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 Mechanistically different effects of fat and sugar on insulin resistance, hypertension, and gut microbiota in rats

2018 ◽  
Vol 314 (6) ◽  
pp. E552-E563 ◽  
Author(s):  
Sara Ramos-Romero ◽  
Mercè Hereu ◽  
Lidia Atienza ◽  
Josefina Casas ◽  
Olga Jáuregui ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Gut Microbiota ◽  
Systemic Inflammation ◽  
Dietary Fat ◽  
Short Chain Fatty Acids ◽  
Low Grade ◽  
Long Term Effects ◽  
Inflammatory Infiltration ◽  
Wky Rats ◽  
Wistar Kyoto

Insulin resistance (IR) and impaired glucose tolerance (IGT) are the first manifestations of diet-induced metabolic alterations leading to Type 2 diabetes, while hypertension is the deadliest risk factor of cardiovascular disease. The roles of dietary fat and fructose in the development of IR, IGT, and hypertension are controversial. We tested the long-term effects of an excess of fat or sucrose (fructose/glucose) on healthy male Wistar-Kyoto (WKY) rats. Fat affects IR and IGT earlier than fructose through low-grade systemic inflammation evidenced by liver inflammatory infiltration, increased levels of plasma IL-6, PGE2, and reduced levels of protective short-chain fatty acids without triggering hypertension. Increased populations of gut Enterobacteriales and Escherichia coli may contribute to systemic inflammation through the generation of lipopolysaccharides. Unlike fat, fructose induces increased levels of diacylglycerols (lipid mediators of IR) in the liver, urine F2-isoprostanes (markers of systemic oxidative stress), and uric acid, and triggers hypertension. Elevated populations of Enterobacteriales and E. coli were only detected in rats given an excess of fructose at the end of the study. Dietary fat and fructose trigger IR and IGT in clearly differentiated ways in WKY rats: early low-grade inflammation and late direct lipid toxicity, respectively; gut microbiota plays a role mainly in fat-induced IR, and hypertension is independent of inflammation-mediated IR. The results provide evidence that suggests that the combination of fat and sugar is potentially more harmful than fat or sugar alone when taken in excess.

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 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.

scholarly journals Severe COVID-19 Is Fueled by Disrupted Gut Barrier Integrity

2020 ◽  
Author(s):  
Leila B. Giron ◽  
Harsh Dweep ◽  
Xiangfan Yin ◽  
Han Wang ◽  
Mohammad Damra ◽  
...  
Keyword(s):  
Systems Biology ◽  
Lung Injury ◽  
Gut Microbiota ◽  
Systemic Inflammation ◽  
Clinical Implications ◽  
Metabolic Function ◽  
Gut Barrier ◽  
Barrier Integrity ◽  
Tight Junction Permeability ◽  
Injury Causes

ABSTRACTA disruption of the crosstalk between gut microbiota and the lung (gut-lung axis) has been implicated as a driver of severity during respiratory-related diseases. Lung injury causes systemic inflammation, which disrupts gut barrier integrity, increasing the permeability to gut microbes and their products. This exacerbates inflammation, resulting in positive feedback. To test the possibility that a disrupted gut contributes to Coronavirus disease 2019 (COVID-19) severity, we used a systems biology approach to analyze plasma from COVID-19 patients with varying disease severity and controls. Severe COVID-19 is associated with a dramatic increase in tight junction permeability and translocation of bacterial and fungal products into blood. This intestinal disruption and microbial translocation correlate strongly with increased systemic inflammation and complement activation, lower gut metabolic function, and higher mortality. Our study highlights a previously unappreciated factor with significant clinical implications, disruption in gut barrier integrity, as a force that contributes to COVID-19 severity.

Type 3 resistant starch from Canna edulis modulates obesity and obesity-related low-grade systemic inflammation in mice by regulating gut microbiota composition and metabolism

2021 ◽  
Author(s):  
Jiahui Wu ◽  
Minyi Qiu ◽  
Chi Zhang ◽  
Caijuan Zhang ◽  
Nan Wang ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Systemic Inflammation ◽  
Resistant Starch ◽  
Low Grade ◽  
Microbiota Composition ◽  
Metabolic Inflammation ◽  
Beneficial Effects ◽  
Type 3 ◽  
Gut Microbiota Composition

The beneficial effects of Ce-RS3 might derive from gut microbiota changes, which might improve obesity and metabolic inflammation by altering host-microbiota interactions with impacts on the metabolome.

scholarly journals Oral-Gut-Brain Axis in Experimental Models of Periodontitis: Associating Gut Dysbiosis With Neurodegenerative Diseases

2021 ◽  
Vol 2 ◽  
Author(s):  
Luis Daniel Sansores-España ◽  
Samanta Melgar-Rodríguez ◽  
Katherine Olivares-Sagredo ◽  
Emilio A. Cafferata ◽  
Víctor Manuel Martínez-Aguilar ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Neurodegenerative Diseases ◽  
Systemic Inflammation ◽  
Experimental Models ◽  
Oral Bacteria ◽  
Oral Microbiota ◽  
Low Grade ◽  
Vagus Nerves ◽  
Intestinal Dysbiosis ◽  
The Brain

