scholarly journals The Effect of Inulin on Lifespan, Related Gene Expression and Gut Microbiota in InRp5545/TM3 Mutant Drosophila melanogaster: A Preliminary Study

Nutrients ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 636 ◽  
Author(s):  
Yuling Dong ◽  
Hao Sun ◽  
Weichao Yang ◽  
Shuang Ma ◽  
Beibei Du ◽  
...  
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Gut Microbiota ◽  
Metabolic Diseases ◽  
Insulin Signalling ◽  
Short Chain Fatty Acids ◽  
Preliminary Evidence ◽  
Diet Group ◽  
Standard Diet ◽  
Related Gene

Inulin is considered an efficient prebiotic and is beneficial for metabolic diseases via promoting intestinal probiotic enrichment and the metabolites of short-chain fatty acids (SCFAs). However, the effect of inulin on patients with InR deficiencies has seldom been reported. In this study, the lifespan, related gene expression, and gut microbiota of InRp5545/TM3 (insulin receptor mutant) Drosophila melanogaster under inulin treatment were investigated. The results showed that the lifespan was extended in only males and not in females. Furthermore, distinctly different patterns of gene expression were found between males and females, especially in the insulin/insulin-like growth factor (IGF)-like signalling (IIS) and target of rapamycin (TOR) pathways. Additionally, as a link between inulin and lifespan responses, the gut microbiota was distinctly separated by gender in both the standard diet group and the inulin treatment group, and the relationship between lifespan and the gut microbiota community was stronger in male flies than in females. This study provides preliminary evidence for the gender-dependent lifespan responses to inulin in insulin signalling-deficient Drosophila. However, controls such as wild-type and TM3 flies, and more InR mutant strains with different genetic backgrounds need to be further investigated to elucidate the mechanisms underlying the phenomenon.

scholarly journals The Relationship between Frequently Used Glucose-Lowering Agents and Gut Microbiota in Type 2 Diabetes Mellitus

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
You Lv ◽  
Xue Zhao ◽  
Weiying Guo ◽  
Ying Gao ◽  
Shuo Yang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Gut Microbiota ◽  
Metabolic Diseases ◽  
Short Chain Fatty Acids ◽  
Current Evidence ◽  
Diabetic Patients ◽  
Glucose Lowering ◽  
Patients With Diabetes ◽  
Gastrointestinal Side Effects ◽  
Underlying Mechanisms

Metabolic diseases, especially diabetes mellitus, have become global health issues. The etiology of diabetes mellitus can be attributed to genetic and/or environmental factors. Current evidence suggests the association of gut microbiota with metabolic diseases. However, the effects of glucose-lowering agents on gut microbiota are poorly understood. Several studies revealed that these agents affect the composition and diversity of gut microbiota and consequently improve glucose metabolism and energy balance. Possible underlying mechanisms include affecting gene expression, lowering levels of inflammatory cytokines, and regulating the production of short-chain fatty acids. In addition, gut microbiota may alleviate adverse effects caused by glucose-lowering agents, and this can be especially beneficial in diabetic patients who experience severe gastrointestinal side effects and have to discontinue these agents. In conclusion, gut microbiota may provide a novel viewpoint for the treatment of patients with diabetes mellitus.

scholarly journals A ‘phenotypic hangover’ – the predictive adaptive response and multigenerational effects of altered nutrition on the transcriptome of Drosophila melanogaster

2017 ◽  
Author(s):  
Amy J. Osborne ◽  
Peter K. Dearden
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Adaptive Response ◽  
Communicable Disease ◽  
Later Life ◽  
Standard Diet ◽  
Expression Of Genes ◽  
Postnatal Environment ◽  
Predictive Adaptive Response ◽  
Epigenetic Processes

