Gut microbial metabolite short-chain fatty acids and obesity

Li, Xuan; Shimizu, Yuuki; Kimura, Ikuo

doi:10.12938/bmfh.17-010

Cited by 91 publications

(83 citation statements)

References 44 publications

(54 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Recent studies have also shown the influence of gut dysbiosis in the development and progression of atherosclerosis and subsequently CVD [76]. Furthermore, the Akkermansia muciniphila was identified to promote gut barrier functions and have attenuating effects against atherosclerosis [77]. Additionally, the human gut microbiota is associated with obesity, and some members of the gut microbiota found to be present in the feces of atherosclerotic patients, are also present in their plaques [78,79].…”

Section: Impact Of Human Gut Microbiota On Vascular Endothelimmentioning

confidence: 99%

Endothelial Dysfunction in Obesity-Induced Inflammation: Molecular Mechanisms and Clinical Implications

et al. 2020

View full text Add to dashboard Cite

Obesity is characterized by the excessive deposition of fat that may interfere with the normal metabolic process of the body. It is a chronic condition associated with various metabolic syndromes, whose prevalence is grossly increasing, and affects both children and adults. Accumulation of excessive macronutrients on the adipose tissues promotes the secretion and release of inflammatory mediators, including interleukin-6 (IL-6), interleukin 1β, tumor necrotic factor-α (TNF-α), leptin, and stimulation of monocyte chemoattractant protein-1 (MCP-1), which subsequently reduce the production of adiponectin thereby initiating a proinflammatory state. During obesity, adipose tissue synthesizes and releases a large number of hormones and cytokines that alter the metabolic processes, with a profound influence on endothelial dysfunction, a situation associated with the formation of atherosclerotic plaque. Endothelial cells respond to inflammation and stimulation of MCP-1, which is described as the activation of adhesion molecules leading to proliferation and transmigration of leukocytes, which facilitates their increase in atherogenic and thromboembolic potentials. Endothelial dysfunction forms the cornerstone of this discussion, as it has been considered as the initiator in the progression of cardiovascular diseases in obesity. Overexpression of proinflammatory cytokines with subsequent reduction of anti-inflammatory markers in obesity, is considered to be the link between obesity-induced inflammation and endothelial dysfunction. Inhibition of inflammatory mechanisms and management and control of obesity can assist in reducing the risks associated with cardiovascular complications.

show abstract

Section: Impact Of Human Gut Microbiota On Vascular Endothelimmentioning

confidence: 99%

Endothelial Dysfunction in Obesity-Induced Inflammation: Molecular Mechanisms and Clinical Implications

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Diverse microbes in the gut possess the ability to produce SCFAs. Among these, Bacteroides, Ruminococcaceae, Lachnospiraceae, Clostridia, Prevotella, Oscillospira and Verrucomicrobia ( Akkermansia muciniphila ), and Faecalibacteria are most commonly associated with the production of SCFAs 33,34,36,61,88–91 . Fan et al observed that bacteroides including Blautia producta and Bacteroides thetaiotaomicron directly affect C. albicans colonization through SCFAs 2 .…”

Section: Discussionmentioning

confidence: 99%

Antibiotic-induced decreases in the levels of microbial-derived short-chain fatty acids promote gastrointestinal colonization ofCandida albicans

