Hepatic Steatosis After Intestinal Bypass—Prevention and Reversal by Metronidazole, Irrespective of Protein-Calorie Malnutrition

Drenick, Ernst J.; Fisler, Janis S.; Johnson, D G

doi:10.1016/s0016-5085(82)80403-4

Cited by 204 publications

(75 citation statements)

References 41 publications

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“…Previous clinical studies have reported that serum LPS levels are increased in patients with hepatic steatosis, whereas antibiotic treatment of these patients resulted in a significant decrease in circulating LPS levels together with attenuated hepatic steatosis, suggesting that the LPS may lead to hepatic lipid accumulation. [15][16][17] A recent study reported that fructose-induced NAFLD is associated with intestinal bacterial overgrowth and increased intestinal permeability, subsequently leading to an endotoxindependent activation of hepatic Kupffer cells mediated by TLR4. 18 Furthermore, inactivation of TLR4 results in a marked decrease in high-fructose diet-induced hepatic steatosis.…”

Section: Discussionmentioning

confidence: 99%

Toll‐like receptor‐4 signalling in the progression of non‐alcoholic fatty liver disease induced by high‐fat and high‐fructose diet in mice

Liu

Zhuang

Bian

et al. 2014

Clin Exp Pharma Physio

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The aim of the present study was to investigate Toll-like receptor-4 (TLR4) signalling at different stages of non-alcoholic fatty liver disease (NAFLD) induced by a high-fat, high-fructose (HFHFr) diet in mice. Both TLR4 wild-type (WT) and mutant (TLR4(mut) ) mice were fed either standard chow (SC) or the HFHFr diet for different periods of time from 4 to 16 weeks. Pathological characteristics and function of the liver were assessed. Simple steatosis, steatohepatitis and hepatic fibrosis occurred sequentially in Week 4, 8 and 16 in WT mice fed with the HFHFr. Expression of TLR4, myeloid differentiation factor 88 (MyD88), interferon regulatory factor (IRF) 3 and IRF7 started to increase at Week 4, peaked at Week 8 and then declined to basal levels at Week 16. This pattern was consistent with changes in inflammation in the liver revealed by haematoxylin and eosin staining. However, lipid accumulation, inflammation and fibrosis in livers of TLR4(mut) mice fed the HFHFr diet were significantly alleviated. In addition, the expression of activin A in WT mice fed the HFHFr diet increased at Week 16. The data suggest that TLR4 signalling mediates non-alcoholic steatohepatitis before fibrosis and that activin A is subsequently involved in NAFLD.

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Section: Discussionmentioning

confidence: 99%

Toll‐like receptor‐4 signalling in the progression of non‐alcoholic fatty liver disease induced by high‐fat and high‐fructose diet in mice

Liu

Zhuang

Bian

et al. 2014

Clin Exp Pharma Physio

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“…Older studies of the now abandoned jejunoileal intestinal bypass procedure supported a role for antibiotics and amino acid supplementation for patients who experienced decompensation. 168,169 Cytoprotective Agents. These agents combine an attractive safety profile, few drug interactions, and a plausible mechanism of action at the cellular or subcellular level.…”

Section: Managementmentioning

confidence: 99%

Nonalcoholic Steatohepatitis: Summary of An Aasld Single Topic Conference

2003

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“…NASH may be prevented or reversed in some patients following jejuno-ileal bypass by the use of metronidazole. 79 Patients with bacterial contamination of the small intestine associated with duodenal or jejunal diverticulum have been often diagnosed with steatohepatitis. 80 Cani et al reported that high-fat diet modulated the dominant bacterial populations within the intestinal microbiota and caused a continuous increase in plasma LPS in mice.…”

Section: Endotoxinmentioning

confidence: 99%

Clinicopathological features of non‐alcoholic fatty liver disease

Sugimoto

Takei

2011

Hepatology Research

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Non-alcoholic fatty liver disease (NAFLD) is the most common form of chronic liver disease worldwide and its incidence is increasing concomitantly with the increase in the prevalence of metabolic syndrome. Fatty liver encompasses a broad pathological spectrum of disease, from relatively benign accumulation of fat (simple steatosis) to progressive non-alcoholic steatohepatitis (NASH), which is associated with necroinflammation and fibrosis. Approximately 20-30% of the Japanese population is estimated to have NAFLD, 10% of which is suggested to have NASH. The most worrisome feature of NASH is the potential progression to cirrhosis, hepatocellular carcinoma (HCC), and finally, mortality. Several factors, such as insulin resistance, adipokines, endotoxins and oxidative stress, are involved in the pathogenesis of NASH. However, the precise etiological mechanism of NAFLD/NASH has yet to be elucidated. This article reviews the clinical background, pathogenesis, new diagnostic approaches and future directions regarding NAFLD/NASH.

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Hepatic Steatosis After Intestinal Bypass—Prevention and Reversal by Metronidazole, Irrespective of Protein-Calorie Malnutrition

Cited by 204 publications

References 41 publications

Toll‐like receptor‐4 signalling in the progression of non‐alcoholic fatty liver disease induced by high‐fat and high‐fructose diet in mice

Toll‐like receptor‐4 signalling in the progression of non‐alcoholic fatty liver disease induced by high‐fat and high‐fructose diet in mice

Nonalcoholic Steatohepatitis: Summary of An Aasld Single Topic Conference

Clinicopathological features of non‐alcoholic fatty liver disease

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