AbstractThe Developmental Origins of Health and Disease (DOHaD) hypothesis predicts that early-life environmental exposures can be detrimental to later-life health, and that mismatch between the pre- and postnatal environment may contribute to the growing non-communicable disease (NCD) epidemic. Within this is an increasingly recognised role for epigenetic mechanisms; epigenetic modifications can be influenced by, e.g., nutrition, and can alter gene expression in mothers and offspring. Currently, there are no whole-genome transcriptional studies of response to nutritional alteration. Thus, we sought to explore how nutrition affects the expression of genes involved in epigenetic processes in Drosophila melanogaster. We manipulated Drosophila food macronutrient composition at the F0 generation, mismatched F1 offspring back to a standard diet, and analysed the transcriptome of the F0 – F3 generations by RNA-sequencing. At F0, the altered (high protein, low carbohydrate, HPLC) diet increased expression of genes involved in epigenetic processes, with coordinated downregulation of genes involved in immunity, neurotransmission and neurodevelopment, oxidative stress and metabolism. Upon reversion to standard nutrition, mismatched F1 and F2 generations displayed multigenerational inheritance of altered gene expression. By the F3 generation, gene expression had reverted to F0 (matched) levels. These nutritionally-induced gene expression changes demonstrate that dietary alteration can upregulate epigenetic genes, which may influence the expression of genes with broad biological functions. Further, the multigenerational inheritance of the gene expression changes in F1 and F2 mismatched generations suggests a predictive adaptive response (PAR) to maternal nutrition. Our findings may help to understand the interaction between maternal diet and future offspring health, and have direct implications for the current NCD epidemic.

scholarly journals MECHANISMS IN ENDOCRINOLOGY: Gut microbiota in patients with type 2 diabetes mellitus

2015 ◽  
Vol 172 (4) ◽  
pp. R167-R177 ◽  
Author(s):  
Kristine H Allin ◽  
Trine Nielsen ◽  
Oluf Pedersen
Keyword(s):  
Type 2 Diabetes ◽  
Gut Microbiota ◽  
Metabolic Diseases ◽  
Short Chain Fatty Acids ◽  
Intestinal Content ◽  
Low Grade ◽  
Bacterial Fermentation ◽  
Underlying Mechanisms

Perturbations of the composition and function of the gut microbiota have been associated with metabolic disorders including obesity, insulin resistance and type 2 diabetes. Studies on mice have demonstrated several underlying mechanisms including host signalling through bacterial lipopolysaccharides derived from the outer membranes of Gram-negative bacteria, bacterial fermentation of dietary fibres to short-chain fatty acids and bacterial modulation of bile acids. On top of this, an increased permeability of the intestinal epithelium may lead to increased absorption of macromolecules from the intestinal content resulting in systemic immune responses, low-grade inflammation and altered signalling pathways influencing lipid and glucose metabolism. While mechanistic studies on mice collectively support a causal role of the gut microbiota in metabolic diseases, the majority of studies in humans are correlative of nature and thus hinder causal inferences. Importantly, several factors known to influence the risk of type 2 diabetes, e.g. diet and age, have also been linked to alterations in the gut microbiota complicating the interpretation of correlative studies. However, based upon the available evidence, it is hypothesised that the gut microbiota may mediate or modulate the influence of lifestyle factors triggering development of type 2 diabetes. Thus, the aim of this review is to critically discuss the potential role of the gut microbiota in the pathophysiology and pathogenesis of type 2 diabetes.

scholarly journals Effect of Kefir, Yacon (Smallanthus sonchifolius) and the Association Between Yacon and Kefir on Intestinal Physiology in Rats With Colon Cancer

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 309-309
Author(s):  
Neuza Costa ◽  
Keila Zanardi ◽  
Caroline Woelffel ◽  
Andre Costa ◽  
Mirelle Viana ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Intestinal Permeability ◽  
Wistar Rats ◽  
Short Chain Fatty Acids ◽  
Diet Group ◽  
Standard Diet ◽  
Smallanthus Sonchifolius ◽  
Intestinal Physiology ◽  
Significant Difference ◽  
Male Wistar Rats

