Gut microbiota-mediated tributyltin-induced metabolic disorder in rats

Yuan, Gehui; Zhang, Zhan; Gao, Xingsu; Zhu, Jun; Guo, Wenhui; Wang, Li; Ding, Ping; Jiang, Ping; Li, Lei

doi:10.1039/d0ra07502g

Cited by 17 publications

(16 citation statements)

References 69 publications

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“…Moreover, Bilophila, a genus which is aggravated in response to high-fat diet (HFD) ( Natividad et al., 2018 ), was increased when treated with high ALA diet ( Figures 5 B and S2 ), suggesting that fatty acid supplementation could promote the growth of yet poorly characterized lipophilic bacteria ( Agans et al., 2018 ). Compared with low ALA diet, Desulfovibrio ( Figure 5 B), a genus that associate with increased plasma TMAO levels ( Fu et al., 2020 ) and production of inflammatory cytokines ( Zhang-Sun et al., 2015 ) and Anaerovorax, which observed to mediate inflammation and lipid metabolism abnormalities ( Yuan et al., 2020 ; Figure S2 ), as well as diverse members of the family Lachnospiraceae (particularly, Acetatifactor , Lachnospiraceae_FCS020_group , Lachnospiraceae_NK4A136 , and Eisenbergiella groups), were strikingly reduced in old mice fed a high ALA diet. Consistently, dietary supplementation with high ALA (>16 months) induced a remarkable decrease in plasma TMAO levels in old mice (p < 0.05; Figure 5 C), whereas fecal level of SCFA acetate, but not propionate, was significantly increased in high versus low ALA-fed old mice (p < 0.05; Figures 5 D and 5E).…”

Section: Resultsmentioning

confidence: 99%

Lifelong dietary omega-3 fatty acid suppresses thrombotic potential through gut microbiota alteration in aged mice

et al. 2021

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Summary Aging is a major risk factor for cardiovascular diseases, including thrombotic events. The gut microbiota has been implicated in the development of thrombotic risk. Plant-derived omega-3 fatty acid ɑ-linolenic acid (ALA) confers beneficial anti-platelet and anti-inflammatory effects. Hence, antithrombotic activity elicited by ALA may be partly dependent on its interaction with gut microbiota during aging. Here, we demonstrate that lifelong dietary ALA decreases platelet hyperresponsiveness and thrombus formation in aged mice. These phenotypic changes can be partly attributed to alteration of microbial composition and reduction of its metabolite trimethylamine N-oxide and inflammatory mediators including TNF-α, as well as the upregulated production of short-chain fatty acid acetate. ALA-rich diet also dampens secretion of increased procoagulant factors, tissue factor and plasminogen activator inhibitor-1, in aged mice. Our results suggest long-term ALA supplementation as an attractive, accessible, and well-tolerated nutritional strategy against age-associated platelet hyperreactivity and thrombotic potential.

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Section: Resultsmentioning

confidence: 99%

Lifelong dietary omega-3 fatty acid suppresses thrombotic potential through gut microbiota alteration in aged mice

et al. 2021

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“…At the genus level, OKG increased Actinobacillus , but decreased Turicibacter and [Acetivibrio]_ethanolgignens_group . Intestinal fora [Acetivibrio]_ethanolgignens_group and Turicibacter are involved in immune function ( 47 , 48 ). [Acetivibrio]_ethanolgignens_group can induce metabolic disorder and liver inflammation ( 48 ).…”

Section: Discussionmentioning

confidence: 99%

Ornithine α-Ketoglutarate Alleviates Inflammation via Regulating Ileal Mucosa Microbiota and Metabolites in Enterotoxigenic Escherichia coli-Infected Pigs

Bao

Yang

et al. 2022

Front. Nutr.

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Enterotoxigenic Escherichia coli (ETEC) is one of the main causes of diarrhea in weaned piglets, and ornithine α-ketoglutarate (OKG) as a food supplement has been shown to improve intestinal immune status in animals and humans. However, it remains unknown whether OKG alleviates inflammation through the regulation of gut microbiota and its metabolites on ETEC-infected piglets. This study was conducted to explore the impact of OKG on growth performance, immunity, and ileal mucosa microbiota and its metabolites in piglets infected with ETEC. On a total of 40 pigs, a 2 × 2 factor design was performed; the major factors were diet (basal diet or 1% OKG diet) and challenge (E. coli or LB Broth). The results showed that ETEC-infection inhibited growth performance, and OKG supplementation alleviated growth performance. Interestingly, ETEC-infection increased the serum TNF-α and IL-6, decreased the serum IL-10, downregulated the mRNA expression of IL-1β, IL-6, MyD88, and improved the mRNA expression of IL-8, IL-18, and TLR4. OKG inhibited serum IL-6, suppressed the phosphorylation of downstream signals of NF-κB/JNK in the ileum, and enhanced serum IL-10 and ileum SIgA in ETEC-challenged piglets. OKG supplementation enhanced the mRNA expression of IL-1β and IL-10 and reduced NF-κB and MyD88 in the ileum. Importantly, OKG reversed intestinal microbiota dysfunction, including the diversity of ileal microbiota, the relative abundances of Actinobacillus, Turicibacter, and [Acetivibrio]_ethanolgignens_group, which significantly affected arachidonic acid metabolism and primary bile acid biosynthesis. Collectively, our results suggest that OKG improves growth performance, regulates immunity, and ileal mucosa microbiota and its metabolites in ETEC-infected piglets.

