cholestyramine can decrease glucose and epidydimal fat levels. Next, while investigating gut microbiota we found increased alpha diversity of the gut microbiome of cholestyramine-treated mice, with fourteen taxa showing restoration of abundance to levels resembling those in mice fed with a control diet. Analyzing expression of genes known to be regulated by cholestyramine (including Cyp7a1), we confirmed the expected effect of this drug in the liver and ileum. Finally, using a transkingdom network analysis we inferred Acetatifactor muris and Muribaculum intestinale as potential mediators/modifiers of cholestyramine effects on the mammalian host. In addition, A. muris correlated positively with glucagon (Gcg) expression in the ileum and negatively correlated with small heterodimer partner (Shp) expression in the liver. Interestingly, A. muris also correlated negatively with glucose levels, further indicating the potential probiotic role for A. muris. In conclusion, our results indicate the gut microbiome has a role in the beneficial effects of cholestyramine and suggest specific microbes as targets of future investigations.

scholarly journals Gut Microbiota as the Link between Elevated BCAA Serum Levels and Insulin Resistance

Biomolecules ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 1414
Author(s):  
Jan Gojda ◽  
Monika Cahova
Keyword(s):  
Insulin Resistance ◽  
Gut Microbiota ◽  
Current Knowledge ◽  
Serum Levels ◽  
Signal Molecules ◽  
Resistance Development ◽  
Obesity And Diabetes ◽  
Branched Chain ◽  
Scientific Attention

The microbiota-harboring human gut is an exquisitely active ecosystem that has evolved in a constant symbiosis with the human host. It produces numerous compounds depending on its metabolic capacity and substrates availability. Diet is the major source of the substrates that are metabolized to end-products, further serving as signal molecules in the microbiota-host cross-talk. Among these signal molecules, branched-chain amino acids (BCAAs) has gained significant scientific attention. BCAAs are abundant in animal-based dietary sources; they are both produced and degraded by gut microbiota and the host circulating levels are associated with the risk of type 2 diabetes. This review aims to summarize the current knowledge on the complex relationship between gut microbiota and its functional capacity to handle BCAAs as well as the host BCAA metabolism in insulin resistance development. Targeting gut microbiota BCAA metabolism with a dietary modulation could represent a promising approach in the prevention and treatment of insulin resistance related states, such as obesity and diabetes.

scholarly journals Upregulation of Mir342 in Diet-Induced Obesity Mouse and the Hypothalamic Appetite Control

2021 ◽  
Vol 12 ◽  
Author(s):  
Dongxiao Zhang ◽  
Satoshi Yamaguchi ◽  
Xinhao Zhang ◽  
Boxuan Yang ◽  
Naoko Kurooka ◽  
...  
Keyword(s):  
Food Intake ◽  
Target Gene ◽  
Potential Candidate ◽  
Appetite Control ◽  
Diet Induced Obesity ◽  
Obesity And Diabetes ◽  
Hypothalamic Arcuate Nucleus ◽  
High Sucrose ◽  
Major Target

In obesity and type 2 diabetes, numerous genes are differentially expressed, and microRNAs are involved in transcriptional regulation of target mRNAs, but miRNAs critically involved in the appetite control are not known. Here, we identified upregulation of miR-342-3p and its host gene Evl in brain and adipose tissues in C57BL/6 mice fed with high fat-high sucrose (HFHS) chow by RNA sequencing. Mir342 (-/-) mice fed with HFHS chow were protected from obesity and diabetes. The hypothalamic arcuate nucleus neurons co-express Mir342 and EVL. The percentage of activated NPY+pSTAT3+ neurons were reduced, while POMC+pSTAT3+ neurons increased in Mir342 (-/-) mice, and they demonstrated the reduction of food intake and amelioration of metabolic phenotypes. Snap25 was identified as a major target gene of miR-342-3p and the reduced expression of Snap25 may link to functional impairment hypothalamic neurons and excess of food intake. The inhibition of miR-342-3p may be a potential candidate for miRNA-based therapy.

scholarly journals The Synbiotic Combination of Akkermansia muciniphila and Quercetin Ameliorates Early Obesity and NAFLD through Gut Microbiota Reshaping and Bile Acid Metabolism Modulation

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 2001
Author(s):  
María Juárez-Fernández ◽  
David Porras ◽  
Petar Petrov ◽  
Sara Román-Sagüillo ◽  
María Victoria García-Mediavilla ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Control Diet ◽  
Liver Lipid ◽  
Nutritional Intervention ◽  
In Vivo Model ◽  
Bile Acid Metabolism ◽  
Alcoholic Fatty Liver ◽  
Akkermansia Muciniphila ◽  
Hepatic Expression

Gut microbiota plays a key role in obesity and non-alcoholic fatty liver disease (NAFLD), so synbiotics could be a therapeutic alternative. We aim to evaluate a nutritional intervention together with the administration of the bacteria Akkermansia muciniphila and the antioxidant quercetin in an in vivo model of early obesity and NAFLD. 21-day-old rats were fed with control or high-fat diet for six weeks. Then, all animals received control diet supplemented with/without quercetin and/or A. muciniphila for three weeks. Gut microbiota, NAFLD-related parameters, circulating bile acids (BAs) and liver gene expression were analyzed. The colonization with A. muciniphila was associated with less body fat, while synbiotic treatment caused a steatosis remission, linked to hepatic lipogenesis modulation. The synbiotic promoted higher abundance of Cyanobacteria and Oscillospira, and lower levels of Actinobacteria, Lactococcus, Lactobacillus and Roseburia. Moreover, it favored elevated unconjugated hydrophilic BAs plasma levels and enhanced hepatic expression of BA synthesis and transport genes. A. muciniphila correlated with circulating BAs and liver lipid and BA metabolism genes, suggesting a role of this bacterium in BA signaling. Beneficial effects of A. muciniphila and quercetin combination are driven by gut microbiota modulation, the shift in BAs and the gut-liver bile flow enhancement.

Sign in / Sign up

Export Citation Format

Share Document