Abstract Objectives To evaluate the effect of consumption of yacon flour, kefir and the association between them on colon cancer induced by 1,2-dimethylhydrazine (DMH) in male Wistar rats, SCFA production, fecal pH and intestinal permeability. Methods The study was conducted with 60 adult Wistar rats divided into 5 groups. For 5 weeks, groups T, Y, K and YK received 1,2-dimethylhydrazine (DMH) to induce colon cancer. After 5 weeks of DMH administration, animals in groups C and T received the standard diet, group Y received a diet with yacon flour with 5% FOS, group K received 1mL /day of kefir and the YK group received a diet with yacon and kefir, for 15 weeks. After euthanasia, intestinal lesions, intraluminal pH, short-chain fatty acids (SCFA) and intestinal permeability were analyzed. Results An increase in macroscopic lesions was observed in groups K (58%) and YK (42%) and a reduction of 5% in group Y, compared to group T. In addition, an increase in neoplastic changes was observed in all groups compared to group T: Y (33%), K (67%) and YK (78%). There was no significant difference in the concentrations of acetate and proprionate, pH, lactulose and mannitol between groups, and butyrate was not found in the samples. Conclusions The consumption of yacon flour, kefir and their association did not influence intestinal physiology and promoted the worsening of the development of colon carcinogenesis in rats. Funding Sources FAPES - Fundação de Amparo à Pesquisa e Inovação do Espírito Santo CNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológico

scholarly journals Synbiotic Supplementation Modulates Gut Microbiota, Regulates Beta-Catenin Expression And Prevents Weight Gain in ob/ob Mice

2021 ◽  
Author(s):  
Sebastião Mauro Bezerra Duarte ◽  
José Tadeu Stefano ◽  
Lucas A. M. Franco ◽  
Roberta C. Martins ◽  
Bruna D. G. C. Moraes ◽  
...  
Keyword(s):  
Gene Expression ◽  
Weight Gain ◽  
Gut Microbiota ◽  
Body Weight Gain ◽  
Standard Diet ◽  
Beta Catenin ◽  
Reduced Body ◽  
Synbiotic Supplementation ◽  
And Control ◽  
The Impact

Abstract Background: The aim of this study was to examine the impact of synbiotic supplementation in obesity and microbiota in ob/ob mice. 20 animals were divided into four groups: Obese Treated (OT), Control (OC), Lean Treated (LT) and Control (LC). All animals received standard diet for 8 weeks. Treated groups received a synbiotic in water while nontreated groups received water. After 8 weeks, all animals were sacrificed and gut tissue mRNA isolation and stool samples by microbiota analysis were collected. Beta-catenin, occludin, cadherin and zonulin were analyzed in gut tissue by RT-qPCR. Results: The synbiotic supplementation reduced body weight gain in OT comparing with OC (p=0.0398), increase of Enterobacteriaceae (p=0.005) and decrease of Cyanobacteria (p=0.047), Clostridiaceae (p=0.026), Turicibacterales (p=0.005) and Coprococcus (p=0.047). A significant reduction of Sutterella bacteria (p=0.009) and Turicibacter (p=0.005) was observed in LT compared to LC. Alpha and beta diversities were differ between all treated groups. Beta-catenin gene expression was significantly decreased in the gut tissue of OT (p≤0.0001) when compared to other groups. No changes were observed in occludin, cadherin and zonulin gene expression in the gut tissue. Conclusion: The synbiotics supplementation prevents excessive weight gain, modulates the gut microbiota, and reduces beta-catenin expression in ob/ob mice.

scholarly journals The Genetic Evidence of Burn-Induced Cardiac Mitochondrial Metabolism Confusion

2020 ◽  
Author(s):  
Jake J. Wen ◽  
Claire B. Cummins ◽  
Taylor P. Williams ◽  
Ravi S. Radhakrishnan
Keyword(s):  
Gene Expression ◽  
Mitochondrial Dysfunction ◽  
Burn Injury ◽  
Mitochondrial Gene ◽  
Preliminary Evidence ◽  
Mitochondrial Metabolism ◽  
Genetic Evidence ◽  
Differentially Expressed ◽  
Related Gene