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“…There is a growing appreciation that xenobiotics may exert their impacts on animal health by altering the composition of their microbiotas (15,16,(59)(60)(61)(98)(99)(100).…”

Section: Discussionmentioning

confidence: 99%

“…While TBT has well-documented direct actions on adipocyte differentiation and other aspects of host physiology (27,28,(35)(36)(37)(38)(39)(40), it was only recently shown to alter the composition of gut microbiota in rodents (59)(60)(61). In attempt to test if TBT-modified gut microbiota is sufficient to affect host physiology, Zhan and coworkers transplanted TBTmodified fecal microbiota into recipient mice pre-treated with antibiotics to deplete their resident microbiota, and recapitulated adiposity and metabolic phenotypes observed in donors (60).…”

Section: Discussionmentioning

confidence: 99%

“…It is therefore possible that TBT could also directly impact the composition and activity of host-associated microbial communities. Indeed, recent studies showed TBT exposure affects gut microbiota composition in rats and mice (59)(60)(61). However, the specific role of TBT-modified microbes on host adiposity remains untested, and such TBT-microbiota interactions in other vertebrates are yet unexplored.…”

Section: Introductionmentioning

confidence: 99%

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Tributyltin exposure leads to increased adiposity and reduced abundance of leptogenic bacteria in the zebrafish intestine

Mueller

et al. 2021

Preprint

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The chemical obesogen tributyltin (TBT) is known to promote fat storage in adipose tissue through direct action on vertebrate cells. TBT also has direct toxic effects on microorganisms, raising the possibility that TBT may also promote fat storage in vertebrates by altering their microbiota. Here we show that exposure of conventionally-reared post-embryonic zebrafish to TBT results in increased adiposity, reduced body size, and altered intestinal microbiota composition including reduced relative abundance of Plesiomonas bacteria. To test if those microbiota alterations affected host adiposity, we exposed conventionally-reared zebrafish to intestinal bacterial strains representative of TBT-altered taxa. We found that introduction of a Plesiomonas strain into conventionally-reared zebrafish was sufficient to reduce adiposity and alter intestinal microbiota composition. Using new long-term gnotobiotic zebrafish husbandry methods, we found that colonization of germ-free zebrafish with Plesiomonas was sufficient to reduce host adiposity. Together these results show the leptogenic activity of Plesiomonas on zebrafish hosts, indicating that the ability of TBT to increase adiposity in vivo may be due in part to TBT-mediated modification of the abundance of leptogenic bacteria like Plesiomonas. These findings underscore how complex reciprocal interactions between animals and their microbial and chemical environments can influence energy balance and metabolic health.IMPORTANCEObesogens are environmental chemicals that promote fat storage and are generally thought to exert this effect directly on animal cells. Using zebrafish, we show that the obesogen tributyltin can also promote fat storage by acting upon intestinal microbiota via reduction of bacteria that are sufficient to reduce fat storage.

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Gut microbiota-mediated tributyltin-induced metabolic disorder in rats

Abstract: Tributyltin (TBT), an environmental pollutant widely used in antifouling coatings, can cause multiple-organ toxicity and gut microbiome dysbiosis in organisms, and can even cause changes in the host metabolomic profiles.

Cited by 17 publications

References 69 publications

Lifelong dietary omega-3 fatty acid suppresses thrombotic potential through gut microbiota alteration in aged mice

Lifelong dietary omega-3 fatty acid suppresses thrombotic potential through gut microbiota alteration in aged mice

Ornithine α-Ketoglutarate Alleviates Inflammation via Regulating Ileal Mucosa Microbiota and Metabolites in Enterotoxigenic Escherichia coli-Infected Pigs

Tributyltin exposure leads to increased adiposity and reduced abundance of leptogenic bacteria in the zebrafish intestine

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