Periodontitis is considered a non-communicable chronic disease caused by a dysbiotic microbiota, which generates a low-grade systemic inflammation that chronically damages the organism. Several studies have associated periodontitis with other chronic non-communicable diseases, such as cardiovascular or neurodegenerative diseases. Besides, the oral bacteria considered a keystone pathogen, Porphyromonas gingivalis, has been detected in the hippocampus and brain cortex. Likewise, gut microbiota dysbiosis triggers a low-grade systemic inflammation, which also favors the risk for both cardiovascular and neurodegenerative diseases. Recently, the existence of an axis of Oral-Gut communication has been proposed, whose possible involvement in the development of neurodegenerative diseases has not been uncovered yet. The present review aims to compile evidence that the dysbiosis of the oral microbiota triggers changes in the gut microbiota, which creates a higher predisposition for the development of neuroinflammatory or neurodegenerative diseases.The Oral-Gut-Brain axis could be defined based on anatomical communications, where the mouth and the intestine are in constant communication. The oral-brain axis is mainly established from the trigeminal nerve and the gut-brain axis from the vagus nerve. The oral-gut communication is defined from an anatomical relation and the constant swallowing of oral bacteria. The gut-brain communication is more complex and due to bacteria-cells, immune and nervous system interactions. Thus, the gut-brain and oral-brain axis are in a bi-directional relationship. Through the qualitative analysis of the selected papers, we conclude that experimental periodontitis could produce both neurodegenerative pathologies and intestinal dysbiosis, and that periodontitis is likely to induce both conditions simultaneously. The severity of the neurodegenerative disease could depend, at least in part, on the effects of periodontitis in the gut microbiota, which could strengthen the immune response and create an injurious inflammatory and dysbiotic cycle. Thus, dementias would have their onset in dysbiotic phenomena that affect the oral cavity or the intestine. The selected studies allow us to speculate that oral-gut-brain communication exists, and bacteria probably get to the brain via trigeminal and vagus nerves.

scholarly journals Impact of a Healthy Dietary Pattern on Gut Microbiota and Systemic Inflammation in Humans

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1783 ◽  
Author(s):  
Vibeke Telle-Hansen ◽  
Kirsten Holven ◽  
Stine Ulven
Keyword(s):  
Gut Microbiota ◽  
Systemic Inflammation ◽  
Intervention Studies ◽  
Short Chain Fatty Acid ◽  
Dietary Intervention ◽  
Low Grade ◽  
Cardiometabolic Disorders ◽  
Healthy Diets ◽  
Dietary Components ◽  
Gut Microbiota Composition

Gut microbiota have recently been suggested to play a part in low-grade systemic inflammation, which is considered a key risk factor for cardiometabolic disorders. Diet is known to affect gut microbiota; however, the effects of diet and dietary components on gut microbiota and inflammation are not fully understood. In the present review, we summarize recent research on human dietary intervention studies, investigating the effects of healthy diets or dietary components on gut microbiota and systemic inflammation. We included 18 studies that reported how different dietary components altered gut microbiota composition, short-chain fatty acid levels, and/or inflammatory markers. However, the heterogeneity among the intervention studies makes it difficult to conclude whether diets or dietary components affect gut microbiota homeostasis and inflammation. More appropriately designed studies are needed to better understand the effects of diet on the gut microbiota, systemic inflammation, and risk of cardiometabolic disorders.

Modifiable Risk Factors for Dementia: The Role of Gut Microbiota

2021 ◽  
Vol 18 ◽  
Author(s):  
Cristian Cabrera ◽  
Paloma Vicens ◽  
Margarita Torrente
Keyword(s):  
Risk Factors ◽  
Gut Microbiota ◽  
Physical Inactivity ◽  
Metabolic Diseases ◽  
Clinical Implications ◽  
Low Grade ◽  
Modifiable Risk Factors ◽  
Excessive Alcohol Consumption ◽  
Excessive Alcohol

: Dementia is a syndrome resulting from chronic or progressive brain disease. Around 40% of worldwide dementia can be prevented or delayed by modifying 12 risk factors: low educational attainment in early life, mid-life hypertension, mid-life obesity, hearing loss, traumatic brain injury, excessive alcohol consumption, smoking, depression, physical inactivity, social isolation, diabetes mellitus, and air pollution. There is growing evidence that gastrointestinal tract microbiota may significantly contribute to dementia pathogenesis. In particular, gut dysbiosis can trigger metabolic diseases and the progression of low-grade systemic inflammation, being involved in much of the major modifiable risk factors. In this review, we focus on studies that have evaluated the association between modifiable risk factors for dementia and the role of gut microbiota. We also suggest clinical implications for researchers in dementia-gut microbiota related fields.

STUDY OF HS-CRP AND TNF-A LEVELS IN COPD PATIENTS ACCOMPANIED WITH CORONARY ARTERY DISEASE

2014 ◽  
pp. 48-56
Author(s):  
Van Thi Tran ◽  
Van Bang Le ◽  
Thị Thu Huong Hoang
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Systemic Inflammation ◽  
Chronic Obstructive ◽  
Low Grade ◽  
Cross Sectional ◽  
Copd Patients ◽  
Coronary Artery Angiography ◽  
Hs Crp ◽  
Artery Disease

Aim: Some studies have linked the present of chronic obstructive oulmonary disease (COPD) to coronary artery disease (CAD). Low grade systemic inflammation occurs in patients with COPD as well as patients with CAD. This study was designed to find out the concentration differences of hs-CRP and TNF-a in patients having both chronic obstructive pulmonary and coronary artery diseases with those having either. Methods: A cross - sectional descriptive study was conducted in 200 patients undergoing a coronary artery angiography in the Heart Institute, Thong Nhat Hospital and 115 People Hospital. COPD was diagnosed using GOLD classification. Result: Our study had shown that the levels of hs-CRP and TNF-a were statistically increased in patients with COPD, CAD as well as in patients who had COPD with CAD (p<0,05). The levels of hs-CRP were higher in CAD than in COPD nad the levels of TNF-a were higher in COPD than in CAD. In patients with COPD and CAD, there were increased the levels of both hs-CRP and TNF-a in serum. Conclusion: Systemic inflammation presents in both COPD and CAD. Key words: hs-CRP, TNF-a, coronary artery disease (CAD).

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