Burn-induced cardiac dysfunction is thought to involve mitochondrial dysfunction although the mechanisms responsible are unclear. In this study, we used our established model of in vivo burn injury to understand the genetic evidence of burn-induced mitochondrial metabolism confusion by describing cardiac mitochondrial metabolism-related gene expression after burn. Cardiac tissue was collected at 24 hours after burn injury. An O2K respirometer system was utilized to measure cardiac mitochondrial function. Oxidative phosphorylation complex activities were determined using enzyme activity assays. RT Profiler PCR array was used to identify differential regulation of genes involved in mitochondrial biogenesis and metabolism. Quantitative qPCR and Western Blotting were applied to validate differentially expressed genes. Burn-induced cardiac mitochondrial dysfunction was supported by the finding of decreased state 3 respiration and decreased mitochondrial electron transport chain activity in complex I, III, IV, and V following burn injury. Eighty-four mitochondrial metabolism-related gene profiles were measured. The mitochondrial gene profile showed that one third of genes related to mitochondrial energy and metabolism was differentially expressed. Of these 28 genes, 15 were more than 2-fold upregulated and 13 were more than 2-fold downregulated. All genes were validated using qPCR; 4 genes had a protein level which correlated with the observed change in gene expression. This study provides preliminary evidence that a large percentage of mitochondrial metabolism-related genes in cardiomyocytes were significantly affected by burn injury.

scholarly journals Inulin Exerts Beneficial Effects on Non-Alcoholic Fatty Liver Disease via Modulating gut Microbiome and Suppressing the Lipopolysaccharide-Toll-Like Receptor 4-Mψ-Nuclear Factor-κB-Nod-Like Receptor Protein 3 Pathway via gut-Liver Axis in Mice

2020 ◽  
Vol 11 ◽  
Author(s):  
Ting Bao ◽  
Fang He ◽  
Xiaoxia Zhang ◽  
Lili Zhu ◽  
Zhen Wang ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Short Chain Fatty Acids ◽  
Nuclear Factor Κb ◽  
Diet Group ◽  
Receptor Protein ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Background: Non-alcoholic fatty liver disease (NAFLD) is a common metabolic disease worldwide with chronic low-grade inflammation and alteration of gut microbiota. Inulin (INU) has been confirmed to exhibit benefit for metabolic diseases. The aim of this study was to clarify the effects and mechanism of INU on NAFLD inflammation via gut-liver axis.Methods: C57BL/6 mice were randomly divided into four groups: normal diet group (ND); high-fat diet group (HFD); ND with INU group (ND-INU); HFD with INU group (HFD-INU). After 14 weeks of feeding, mice were sacrificed and associated indications were investigated.Results: Significant increases of body weight, liver weight, liver biochemical aspartate aminotransferase, alanine aminotransferase, triglyceride, total cholesterol and pro-inflammatory indicators (Lipopolysaccharide, interleukin (IL)-18, IL-1β, TNF-α and IL-6), as well as a reduction of plasma IL-10 were observed in HFD group, while INU treatment restored these abnormal indicators. The ratio of hepatic macrophages (Mψs) and Toll-like receptor 4+ Mψs were both reduced with INU intervention. Nuclear factor-κB, nod-like receptor protein 3, apoptosis-associated speck-like protein and caspase-1 were decreased in HFD-INU group. Additionally, the results of 16S rRNA sequencing and analysis showed that INU administration modulated the composition of gut microbial community in NAFLD mice by up-regulating the abundances of Akkermansia and Bifidobacterium as well as down-regulating the abundances of Blautia and the ratio of Firmicutes/Bacteroidetes. Short-chain fatty acids including acetic acid, propionic acid and butyric acid, were increased with INU treatment. Correlation analysis revealed close relationships among inflammatory indicators, metabolic indicators as well as gut microbiota/its metabolite short-chain fatty acids.Conclusion: INU prevents NAFLD via modulating gut microbiota and suppressing Lipopolysaccharide-Toll-like receptor 4-Mψ-Nuclear factor-κB-nod-like receptor protein 3 inflammatory pathway via the gut-liver axis.

scholarly journals Effects of combined d-fagomine and omega-3 PUFAs on gut microbiota subpopulations and diabetes risk factors in rats fed a high-fat diet

