scholarly journals High-Fat, Western-Style Diet, Systemic Inflammation, and Gut Microbiota: A Narrative Review

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 3164
Author(s):  
Ida Judyta Malesza ◽  
Michał Malesza ◽  
Jarosław Walkowiak ◽  
Nadiar Mussin ◽  
Dariusz Walkowiak ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Systemic Inflammation ◽  
Renin Angiotensin System ◽  
Narrative Review ◽  
Nutrient Ratios ◽  
Low Grade ◽  
High Fat ◽  
Barrier Dysfunction ◽  
Inflammatory Status ◽  
Fat Consumption

The gut microbiota is responsible for recovering energy from food, providing hosts with vitamins, and providing a barrier function against exogenous pathogens. In addition, it is involved in maintaining the integrity of the intestinal epithelial barrier, crucial for the functional maturation of the gut immune system. The Western diet (WD)—an unhealthy diet with high consumption of fats—can be broadly characterized by overeating, frequent snacking, and a prolonged postprandial state. The term WD is commonly known and intuitively understood. However, the strict digital expression of nutrient ratios is not precisely defined. Based on the US data for 1908–1989, the calory intake available from fats increased from 32% to 45%. Besides the metabolic aspects (hyperinsulinemia, insulin resistance, dyslipidemia, sympathetic nervous system and renin-angiotensin system overstimulation, and oxidative stress), the consequences of excessive fat consumption (high-fat diet—HFD) comprise dysbiosis, gut barrier dysfunction, increased intestinal permeability, and leakage of toxic bacterial metabolites into the circulation. These can strongly contribute to the development of low-grade systemic inflammation. This narrative review highlights the most important recent advances linking HFD-driven dysbiosis and HFD-related inflammation, presents the pathomechanisms for these phenomena, and examines the possible causative relationship between pro-inflammatory status and gut microbiota changes.

The ameliorative effect of the Pyracantha fortuneana (Maxim.) H. L. Li extract on intestinal barrier dysfunction through modulating glycolipid digestion and gut microbiota in high fat diet-fed rats

2019 ◽  
Vol 10 (10) ◽  
pp. 6517-6532 ◽  
Author(s):  
Hang Xu ◽  
Chunfang Zhao ◽  
Yutian Li ◽  
Ruiyu Liu ◽  
Mingzhang Ao ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
High Fat Diet ◽  
Intestinal Barrier ◽  
High Fat ◽  
Barrier Dysfunction ◽  
Fruit Extract ◽  
Intestinal Barrier Dysfunction ◽  
Beneficial Effects ◽  
Obese Rats ◽  
Ameliorative Effect

Pyracantha fortuneana fruit extract (PFE) exhibits beneficial effects on IBF in association with the modulation of glycolipid digestion and gut microbiota in HFD-fed obese rats.

Impact of dietary fat on gut microbiota and low-grade systemic inflammation: mechanisms and clinical implications on obesity

2017 ◽  
Vol 69 (2) ◽  
pp. 125-143 ◽  
Author(s):  
Flávia Galvão Cândido ◽  
Flávia Xavier Valente ◽  
Łukasz Marcin Grześkowiak ◽  
Ana Paula Boroni Moreira ◽  
Daniela Mayumi Usuda Prado Rocha ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Systemic Inflammation ◽  
Dietary Fat ◽  
Clinical Implications ◽  
Low Grade

scholarly journals Modulation of the Gut Microbiota by Shen-Yan-Fang-Shuai Formula Improves Obesity Induced by High-Fat Diets

2020 ◽  
Vol 11 ◽  
Author(s):  
Zhen Wang ◽  
Junfeng Lu ◽  
Jingwei Zhou ◽  
Weiwei Sun ◽  
Yang Qiu ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Metabolic Disorders ◽  
Intestinal Barrier ◽  
Fecal Microbiota ◽  
16S Rrna Genes ◽  
Rrna Genes ◽  
Therapeutic Effects ◽  
Low Grade ◽  
High Fat ◽  
Gut Barrier Function

