Temporal changes in insulin sensitivity following the development of acute liver failure secondary to acetaminophen

Clark, Sarah J.; Shojaee‐Moradie, Fariba; Croos, P; Seed, Paul; Umpleby, A. Margot; Wendon, Julia; Miell, John

doi:10.1053/jhep.2001.25514

Cited by 35 publications

(13 citation statements)

References 43 publications

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“…Therefore, MUFAs replacement instead of SFAs and carbohydrate may be beneficial for patients with NAFLD. The probable mechanism for MUFA beneficial effect on liver fat content might be related to its expression regulation potency of involved genes in peripheral insulin sensitivity (56), anti-inflammatory (57) and inhibitory effects on nuclear factor- κB (NF-κB) (58). In a study, MUFA decreased the expression of hepatic lipogenesis and gluconeogenesis genes and SREBP in fatty rats (59).…”

Section: Resultsmentioning

confidence: 99%

Diet Macronutrients Composition in Nonalcoholic Fatty Liver Disease: A Review on the Related Documents

Kani¹,

Alavian²,

Haghighatdoost³

et al. 2014

Hepat Mon

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Context:Non-alcoholic fatty liver disease (NAFLD) is a growing health problem in both developed and developing countries. Metabolic abnormalities, specially insulin resistance and hyperglycemia are highly correlated with NAFLD. Lifestyle modifications including physical activity and promoting nutrient intakes are critical in prevention and treatment of NAFLD. Hence, in this article we aimed to review the evidence regarding the effects of various macronutrients on fat accumulation in hepatic cells as well as the level of liver enzymes.Evidence Acquisitions:The relevant English and non-English published papers were searched using online databases of PubMed, ISI Web of Science, SCOPUS, Science Direct and EMBASE from January 2000 to January 2013. We summarized the findings of 40 relevant studies in this review.Results:Although a hypocaloric diet could prevent the progression of fat accumulation in liver, the diet composition is another aspect which should be considered in diet therapy of patients with NAFLD.Conclusions:Several studies assessed the effects of dietary composition on fat storage in liver; however, their findings are inconsistent. Most studies focused on the quantity of carbohydrate and dietary fat; whilst there is very limited information regarding the role of protein intake.

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Section: Resultsmentioning

confidence: 99%

Diet Macronutrients Composition in Nonalcoholic Fatty Liver Disease: A Review on the Related Documents

Kani¹,

Alavian²,

Haghighatdoost³

et al. 2014

Hepat Mon

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“…An olive oil-enriched diet contributes to redistribution of body fat and modifies the lipolytic efficiency of fat cells [57] . Furthermore, n-9 fatty acids may regulate gene expression related to peripheral insulin sensitivity [58] , increased endothelial vasoreactivity [59] , up-regulation of uncoupling protein mRNA in adipose tissue and muscle [60] , and expression of upregulates glucose transporter-2 in the liver [61] . Oleic acid decreases the expression of genes involved in hepatic gluconeogenesis and lipogenesis and SREBP in Zucker fatty rats [62] .…”

Section: The Special Mechanism Of Olive Oilmentioning

confidence: 99%

Olive oil consumption and non-alcoholic fatty liver disease

Assy

Nassar²,

Nasser³

et al. 2009

WJG

145

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The clinical implications of non-alcoholic fatty liver diseases (NAFLD) derive from their potential to progress to fibrosis and cirrhosis. Inappropriate dietary fat intake, excessive intake of soft drinks, insulin resistance and increased oxidative stress results in increased free fatty acid delivery to the liver and increased hepatic triglyceride (TG) accumulation. An olive oil-rich diet decreases accumulation of TGs in the liver, improves postprandial TGs, glucose and glucagonlike peptide-1 responses in insulin-resistant subjects, and upregulates glucose transporter-2 expression in the liver. The principal mechanisms include: decreased nuclear factor-kappaB activation, decreased lowdensity lipoprotein oxidation, and improved insulin resistance by reduced production of inflammatory cytokines (tumor necrosis factor, interleukin-6) and improvement of jun N-terminal kinase-mediated phosphorylation of insulin receptor substrate-1. The beneficial effect of the Mediterranean diet is derived from monounsaturated fatty acids, mainly from olive oil. In this review, we describe the dietary sources of the monounsaturated fatty acids, the composition of olive oil, dietary fats and their relationship to insulin resistance and postprandial lipid and glucose responses in non-alcoholic steatohepatitis, clinical and experimental studies that assess the relationship between olive oil and NAFLD, and the mechanism by which olive oil ameliorates fatty liver, and we discuss future perspectives.

