Heat Killed Lactobacillus reuteri GMNL-263 Reduces Fibrosis Effects on the Liver and Heart in High Fat Diet-Hamsters via TGF-β Suppression

Wei, Ting; Kuo, Wei Wen; Hsieh, Dennis Jine Yuan; Yeh, Yu Lan; Day, Cecilia Hsuan; Chen, Ya Hui; Chen, Ray Jade; Padma, Viswanadha Vijaya; Chen, Yi Hsing; Huang, Chih Yang

doi:10.3390/ijms161025881

Cited by 52 publications

(37 citation statements)

References 43 publications

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“…In other studies, heat-killed non-viable forms of L. reuteri GMNL-263 were potent enough to prevent weight gain in a diet-induced obesity rat model (Hsieh et al, 2016). In high-fat diet fed hamsters, the same heat- treated material reduced liver fibrosis, blood LDL-cholesterol and plasma malondialdehyde and myocardial cell apoptosis (Ting et al, 2015a,b). A heat-killed L. reuteri ATCC 23272 also reduced pro-inflammatory cytokines, but was less potent than viable forms in reducing eosinophil influx and airway damage (Forsythe et al, 2007); however, killed bacteria were able to reduce visceral pain (Kamiya et al, 2006).…”

Section: Discussionmentioning

confidence: 92%

Microbial lysate upregulates host oxytocin

Varian

Poutahidis

DiBenedictis

et al. 2017

Brain, Behavior, and Immunity

120

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Neuropeptide hormone oxytocin has roles in social bonding, energy metabolism, and wound healing contributing to good physical, mental and social health. It was previously shown that feeding of a human commensal microbe Lactobacillus reuteri (L. reuteri) is sufficient to up-regulate endogenous oxytocin levels and improve wound healing capacity in mice. Here we show that oral L. reuteri-induced skin wound repair benefits extend to human subjects. Further, dietary supplementation with a sterile lysate of this microbe alone is sufficient to boost systemic oxytocin levels and improve wound repair capacity. Oxytocin-producing cells were found to be increased in the caudal paraventricular nucleus [PVN] of the hypothalamus after feeding of a sterile lysed preparation of L. reuteri, coincident with lowered blood levels of stress hormone corticosterone and more rapid epidermal closure, in mouse models. We conclude that microbe viability is not essential for regulating host oxytocin levels. The results suggest that a peptide or metabolite produced by bacteria may modulate host oxytocin secretion for potential public or personalized health goals.

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Section: Discussionmentioning

confidence: 92%

Microbial lysate upregulates host oxytocin

Varian

Poutahidis

DiBenedictis

et al. 2017

Brain, Behavior, and Immunity

120

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“…Recent studies have shown that Oscillospira genus appears to be reduced in patients with NAFLD and NASH . Further, several clinical trials have shown an improved disease state associated to the treatment with different species of Lactobacillus genus as a probiotic . The relative abundance of these genera in dHFD− , in addition to its specific profile at phylum and class levels, could be related to a protective functionality against NAFLD.…”

Section: Discussionmentioning

confidence: 99%

Functional Interactions between Gut Microbiota Transplantation, Quercetin, and High‐Fat Diet Determine Non‐Alcoholic Fatty Liver Disease Development in Germ‐Free Mice

Porras

Nistal

Martínez‐Flórez

et al. 2019

Molecular Nutrition Food Res

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Scope Modulation of intestinal microbiota has emerged as a new therapeutic approach for non‐alcoholic fatty liver disease (NAFLD). Herein, it is addressed whether gut microbiota modulation by quercetin and intestinal microbiota transplantation can influence NAFLD development. Methods and results Gut microbiota donor mice are selected according to their response to high‐fat diet (HFD) and quercetin in terms of obesity and NAFLD‐related biomarkers. Germ‐free recipients displayed metabolic phenotypic differences derived from interactions between microbiota transplanted, diets, and quercetin. Based on the evaluation of hallmark characteristics of NAFLD, it is found that gut microbiota transplantation from the HFD‐non‐responder donor and the HFD‐fed donor with the highest response to quercetin results in a protective phenotype against HFD‐induced NAFLD, in a mechanism that involves gut–liver axis alteration blockage in these receivers. Gut microbiota from the HFD‐responder donor predisposed transplanted germ‐free mice to NAFLD. Divergent protective and deleterious metabolic phenotypes exhibited are related to definite microbial profiles in recipients, highlighting the predominant role of Akkermansia genus in the protection from obesity‐associated NAFLD development. Conclusions The results provide scientific support for the prebiotic capacity of quercetin and the transfer of established metabolic profiles through gut microbiota transplantation as a protective strategy against the development of obesity‐related NAFLD.

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“…Additionally, mice fed methionine-choline diet, a model of severe NASH not associated with obesity or the metabolic syndrome, developed less liver fibrosis when treated with VSL#3 [ 130 ]. Other probiotics also showed beneficial effects in animal models of NAFLD/NASH [ 131 , 132 , 133 , 134 , 135 , 136 , 137 , 138 , 139 ].…”

Section: Microbiota As a Therapeutic Targetmentioning

confidence: 99%

Diet, Microbiota, Obesity, and NAFLD: A Dangerous Quartet

Machado

Cortez‐Pinto

2016

IJMS

107

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Recently, the importance of the gut-liver-adipose tissue axis has become evident. Nonalcoholic fatty liver disease (NAFLD) is the hepatic disease of a systemic metabolic disorder that radiates from energy-surplus induced adiposopathy. The gut microbiota has tremendous influences in our whole-body metabolism, and is crucial for our well-being and health. Microorganisms precede humans in more than 400 million years and our guest flora evolved with us in order to help us face aggressor microorganisms, to help us maximize the energy that can be extracted from nutrients, and to produce essential nutrients/vitamins that we are not equipped to produce. However, our gut microbiota can be disturbed, dysbiota, and become itself a source of stress and injury. Dysbiota may adversely impact metabolism and immune responses favoring obesity and obesity-related disorders such as insulin resistance/diabetes mellitus and NAFLD. In this review, we will summarize the latest evidence of the role of microbiota/dysbiota in diet-induced obesity and NAFLD, as well as the potential therapeutic role of targeting the microbiota in this set.

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Heat Killed Lactobacillus reuteri GMNL-263 Reduces Fibrosis Effects on the Liver and Heart in High Fat Diet-Hamsters via TGF-β Suppression

Cited by 52 publications

References 43 publications

Microbial lysate upregulates host oxytocin

Microbial lysate upregulates host oxytocin

Functional Interactions between Gut Microbiota Transplantation, Quercetin, and High‐Fat Diet Determine Non‐Alcoholic Fatty Liver Disease Development in Germ‐Free Mice

Diet, Microbiota, Obesity, and NAFLD: A Dangerous Quartet

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