Obesity and related metabolic disorders are associated with intestinal microbiota dysbiosis, disrupted intestinal barrier and chronic inflammation. Shen-Yan-Fang-Shuai formula (SYFSF) is a traditional Chinese herbal formula composed of Astragali Radix, Radix Angelicae Sinensis, Rheum Officinale Baill, and four other herbs. In this study, we identified that SYFSF treatment prevented weight gain, low-grade inflammation and insulin resistance in high-fat diet (HFD)-fed mice. SYFSF also substantially improved gut barrier function, reduced metabolic endotoxemia, as well as systemic inflammation. Sequencing of 16S rRNA genes obtained from fecal samples demonstrated that SYFSF attenuated HFD-induced gut dysbiosis, seen an decreased Firmicutes to Bacteroidetes ratios. Microbial richness and diversity were also higher in the SYFSF-treated HFD group. Furthermore, similar therapeutic effects and changes in gut microbiota profile caused by SYFSF could be replicated by fecal microbiota transfer (FMT). Taken together, our study highlights the efficacy of SYFSF in preventing obesity and related metabolic disorders. Its therapeutic effect is associated with the modulation of gut microbiota, as a prebiotic.

scholarly journals Potato-Resistant Starch Supplementation Improves Microbiota Dysbiosis, Inflammation, and Gut–Brain Signaling in High Fat-Fed Rats

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2710 ◽  
Author(s):  
Elizabeth A. Klingbeil ◽  
Carolina Cawthon ◽  
Rebecca Kirkland ◽  
Claire B. de La Serre
Keyword(s):  
Systemic Inflammation ◽  
Resistant Starch ◽  
High Fat ◽  
Epithelial Barrier Function ◽  
Bacterial Fermentation ◽  
Inflammatory Status ◽  
Afferent Fibers ◽  
Male Wistar Rats ◽  
Compositional Changes ◽  
Gut Microbiota Dysbiosis

(1) High-fat (HF) diet leads to gut microbiota dysbiosis which is associated with systemic inflammation. Bacterial-driven inflammation is sufficient to alter vagally mediated satiety and induce hyperphagia. Promoting bacterial fermentation improves gastrointestinal (GI) epithelial barrier function and reduces inflammation. Resistant starch escape digestion and can be fermented by bacteria in the distal gut. Therefore, we hypothesized that potato RS supplementation in HF-fed rats would lead to compositional changes in microbiota composition associated with improved inflammatory status and vagal signaling. (2) Male Wistar rats (n = 8/group) were fed a low-fat chow (LF, 13% fat), HF (45% fat), or an isocaloric HF supplemented with 12% potato RS (HFRS) diet. (3) The HFRS-fed rats consumed significantly less energy than HF animals throughout the experiment. Systemic inflammation and glucose homeostasis were improved in the HFRS compared to HF rats. Cholecystokinin-induced satiety was abolished in HF-fed rats and restored in HFRS rats. HF feeding led to a significant decrease in positive c fiber staining in the brainstem which was averted by RS supplementation. (4) The RS supplementation prevented dysbiosis and systemic inflammation. Additionally, microbiota manipulation via dietary potato RS prevented HF-diet-induced reorganization of vagal afferent fibers, loss in CCK-induced satiety, and hyperphagia.

scholarly journals Gut Microbiota Mediates the Protective Effects of Dietary Capsaicin against Chronic Low-Grade Inflammation and Associated Obesity Induced by High-Fat Diet

mBio ◽  
2017 ◽  
Vol 8 (3) ◽  
Author(s):  
Chao Kang ◽  
Bin Wang ◽  
Kanakaraju Kaliannan ◽  
Xiaolan Wang ◽  
Hedong Lang ◽  
...  
Keyword(s):  
16S Rrna ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Rrna Gene ◽  
Low Grade ◽  
High Fat ◽  
Microbial Dysbiosis ◽  
Low Grade Inflammation ◽  
Metabolic Endotoxemia

