Gut microbiota‐derived lipopolysaccharide uptake and trafficking to adipose tissue: implications for inflammation and obesity

Hersoug, Lars-Georg; Møller, Pia Krause; Loft, Steffen

doi:10.1111/obr.12370

Cited by 234 publications

(164 citation statements)

References 180 publications

(223 reference statements)

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“…Higher peripheral levels of LPS in obese compared to lean individuals have also been demonstrated [140] . In addition, 4 h after the ingestion of a high-fat diet, obese individuals displayed higher peripheral increments in LPS compared to healthy controls [141] .…”

Section: Obesity and Type 2 Diabetesmentioning

confidence: 94%

Gut Microbiota, Bacterial Translocation, and Interactions with Diet: Pathophysiological Links between Major Depressive Disorder and Non-Communicable Medical Comorbidities

Slyepchenko

Maes

Jacka

et al. 2016

Psychother Psychosom

220

136

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Background: Persistent low-grade immune-inflammatory processes, oxidative and nitrosative stress (O&NS), and hypothalamic-pituitary-adrenal axis activation are integral to the pathophysiology of major depressive disorder (MDD). The microbiome, intestinal compositional changes, and resultant bacterial translocation add a new element to the bidirectional interactions of the gut-brain axis; new evidence implicates these pathways in the patho-aetiology of MDD. In addition, abnormalities in the gut-brain axis are associated with several chronic non-communicable disorders, which frequently co-occur in individuals with MDD, including but not limited to irritable bowel syndrome (IBS), chronic fatigue syndrome (CFS), obesity, and type 2 diabetes mellitus (T2DM). Methods: We searched the PubMed/MEDLINE database up until May 1, 2016 for studies which investigated intestinal dysbiosis and bacterial translocation (the ‘leaky gut') in the pathophysiology of MDD and co-occurring somatic comorbidities with an emphasis on IBS, CFS, obesity, and T2DM. Results: The composition of the gut microbiota is influenced by several genetic and environmental factors (e.g. diet). Several lines of evidence indicate that gut-microbiota-diet interactions play a significant pathophysiological role in MDD and related medical comorbidities. Gut dysbiosis and the leaky gut may influence several pathways implicated in the biology of MDD, including but not limited to immune activation, O&NS, and neuroplasticity cascades. However, methodological inconsistencies and limitations limit comparisons across studies. Conclusions: Intestinal dysbiosis and the leaky gut may constitute a key pathophysiological link between MDD and its medical comorbidities. This emerging literature opens relevant preventative and therapeutic perspectives.

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Section: Obesity and Type 2 Diabetesmentioning

confidence: 94%

Gut Microbiota, Bacterial Translocation, and Interactions with Diet: Pathophysiological Links between Major Depressive Disorder and Non-Communicable Medical Comorbidities

Slyepchenko

Maes

Jacka

et al. 2016

Psychother Psychosom

220

136

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show abstract

“…They identified a depletion of Parabaceroides distasonis , which has been shown to be anti-inflammatory in the gut and to reduce dextran sodium sulfate-induced inflammatory cytokines and colitis in mice [95]. HFD-fed mice have also been shown to have increased levels of circulating lipopolysaccharide (LPS), a marker of intestinal barrier dysfunction and endotoxemia, which has been shown to promote colorectal cancer development [96]. Another study has suggested that HFD-fed mice have increased colorectal cancer development primarily due to gut dysbiosis associated with obesity.…”

Section: Obesity and Cancermentioning

confidence: 99%

Obesity and cancer: inflammation bridges the two

Kolb

Sutterwala

Zhang

2016

Current Opinion in Pharmacology

321

228

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Obesity is a growing public health problem and affects 35% US adults. Obesity increases the risk of many cancer types and is associated with poor outcomes. Clinical management of cancer patients has been essentially the same between normal weight and obese individuals. Understanding causal mechanisms by which obesity drives cancer initiation and progression is essential for the development of novel precision therapy for obese cancer patients. One caveat is that various mechanisms have been proposed for different cancer types for their progression under obesity. Since obesity is known to have global impact on inflammation, here we will summarize recent literature and discuss the potential of inflammation being the common causal mechanism to promote cancer promotion across cancer types.

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“…Low levels of LPS are physiologically present in the blood of humans and animals. 91 HFD feeding modulates the gut microbiota and increases intestinal permeability, which elevates LPS plasma concentrations. 71,72 In line with these results, LPS also increased miR-155-5p expression in murine pancreatic β-cells in vitro and in vivo.…”

Section: Hyperlipidemia-related Endotoxemia Induces Islet Mir-155-5p mentioning

confidence: 99%

Hyperlipidemia-Induced MicroRNA-155-5p Improves β-Cell Function by TargetingMafb

et al. 2017

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A high-fat diet increases bacterial lipopolysaccharide (LPS) in the circulation and thereby stimulates glucagon-like peptide 1 (GLP-1)–mediated insulin secretion by upregulating interleukin-6 (IL-6). Although microRNA-155-5p (miR-155-5p), which increases IL-6 expression, is upregulated by LPS and hyperlipidemia and patients with familial hypercholesterolemia less frequently develop diabetes, the role of miR-155-5p in the islet stress response to hyperlipidemia is unclear. In this study, we demonstrate that hyperlipidemia-associated endotoxemia upregulates miR-155-5p in murine pancreatic β-cells, which improved glucose metabolism and the adaptation of β-cells to obesity-induced insulin resistance. This effect of miR-155-5p is because of suppression of v-maf musculoaponeurotic fibrosarcoma oncogene family, protein B, which promotes β-cell function through IL-6–induced GLP-1 production in α-cells. Moreover, reduced GLP-1 levels are associated with increased obesity progression, dyslipidemia, and atherosclerosis in hyperlipidemic Mir155 knockout mice. Hence, induction of miR-155-5p expression in β-cells by hyperlipidemia-associated endotoxemia improves the adaptation of β-cells to insulin resistance and represents a protective mechanism in the islet stress response.

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Gut microbiota‐derived lipopolysaccharide uptake and trafficking to adipose tissue: implications for inflammation and obesity

Cited by 234 publications

References 180 publications

Gut Microbiota, Bacterial Translocation, and Interactions with Diet: Pathophysiological Links between Major Depressive Disorder and Non-Communicable Medical Comorbidities

Gut Microbiota, Bacterial Translocation, and Interactions with Diet: Pathophysiological Links between Major Depressive Disorder and Non-Communicable Medical Comorbidities

Obesity and cancer: inflammation bridges the two

Hyperlipidemia-Induced MicroRNA-155-5p Improves β-Cell Function by TargetingMafb

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