High Prevalence of Small Intestinal Bacterial Overgrowth in Patients with Morbid Obesity: A Contributor to Severe Hepatic Steatosis

Sabaté, Jean‐Marc; Jouët, Pauline; Harnois, Florence; Mechler, Charlotte; Msika, Simon; Grossin, M; Coffin, Benoït

doi:10.1007/s11695-007-9398-2

Cited by 233 publications

(167 citation statements)

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“…4,7,9,31 Indeed, Miele et al 32 recently reported that in patients with NASH the increase in intestinal permeability was associated with lower levels of protein levels of ZO-1. In genetically obese mice (eg, ob/ob mice), the development of NAFLD was associated with a loss of the tight junction proteins ZO-1 and occludin and increased levels of the endotoxin receptor CD14 in the liver.…”

Section: Discussionmentioning

confidence: 99%

Metformin protects against the development of fructose-induced steatosis in mice: role of the intestinal barrier function

Spruss

Kanuri

Stahl

et al. 2012

Laboratory Investigation

146

151

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To test the hypothesis that metformin protects against fructose-induced steatosis, and if so, to elucidate underlying mechanisms, C57BL/6J mice were either fed 30% fructose solution or plain water for 8 weeks. Some of the animals were concomitantly treated with metformin (300 mg/kg body weight/day) in the drinking solution. While chronic consumption of 30% fructose solution caused a significant increase in hepatic triglyceride accumulation and plasma alanineaminotransferase levels, this effect of fructose was markedly attenuated in fructose-fed mice concomitantly treatment with metformin. The protective effects of the metformin treatment on the onset of fructose-induced non-alcoholic fatty liver disease (NAFLD) were associated with a protection against the loss of the tight junction proteins occludin and zonula occludens 1 in the duodenum of fructose-fed mice and the increased translocation of bacterial endotoxin found in mice only fed with fructose. In line with these findings, in metformin-treated fructose-fed animals, hepatic expression of genes of the toll-like receptor-4-dependent signalling cascade as well as the plasminogen-activator inhibitor/cMet-regulated lipid export were almost at the level of controls. Taken together, these data suggest that metformin not only protects the liver from the onset of fructose-induced NAFLD through mechanisms involving its direct effects on hepatic insulin signalling but rather through altering intestinal permeability and subsequently the endotoxin-dependent activation of hepatic Kupffer cells.

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Section: Discussionmentioning

confidence: 99%

Metformin protects against the development of fructose-induced steatosis in mice: role of the intestinal barrier function

Spruss

Kanuri

Stahl

et al. 2012

Laboratory Investigation

146

151

View full text Add to dashboard Cite

show abstract

“…Currently, NAFLD represents one of the most common liver diseases worldwide (35). One study reported that the occurrence of benign digestive disorders, including diverticular disease, gallstones, and inflammatory bowel disease, is closely related to NAFLD (36,37). The development of GD in NAFLD involves a multifactorial process, which remains unelucidated.…”

Section: Discussionmentioning

confidence: 99%

Promotional effect of nonalcoholic fatty liver disease on Gallstone disease: A systematic review and meta-analysis

Shen¹,

Gong²,

Wang³

et al. 2020

Turk J Gastroenterol

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“…A bakteriális túlbur-jánzás összefügg a májelzsírosodás mértékével [11]. A gyomor-bél rendszerből származó lymphocyták a májba vándorolnak és ott hepaticus CD4 + és CD8 + T-sejtek aktiválódását váltják ki nem alkoholos zsírmáj egérmodell-jében.…”

Section: Intestinalis Bélflóra: Portalis Endotoxinaemiaunclassified

Az idült májbetegségek progressziójához vezető folyamatok

et al. 2016

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Különböző károsító hatások miatt (vírusok, anyagcserezavarok, táplálkozási tényezők, toxikus ártalmak, autoimmun folyamatok) kóros májműködés lép fel, amely a máj elzsírosodásához és kötőszövetes átépüléséhez vezet. A progreszszió folyamata összetett, több útvonalon megy végbe, számos tényező befolyásolja. A szerzők összefoglaló közlemé-nyükben áttekintik a krónikus májbetegségek progressziójában részt vevő tényezőket. Bemutatják a sejtek szerepét, az általuk termelt főbb citokineket és gyulladásos mediátorokat, valamint az intestinalis bélflóra kapcsolatát a betegséggel. Kitérnek az oxidatív stressz, a mitokondriális diszfunkció és a sejthalál kórlefolyásban betöltött szerepére. Ismertetik az inzulinrezisztencia és a mikroelemek (vas, réz) kapcsolatát a májkárosodással. Összefoglalják a progreszszió hátterében álló genetikai és epigenetikai vonatkozásokat is. Az új kezelési lehetőségek felismerése, a kezelés hatékonyságának megítélése vagy a májátültetés időpontjának megválasztása, sikeressége függhet a kórlefolyás pontosabb megismerésétől. Orv. Hetil., 2016, 157(8), 290-297.Kulcsszavak: májelzsírosodás, progresszió, hepatitis, fibrosis, oxidatív stressz, mitokondriális diszfunkció, csillagsejtek, intestinalis bélflóra Various pathways leading to the progression of chronic liver diseasesAs the result of various effects (viruses, metabolic diseases, nutritional factors, toxic agents, autoimmune processes) abnormal liver function, liver steatosis and connective tissue remodeling may develop. Progression of this process is complex including various pathways and a number of factors. The authors summarize the factors involved in the progression of chronic liver disease. They describe the role of cells and the produced inflammatory mediators and cytokines, as well as the relationship between the disease and the intestinal flora. They emphasize the role of oxidative stress, mitochondrial dysfunction and cell death in disease progression. Insulin resistance and micro-elements (iron, copper) in relation to liver damage are also discussed, and genetic and epigenetic aspects underlying disease progression are summarized. Discovery of novel treatment options, assessment of the effectiveness of treatment, as well as the success and proper timing of liver transplantation may depend on a better understanding of the process of disease progression.Keywords: liver steatosis, progression, hepatitis, fibrosis, oxidative stress, mitochondrial dysfunction, stellate cells, intestinal flora Egresi, A., Lengyel, G., Somogyi, A., Blázovics, A., Hagymási, K. [Various pathways leading to the progression of chronic liver diseases]. Orv. Hetil., 2016, 157(8), 290-297. (Beérkezett: 2015 elfogadva: 2016. január Rövidítések AFLD = alkoholos zsírmájbetegség; ATP = adenozin-5'-trifoszfát; CCR5 = kemokinligand-5; CRP = C-reaktív protein; Cu = réz; DM = diabetes mellitus; DNS = deoxiribonukleinsav; ECM = extracelluláris mátrix; ETC = elektrontranszportlánc; FXR = farnezoid X-receptor; HBV = hepatitis B-vírus; HCV = hepatitis C-vírus; HSC = (h...

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High Prevalence of Small Intestinal Bacterial Overgrowth in Patients with Morbid Obesity: A Contributor to Severe Hepatic Steatosis

Abstract: In morbidly obese patients, bacterial overgrowth prevalence is higher than in healthy subjects and is associated with severe hepatic steatosis.

Cited by 233 publications

References 48 publications

Metformin protects against the development of fructose-induced steatosis in mice: role of the intestinal barrier function

Metformin protects against the development of fructose-induced steatosis in mice: role of the intestinal barrier function

Promotional effect of nonalcoholic fatty liver disease on Gallstone disease: A systematic review and meta-analysis

Az idült májbetegségek progressziójához vezető folyamatok

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