ABSTRACT Metabolic endotoxemia originating from dysbiotic gut microbiota has been identified as a primary mediator for triggering the chronic low-grade inflammation (CLGI) responsible for the development of obesity. Capsaicin (CAP) is the major pungent bioactivator in chili peppers and has potent anti-obesity functions, yet the mechanisms linking this effect to gut microbiota remain obscure. Here we show that mice fed a high-fat diet (HFD) supplemented with CAP exhibit lower levels of metabolic endotoxemia and CLGI associated with lower body weight gain. High-resolution responses of the microbiota were examined by 16S rRNA sequencing, short-chain fatty acid (SCFA) measurements, and phylogenetic reconstruction of unobserved states (PICRUSt) analysis. The results showed, among others, that dietary CAP induced increased levels of butyrate-producing Ruminococcaceae and Lachnospiraceae, while it caused lower levels of members of the lipopolysaccharide (LPS)-producing family S24_7. Predicted function analysis (PICRUSt) showed depletion of genes involved in bacterial LPS synthesis in response to CAP. We further identified that inhibition of cannabinoid receptor type 1 (CB1) by CAP also contributes to prevention of HFD-induced gut barrier dysfunction. Importantly, fecal microbiota transplantation experiments conducted in germfree mice demonstrated that dietary CAP-induced protection against HFD-induced obesity is transferrable. Moreover, microbiota depletion by a cocktail of antibiotics was sufficient to block the CAP-induced protective phenotype against obesity, further suggesting the role of microbiota in this context. Together, our findings uncover an interaction between dietary CAP and gut microbiota as a novel mechanism for the anti-obesity effect of CAP acting through prevention of microbial dysbiosis, gut barrier dysfunction, and chronic low-grade inflammation. IMPORTANCE Metabolic endotoxemia due to gut microbial dysbiosis is a major contributor to the pathogenesis of chronic low-grade inflammation (CLGI), which primarily mediates the development of obesity. A dietary strategy to reduce endotoxemia appears to be an effective approach for addressing the issue of obesity. Capsaicin (CAP) is the major pungent component in red chili (genus Capsicum). Little is known about the role of gut microbiota in the anti-obesity effect of CAP. High-throughput 16S rRNA gene sequencing revealed that CAP significantly increased butyragenic bacteria and decreased LPS-producing bacteria (e.g., members of the S24-7 family) and LPS biosynthesis. By using antibiotics and microbiota transplantation, we prove that gut microbiota plays a causal role in dietary CAP-induced protective phenotype against high-fat-diet-induced CLGI and obesity. Moreover, CB1 inhibition was partially involved in the beneficial effect of CAP. Together, these data suggest that the gut microbiome is a critical factor for the anti-obesity effects of CAP. Metabolic endotoxemia due to gut microbial dysbiosis is a major contributor to the pathogenesis of chronic low-grade inflammation (CLGI), which primarily mediates the development of obesity. A dietary strategy to reduce endotoxemia appears to be an effective approach for addressing the issue of obesity. Capsaicin (CAP) is the major pungent component in red chili (genus Capsicum). Little is known about the role of gut microbiota in the anti-obesity effect of CAP. High-throughput 16S rRNA gene sequencing revealed that CAP significantly increased butyragenic bacteria and decreased LPS-producing bacteria (e.g., members of the S24-7 family) and LPS biosynthesis. By using antibiotics and microbiota transplantation, we prove that gut microbiota plays a causal role in dietary CAP-induced protective phenotype against high-fat-diet-induced CLGI and obesity. Moreover, CB1 inhibition was partially involved in the beneficial effect of CAP. Together, these data suggest that the gut microbiome is a critical factor for the anti-obesity effects of CAP.

scholarly journals Propensity to high-fat diet-induced obesity in rats is associated with changes in the gut microbiota and gut inflammation