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Mercè Hereu ◽  
Sara Ramos-Romero ◽  
Cristina Busquets ◽  
Lidia Atienza ◽  
Susana Amézqueta ◽  
...  
Keyword(s):  
Risk Factors ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Short Chain Fatty Acids ◽  
Standard Diet ◽  
Liver Inflammation ◽  
Omega 3 ◽  
Sprague Dawley ◽  
High Fat ◽  
Related Risk

Abstract Food contains bioactive compounds that may prevent changes in gut microbiota associated with Westernized diets. The aim of this study is to explore the possible additive effects of d-fagomine and ω-3 PUFAs (EPA/DHA 1:1) on gut microbiota and related risk factors during early stages in the development of fat-induced pre-diabetes. Male Sprague Dawley (SD) rats were fed a standard diet, or a high-fat (HF) diet supplemented with d-fagomine, EPA/DHA 1:1, a combination of both, or neither, for 24 weeks. The variables measured were fasting glucose and glucose tolerance, plasma insulin, liver inflammation, fecal/cecal gut bacterial subgroups and short-chain fatty acids (SCFAs). The animals supplemented with d-fagomine alone and in combination with ω-3 PUFAs accumulated less fat than those in the non-supplemented HF group and those given only ω-3 PUFAs. The combined supplements attenuated the high-fat-induced incipient insulin resistance (IR), and liver inflammation, while increasing the cecal content, the Bacteroidetes:Firmicutes ratio and the populations of Bifidobacteriales. The functional effects of the combination of d-fagomine and EPA/DHA 1:1 against gut dysbiosis and the very early metabolic alterations induced by a high-fat diet are mainly those of d-fagomine complemented by the anti-inflammatory action of ω-3 PUFAs.

scholarly journals Role of the Gut Microbiota in Stroke Pathogenesis and Potential Therapeutic Implications

2021 ◽  
pp. 1-9
Author(s):  
Kazuo Yamashiro ◽  
Naohide Kurita ◽  
Takao Urabe ◽  
Nobutaka Hattori
Keyword(s):  
Ischemic Stroke ◽  
Gut Microbiota ◽  
Metabolic Diseases ◽  
Short Chain Fatty Acids ◽  
Stroke Treatment ◽  
Therapeutic Implications ◽  
Gut Dysbiosis ◽  
Treatment And Prevention ◽  
Effective Interventions ◽  
Acute Cerebral Ischemia

<b><i>Background:</i></b> Major advances have been made in stroke treatment and prevention in the past decades. However, the burden of stroke remains high. Identification of novel targets and establishment of effective interventions to improve stroke outcomes are, therefore, needed. Recent research highlights the contribution of the gut microbiota to stroke pathogenesis. <b><i>Summary:</i></b> Compositional and functional alterations of the gut microbiota, termed dysbiosis, are linked to stroke risk factors, such as obesity, metabolic diseases, and atherosclerosis. In acute cerebral ischemia, the gut microbiota plays a key role in bidirectional interactions between the gut and brain, referred to as the microbiota-gut-brain axis. Gut dysbiosis prior to ischemic stroke affects outcomes. Additionally, the brain affects the gut microbiota during acute ischemic brain injury, which in turn impacts outcomes. Interactions between the gut microbiota and stroke pathogenesis are mediated by several factors including bacterial components (e.g., lipopolysaccharide), gut microbiota-related metabolites (e.g., short-chain fatty acids and trimethylamine N-oxide), and the immune and nervous systems. Clinical studies have reported that patients with acute ischemic stroke exhibit gut dysbiosis, which is associated with host metabolism and inflammation, as well as functional outcomes. Modulation of the gut microbiota or its metabolites improves conditions related to stroke pathogenesis, including inflammation, cardiometabolic disease, atherosclerosis, and thrombosis. <b><i>Key Messages:</i></b> Accumulating evidence indicates that the gut microbiota plays a possible role in stroke pathogenesis. Modulation of the gut microbiota may provide a novel therapeutic strategy for the treatment and prevention of stroke.

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