Thangamani¹,

Guinan²,

Wang

et al. 2018

Preprint

View full text Add to dashboard Cite

27Candida albicans is the fourth most common cause of systemic nosocomial infections, 28 posing a significant risk in immunocompromised individuals. As the majority of systemic C. 29 albicans infections stem from endogenous gastrointestinal (GI) colonization, understanding the 30 mechanisms associated with GI colonization is essential in the development of novel methods to 31 prevent C. albicans-related mortality. In this study, we investigated the role of microbial-derived 32 short-chain fatty acids (SCFAs) including acetate, butyrate, and propionate on growth, 33 morphogenesis, and GI colonization of C. albicans. Our results indicate that cefoperazone-treated 34 mice susceptible to C. albicans infection had significantly decreased levels of SCFAs in the cecal 35 contents that correlate with a higher fungal load in the feces. Further, using in vivo concentration 36 of SCFAs, we demonstrated that SCFAs inhibit the growth, germ tube, hyphae and biofilm 37 development of C. albicans in vitro. Collectively, results from this study demonstrate that 38 antibiotic-induced decreases in the levels of SCFAs in the cecum enhances the growth and GI 39 colonization of C. albicans. 40 41 42 Keywords: C. albicans, antibiotic treatment, SCFAs, gastrointestinal colonization, hyphae and 43 attachment.44 45 46 47 48 49 50C. albicans, often present in the healthy gastrointestinal (GI) tract, is harmless to the 51 immunocompetent human host with its resident microbiota 1,2 . Though compelling evidence 52 suggests that disturbances in immune regulation contribute to invasive C. albicans infections, 53 antibiotic-induced gut dysbiosis remains a major risk factor for increased C. albicans colonization 54 and dissemination in immunocompromised patients and individuals with antibiotic-associated 55 diarrhea (AAD) [3][4][5][6][7][8][9][10][11][12][13][14][15][16] . Administration of broad-spectrum antibiotics increases the risk of C. albicans 56 colonization in the gut and the source of systemic infections is often found to be the GI tract 13,16-57 20 . In addition, more than 60% of individuals with AAD test positive for C. albicans and patients 58 treated with antibiotics for Clostridium difficile often develop an episode of candidemia 9,10,14,15,21 . 59Taken together, these studies demonstrate that antibiotic-induced gut dysbiosis in 60 immunocompromised individuals and AAD patients leads to increased colonization of C. albicans 61 and this increased intestinal colonization predisposes high-risk patients to systemic candidiasis 62 22,23 . Therefore, understanding the factors involved in antibiotic-induced gut dysbiosis and 63 subsequent GI colonization of C. albicans is critical to treat and prevent C. albicans pathogenesis. 64 65Antibiotic treatment in mice and humans alters the composition of gut microbiota, 66 ultimately leading to changes in the levels of microbial-derived gut metabolites, mainly bile acids 67 and short-chain fatty acids (SCFAs) [24][25][26][27][28] . Alterations in the normal levels of microbial-derive...

show abstract

“…SCFAs ameliorate insulin sensitivity, energy expenditure, dyslipidemia, intestinal gut‐barrier function, and inflammation, in part through initiation of G‐protein‐coupled receptor‐mediated pathways, upregulating mucin genes, and inhibiting histone deacetylases . Gut microbiota modulate body weight by changing energy balance, gut‐barrier function, inflammatory status, impaired synthesis of SCFA, and bile acid metabolism . Research studies have shown that obese individuals have an increased number of Firmicutes and Actinobacteria and decreased number of Bacteroidetes .…”

Section: Impact Of Gut Microbiota On Obesity and Inflammationmentioning

confidence: 99%

Protective Effects of Anthocyanins in Obesity‐Associated Inflammation and Changes in Gut Microbiome

Jayarathne

Stull

Park

et al. 2019

Molecular Nutrition Food Res

View full text Add to dashboard Cite

Obesity is a complex disease and a major public health epidemic. Chronic, low‐grade inflammation is a common underlying feature of obesity and associated metabolic diseases; adipose tissue is a major contributor to this systemic inflammation. Evidence shows that obesity‐associated inflammation may originate from gut dysfunction, including changes in intestinal bacteria or microbiome profiles. Increasingly, food and plant bioactive compounds with antioxidant and anti‐inflammatory properties are proposed to ameliorate obesity‐associated inflammation. Among these, the health‐promoting effects of anthocyanin‐rich foods are of interest here. Specifically, this review summarizes the reported benefits of anthocyanins in obesity‐associated inflammation and underlying molecular mechanisms, including the role of gut microbiome and cell signaling pathways regulated by anthocyanins both in vivo and in vitro.

show abstract

Gut microbial metabolite short-chain fatty acids and obesity

Cited by 91 publications

References 44 publications

Endothelial Dysfunction in Obesity-Induced Inflammation: Molecular Mechanisms and Clinical Implications

Endothelial Dysfunction in Obesity-Induced Inflammation: Molecular Mechanisms and Clinical Implications

Antibiotic-induced decreases in the levels of microbial-derived short-chain fatty acids promote gastrointestinal colonization ofCandida albicans

Protective Effects of Anthocyanins in Obesity‐Associated Inflammation and Changes in Gut Microbiome

Contact Info

Product

Resources

About