2010 ◽  
Vol 299 (2) ◽  
pp. G440-G448 ◽  
Author(s):  
Claire Barbier de La Serre ◽  
Collin L. Ellis ◽  
Jennifer Lee ◽  
Amber L. Hartman ◽  
John C. Rutledge ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
High Fat Diet ◽  
Relative Proportion ◽  
Low Grade ◽  
Sprague Dawley ◽  
High Fat ◽  
Intestinal Alkaline Phosphatase ◽  
Sprague Dawley Rats ◽  
Tlr4 Activation ◽  
Fat Diets

Consumption of diets high in fat and calories leads to hyperphagia and obesity, which is associated with chronic “low-grade” systemic inflammation. Ingestion of a high-fat diet alters the gut microbiota, pointing to a possible role in the development of obesity. The present study used Sprague-Dawley rats that, when fed a high-fat diet, exhibit either an obesity-prone (DIO-P) or obesity-resistant (DIO-R) phenotype, to determine whether changes in gut epithelial function and microbiota are diet or obese associated. Food intake and body weight were monitored daily in rats maintained on either low- or high-fat diets. After 8 or 12 wk, tissue was removed to determine adiposity and gut epithelial function and to analyze the gut microbiota using PCR. DIO-P but not DIO-R rats exhibit an increase in toll-like receptor (TLR4) activation associated with ileal inflammation and a decrease in intestinal alkaline phosphatase, a luminal enzyme that detoxifies lipopolysaccharide (LPS). Intestinal permeability and plasma LPS were increased together with phosphorylation of myosin light chain and localization of occludin in the cytoplasm of epithelial cells. Measurement of bacterial 16S rRNA showed a decrease in total bacterial density and an increase in the relative proportion of Bacteroidales and Clostridiales orders in high-fat-fed rats regardless of phenotype; an increase in Enterobacteriales was seen in the microbiota of DIO-P rats only. Consumption of a high-fat diet induces changes in the gut microbiota, but it is the development of inflammation that is associated with the appearance of hyperphagia and an obese phenotype.

scholarly journals High-fat diet increases the severity of Giardia infection in association with low-grade inflammation and gut microbiota dysbiosis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Thibault Allain ◽  
Elena Fekete ◽  
Olivia Sosnowski ◽  
Dimitri Desmonts de Lamache ◽  
Jean-Paul Motta ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Goblet Cell ◽  
Dietary Fat ◽  
Inflammatory Cells ◽  
Low Grade ◽  
High Fat ◽  
Cell Hyperplasia ◽  
Giardia Infection ◽  
Goblet Cell Hyperplasia ◽  
Β Diversity

AbstractExogenous factors that may influence the pathophysiology of Giardia infection remain incompletely understood. We have investigated the role of dietary fat in the pathogenesis of Giardia infection. Male 3 to 4-week-old C57BL/6 mice were fed either a low fat (LF) or a high fat (HF) diet for 12 days and challenged with G. duodenalis. In infected animals, the trophozoite burden was higher in HF + Giardia mice compared to the LF + Giardia group at day 7 post infection. Fatty acids exerted direct pro-growth effects on Giardia trophozoites. Analysis of disease parameters showed that HF + Giardia mice exhibited more mucosal infiltration by inflammatory cells, decreased villus/crypt ratios, goblet cell hyperplasia, mucus disruption, increased gut motility, and elevated fecal water content compared with LF + Giardia. HF diet-dependent exacerbation of Giardia-induced goblet cell hyperplasia was associated with elevated Atoh1 and Muc2 gene expression. Gut microbiota analysis revealed that the HF diet alone induces a taxonomic shift. HF + Giardia mice exhibited microbiota dysbiosis characterized by an increase of Firmicutes and a decrease of Bacteroidetes and significant changes in α- and β-diversity metrics. Taken together, the findings suggest that a HF diet exacerbates the outcome of Giardia infection. The data demonstrate that elevated dietary fat represents an important exogenous factor promoting the pathophysiology of giardiasis.

