Dietary LPS traces influences disease expression of the diet-induced obese mouse

Lindenberg, Frederikke; Ellekilde, Merete; Thorn, Anders; Kihl, Pernille; Larsen, Christina; Hansen, Christian; Metzdorff, Stine Broeng; Aalbæk, Bent; Hansen, Axel Kornerup

doi:10.1016/j.rvsc.2019.01.005

Cited by 16 publications

(13 citation statements)

References 36 publications

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“…It showed that blood LPS levels were elevated when corn oil and LPS were co-administered. Lindenberg et al reported that LPS concentrations in the blood were higher in mice fed a high-fat diet containing LPS than in mice fed a high-fat diet without LPS [16]. However, the effect of LPS levels in food on blood LPS levels has not been adequately studied in humans and further studies are needed.…”

Section: Fat Intake and Metabolic Endotoxemiamentioning

confidence: 99%

Regulation of Gut Microbiota and Metabolic Endotoxemia with Dietary Factors

Fuke¹,

Nagata

Suganuma³

et al. 2019

Nutrients

177

127

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Metabolic endotoxemia is a condition in which blood lipopolysaccharide (LPS) levels are elevated, regardless of the presence of obvious infection. It has been suggested to lead to chronic inflammation-related diseases such as obesity, type 2 diabetes mellitus, non-alcoholic fatty liver disease (NAFLD), pancreatitis, amyotrophic lateral sclerosis, and Alzheimer’s disease. In addition, it has attracted attention as a target for the prevention and treatment of these chronic diseases. As metabolic endotoxemia was first reported in mice that were fed a high-fat diet, research regarding its relationship with diets has been actively conducted in humans and animals. In this review, we summarize the relationship between fat intake and induction of metabolic endotoxemia, focusing on gut dysbiosis and the influx, kinetics, and metabolism of LPS. We also summarize the recent findings about dietary factors that attenuate metabolic endotoxemia, focusing on the regulation of gut microbiota. We hope that in the future, control of metabolic endotoxemia using dietary factors will help maintain human health.

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Section: Fat Intake and Metabolic Endotoxemiamentioning

confidence: 99%

Regulation of Gut Microbiota and Metabolic Endotoxemia with Dietary Factors

Fuke¹,

Nagata

Suganuma³

et al. 2019

Nutrients

177

127

View full text Add to dashboard Cite

show abstract

“…However, much lower doses are known to induce low-grade inflammation in mice [46]. The unintended dosing of the mothers in our study has been oral, and in a previous study, we did not observe dramatic inflammatory responses after a low oral dose of LPS [30]. On the other hand, it cannot be excluded that some of the effects we observed in the pups of the present study were transferred from the mother and were caused by her ingestion of LPS.…”

Section: Discussionmentioning

confidence: 76%

“…Obviously, we do not know how early before that the effect would have been measurable. However, in a previous study on older diet-induced obese mice, we were unable to register any impact after only two weeks of oral LPS dosing [30]. It is also apparent from the present and previous studies in the low-dose DSS model that such an early-life inflammatory stimulation does not necessarily have major preventive impact on the development of T1D [29, 44], although one study showed a delayed onset if LPS was injected in the prediabetic phase [29].…”

Section: Discussionmentioning

confidence: 97%

“…Consequently, it is relevant to study, which impact early-life ingestion of LPS may have on the pancreatic immune response and T1D development, and whether LPS can be regarded as a part of a mechanistic explanation of the protective effect of vancomycin in NOD mice. As it has been shown that the LPS content of laboratory rodent diets influence the development of regulatory T cells [4] and consequently has a modest impact on rodent models of type 2 diabetes [30], it may also be relevant to elucidate whether it influences the NOD mouse as a model for T1D. We, therefore, hypothesized that administration of LPS in early life would reduce proinflammatory gene expression in the pancreatic lymph node (PLN) and subsequently T1D incidence in NOD mice.…”