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“…(2001) have demonstrated that the overexpression of Lpl , which has been known to be the rate-limiting enzyme involved with triglyceride hydrolysis (Goldberg, 1996), causes profound insulin resistance in liver (Baron et al ., 1988). Insulin resistance can lead to selective accumulation of fatty acid-derived metabolites (i.e., fatty acyl CoA, ceramide, diacylglycerol) in liver and may be implicated in the development of acute liver failure (ALF) (Clark et al ., 2001) through impaired peripheral glucose utilization and a failure to fully suppress endogenous glucose production, contributing to the catabolic state that occurs in ALF. These suggest potential involvement of Lpl in the susceptibility to hepatotoxicity although little is known currently for the exact mechanism on link with the APAP-induced hepatotoxicity.…”

Section: Discussionmentioning

confidence: 99%

Expression Levels of GABA-A Receptor Subunit Alpha 3, Gabra3 and Lipoprotein Lipase, Lpl Are Associated with the Susceptibility to Acetaminophen-Induced Hepatotoxicity

Kim

Yun

Shin

et al. 2016

Biomol Ther (Seoul)

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Drug-induced liver injury (DILI) is the serious and fatal drug-associated adverse effect, but its incidence is very low and individual variation in severity is substantial. Acetaminophen (APAP)-induced liver injury accounts for >50% of reported DILI cases but little is known for the cause of individual variations in the severity. Intrinsic genetic variation is considered a key element but the identity of the genes was not well-established. Here, pre-biopsy method and microarray technique was applied to uncover the key genes for APAP-induced liver injury in mice, and a cause and effect experiment employing quantitative real-time PCR was conducted to confirm the correlation between the uncovered genes and APAP-induced hepatotoxicity. We identified the innately and differentially expressed genes of mice susceptible to APAP-induced hepatotoxicity in the pre-biopsied liver tissue before APAP treatment through microarray analysis of the global gene expression profiles (Affymetrix GeneChip® Mouse Gene 1.0 ST for 28,853 genes). Expression of 16 genes including Gdap10, Lpl, Gabra3 and Ccrn4l were significantly different (t-test: FDR <10%) more than 1.5 fold in the susceptible animals than resistant. To confirm the association with the susceptibility to APAP-induced hepatotoxicity, another set of animals were measured for the expression level of selected 4 genes (higher two and lower two genes) in the liver pre-biopsy and their sensitivity to APAP-induced hepatotoxicity was evaluated by post hoc. Notably, the expressions of Gabra3 and Lpl were significantly correlated with the severity of liver injury (p<0.05) demonstrating that these genes may be linked to the susceptibility to APAP-induced hepatotoxicity.

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Temporal changes in insulin sensitivity following the development of acute liver failure secondary to acetaminophen

Cited by 35 publications

References 43 publications

Diet Macronutrients Composition in Nonalcoholic Fatty Liver Disease: A Review on the Related Documents

Diet Macronutrients Composition in Nonalcoholic Fatty Liver Disease: A Review on the Related Documents

Olive oil consumption and non-alcoholic fatty liver disease

Expression Levels of GABA-A Receptor Subunit Alpha 3, Gabra3 and Lipoprotein Lipase, Lpl Are Associated with the Susceptibility to Acetaminophen-Induced Hepatotoxicity

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