scholarly journals Green Plant Pigment, Chlorophyllin, Ameliorates Non-alcoholic Fatty Liver Diseases (NAFLDs) Through Modulating Gut Microbiome in Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
You Yang ◽  
Xile Jiang ◽  
Stephen J. Pandol ◽  
Yuan-Ping Han ◽  
Xiaofeng Zheng
Keyword(s):  
Insulin Resistance ◽  
Gut Microbiota ◽  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Systemic Inflammation ◽  
Gut Microbiome ◽  
Liver Diseases ◽  
High Fat ◽  
Green Pigment ◽  
Alcoholic Fatty Liver

Non-alcoholic fatty liver diseases (NAFLDs) along with metabolic syndrome and Type-2 diabetes (T2D) are increasingly prevalent worldwide. Without an effective resolution, simple hepatic steatosis may lead to non-alcoholic steatohepatitis (NASH), characterized by hepatocyte damage, chronic inflammation, necrosis, fatty degeneration, and cirrhosis. The gut microbiome is vital for metabolic homeostasis. Conversely, dysbiosis contributes to metabolic diseases including NAFLD. Specifically, diet composition is critical for the enterotype of gut microbiota. We reasoned that green pigment rich in vegetables may modulate the gut microbiome for metabolic homeostasis. In this study, C57BL/6 mice under a high fat diet (HFD) were treated with sodium copper chlorophyllin (CHL), a water-soluble derivative of chlorophyll, in drinking water. After 28 weeks of HFD feeding, liver steatosis was established accompanied by gut microbiota dysbiosis, intestinal impairment, endotoxemia, systemic inflammation, and insulin resistance. Administration of CHL effectively alleviated systemic and intestinal inflammation and maintained tight junction in the intestinal barrier. CHL rebalanced gut microbiota in the mice under high fat feeding and attenuated hepatic steatosis, insulin resistance, dyslipidemia, and reduced body weight. Fecal flora transplants from the CHL-treated mice ameliorated steatosis as well. Thus, dietary green pigment or the administration of CHL may maintain gut eubiosis and intestinal integrity to attenuate systemic inflammation and relieve NASH.

scholarly journals Inflammation-Related Mechanisms in Chronic Kidney Disease Prediction, Progression, and Outcome

2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Simona Mihai ◽  
Elena Codrici ◽  
Ionela Daniela Popescu ◽  
Ana-Maria Enciu ◽  
Lucian Albulescu ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Gut Microbiota ◽  
Clinical Care ◽  
Low Grade ◽  
Public Health Burden ◽  
Inflammatory Status ◽  
Low Grade Inflammation ◽  
Gut Microbiota Dysbiosis

Persistent, low-grade inflammation is now considered a hallmark feature of chronic kidney disease (CKD), being involved in the development of all-cause mortality of these patients. Although substantial improvements have been made in clinical care, CKD remains a major public health burden, affecting 10–15% of the population, and its prevalence is constantly growing. Due to its insidious nature, CKD is rarely diagnosed in early stages, and once developed, its progression is unfortunately irreversible. There are many factors that contribute to the setting of the inflammatory status in CKD, including increased production of proinflammatory cytokines, oxidative stress and acidosis, chronic and recurrent infections, altered metabolism of adipose tissue, and last but not least, gut microbiota dysbiosis, an underestimated source of microinflammation. In this scenario, a huge step forward was made by the increasing progression of omics approaches, specially designed for identification of biomarkers useful for early diagnostic and follow-up. Recent omics advances could provide novel insights in deciphering the disease pathophysiology; thus, identification of circulating biomarker panels using state-of-the-art proteomic technologies could improve CKD early diagnosis, monitoring, and prognostics. This review aims to summarize the recent knowledge regarding the relationship between inflammation and CKD, highlighting the current proteomic approaches, as well as the inflammasomes and gut microbiota dysbiosis involvement in the setting of CKD, culminating with the troubling bidirectional connection between CKD and renal malignancy, raised on the background of an inflammatory condition.

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