Section: Introductionmentioning

confidence: 99%

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Oral LPS Dosing Induces Local Immunological Changes in the Pancreatic Lymph Nodes in Mice

Kihl

Krych

Deng

et al. 2019

Journal of Diabetes Research

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Lacking the initial contact between the immune system and microbial-associated molecular patterns (MAMPs), such as lipopolysaccharides (LPS), early in life, may be regarded as one of the causal factors of the increasing global increase in the incidence of autoimmune diseases, such as type 1 diabetes (T1D). Previously, a reduced incidence of T1D accompanied by dramatically increased abundances of both the mucin-metabolising bacterium Akkermansia muciniphila, and LPS-carrying Proteobacteria was observed, when vancomycin was given to pups of nonobese diabetic (NOD) mice. While the T1D incidence reducing effect of A. muciniphila has been shown in further studies, little is known as to whether the increased abundance of LPS-carrying bacteria also has a protective effect. Therefore, we fed NOD pups with Eschericia coli LPS orally from birth to weaning, which decreased the gene expressions of TNFα, IL-10, IL-6, IFNγ, IL-1β, IL-2, IL-4, and FoxP3 in the pancreatic lymph nodes, while the same gene expression profile in the spleen was unaffected. However, no significant difference in the incidence of T1D, gut microbiota composition, or ileum expression of the genetic markers of gut permeability, Claudin8, Occludin, Zonulin-1 (Tjp1), Claudin15, Muc1, and Muc2 were observed in relation to LPS ingestion. It is, therefore, concluded that early life oral E. coli LPS has an impact on the local immune response, which, however, did not influence T1D incidence in NOD mice later in life.

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“…Intestinal bacterial-derived pathogens such as lipopolysaccharide (LPS) play an important role in obesity-related metabolic disorders 4 . A wide range of studies have found that LPS appears to induce chronic low-grade in ammation and regulate fat deposition, which causes insulin resistance and type 2 diabetes mellitus (T2DM) 5,6 .…”

Section: Introductionmentioning

confidence: 99%

Roux-En-Y Gastric Bypass Improved Intestinal Permeability by Regulating Gut Innate Immunity in Diet-Induced Obese Mice

Jin

Chen

Zhou

et al. 2020

Preprint

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Roux-en-Y gastric bypass (RYGB) has been proven to be the most effective treatment for morbid obesity, yet the impact of RYGB on intestinal permeability is fully unknown. In this work, we subjected obese mice to RYGB and sham operation procedures. Serum lipopolysaccharide (LPS), inflammatory cytokines and intestinal permeability were measured at 8 weeks postsurgery. In contrast to sham surgery, RYGB reduced body weight, improved glucose tolerance and insulin resistance, and decreased serum levels of LPS, IL6 and TNFα. Intestinal permeability of the common limb and colon was significantly improved in the RYGB group compared to the sham group. The mRNA levels of IL1β, IL6, and TLR4 of the intestine were significantly decreased in the RYGB group compared with the sham group. The expression of intestinal islet-derived 3β (REG3β), islet-derived 3γ (REG3γ) and IAP was higher in the RYGB group than in the sham group. In conclusion, in a diet-induced obesity (DIO) mouse model,RYGB improved intestinal permeability and attenuated systemic inflammation by downregulating intestinal inflammation and innate immunity, which might result from enhanced production of IAP and antimicrobial peptides.

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Dietary LPS traces influences disease expression of the diet-induced obese mouse

Cited by 16 publications

References 36 publications

Regulation of Gut Microbiota and Metabolic Endotoxemia with Dietary Factors

Regulation of Gut Microbiota and Metabolic Endotoxemia with Dietary Factors

Oral LPS Dosing Induces Local Immunological Changes in the Pancreatic Lymph Nodes in Mice

Roux-En-Y Gastric Bypass Improved Intestinal Permeability by Regulating Gut Innate Immunity in Diet-Induced Obese Mice

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