Regulation of Gut Microbiota and Metabolic Endotoxemia with Dietary Factors - PubMed (original) (raw)

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Regulation of Gut Microbiota and Metabolic Endotoxemia with Dietary Factors

Nobuo Fuke et al. Nutrients. 2019.

Abstract

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.

Keywords: dietary factors; gut microbiota; lipopolysaccharide; metabolic endotoxemia.

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Conflict of interest statement

The authors, N.F. and H.S., are employees of KAGOME CO., LTD., which has a product and a patent for broccoli sprout extract. N.F. holds stock in KAGOME CO., LTD.

Figures

Figure 1

Figure 1

The number of reported changes of intestinal bacterial genera in dietary factor intervention studies in animals.

Figure 2

Figure 2

A hypothetical schematic of the behavior of Desulfovibrio in the intestine, influx of LPS, and the effects of sulforaphane on Desulfovibrio. Desulfovibrio, a source of LPS, reduces the amount of short-chain fatty acids in the intestinal tract through lactic acid consumption and suppression of growth of Bifidobacterium, thereby attenuating tight junction. In addition, hydrogen sulfide, a metabolite of Desulfovibrio, inhibits peristalsis, thereby retaining the LPS-containing intestinal contents and promoting LPS absorption. The functional component of the broccoli sprouts, glucoraphanin, is metabolized by enteric bacteria to sulforaphane. Sulforaphane inhibits the growth of Desulfovibrio and the entry of LPS into the blood (details are described in the Section 4). LPS: Lipopolysaccharide, GR: Glucoraphanin, SFN: Sulforaphane. Broccoli and sprouts illustrations © irasutoya, 2012 and 2013, respectively.

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