Involvement of lipid droplets in hepatic responses to lipopolysaccharide treatment in mice

Arisqueta, Lino; Núñez-García, Maitane; Ogando, Jesús; García-Arcos, Itsaso; Ochoa, Begoña; Aspichueta, Patricia; Fresnedo, Olatz; Rueda, Yuri

doi:10.1016/j.bbalip.2013.04.015

Cited by 15 publications

(25 citation statements)

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“…Finally in patients with sepsis low apolipoprotein A-I and HDL are associated with poor outcome [6]. The exact mechanism for the protective effects of HDL are not clear yet, but may be related to lipid droplets or microvesicles as carriers of danger-associated molecular patterns [17], [18]. Low HDL could aggravate detrimental effects of immune reactions and inflammatory process in ALF and would thus be indirectly associated to severity of the disease.…”

Section: Discussionmentioning

confidence: 99%

Low Levels of Blood Lipids Are Associated with Etiology and Lethal Outcome in Acute Liver Failure

et al. 2014

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Background/AimsEmerging data links different aspects of lipid metabolism to liver regeneration. In patients with acute liver failure (ALF), low levels of lipids may correlate with disease severity. Thus, we determined whether there is an etiology-specific link between lipid levels in patients suffering from ALF and aimed to investigate an effect of lipid levels on the prognosis of ALF.MethodsIn this retrospective single center study, we reviewed 89 consecutive ALF patients, who met the criteria of the “Acute Liver Failure Study Group”. Patient characteristics, clinical data and laboratory parameters were individually analyzed at admission and correlated with the patients' outcome after a four week follow up. Possible endpoints were either discharge, or death or liver transplantation.ResultsHigh-density lipoprotein (HDL), cholesterol and triglyceride levels were significantly lower in patients who died or required a liver transplant. HDL levels were significantly higher in patients with ALF caused by acetaminophen intoxication, compared to fulminant HBV infection or drug induced liver injury. HDL levels correlated with hepatic injury by ALT levels, and Albumin, and inversely correlated with the MELD score, INR, and bilirubin.ConclusionIn our cohort of patients with ALF, we could show that HDL and cholesterol are suppressed. In addition novel etiology specific patterns between acteminophen and non-acteminophen induced liver failure were detected for serum lipid components. Further studies are needed to address the role of cholesterol and lipid metabolism and the according pathways in different etiologies of ALF.

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Section: Discussionmentioning

confidence: 99%

Low Levels of Blood Lipids Are Associated with Etiology and Lethal Outcome in Acute Liver Failure

et al. 2014

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“…In particular, the intra-abdominal WAT is strategically located to flood the liver with proinflammatory cytokines via the portal circulation, and alter hepatic protein synthesis (Libby et al, 2010). In addition, lipid droplets in hepatocytes, like adipocytes, are seen as inducible organelles with roles in cell signalling, regulation of lipid metabolism, membrane trafficking, and control of the synthesis and secretion of inflammatory mediators (Anderson and Borlak, 2008;Arisqueta et al, 2013;Bozza and Viola, 2010). Presumably, hepatocyte lipid droplets could be implicated in impairment of hepatic protein synthesis.…”

Section: Clinical Biochemistrymentioning

confidence: 99%

Fatty Liver Haemorrhagic Syndrome in Laying Hens: Field and Experimental Investigations

Shini¹

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Field and experimental investigations were conducted to study the fatty liver haemorrhagic syndrome (FLHS) in caged laying hens. The main goal of the research was to gain a greater understanding of the aetiology and pathogenesis of this non-infectious disease. The disease is characterized by excessive accumulation of fat in the liver and abdominal cavity, subsequent liver rupture, haemorrhage and sudden death of hens. It has been shown that the balance between hepatic synthesis and secretion of lipids is the key point that regulates hepatic and extrahepatic fat deposition in hens. Liver fat accumulation can be increased by many factors, especially nutrition, housing conditions, and inflammatory challenges. A description of normal and abnormal lipid metabolism in the hen, and consequences for hen health and disease (including FLHS) is given in the literature review (Chapter 2).The initial study examined mortality of layer flocks kept in three different housing systems (cage, barn and free range) on the Gatton Campus, University of Queensland (Chapter 4). It was shown that there were no significant differences in mortality rates of hens (6.1%, 6.4% and 5.8%, for cages, barns and free range, respectively) between the housing systems but the causes of death were different. The most common cause of death in hens kept in cages was FLHS with 74% of dead hens dying from the condition. In contrast, FLHS only accounted for 0 to 5% of hen mortality in the other systems. Post-mortem of dead hens and body weight monitoring of flocks throughout the laying cycle were recommended as tools to predict FLHS.An epidemiological survey (Chapter 5) of caged flocks in South-Eastern Queensland was undertaken to explore the prevalence of FLHS in commercial layer flocks. From necropsies of dead birds from 7 flocks of different ages, it was found that approximately 40% of hens died due to FLHS. This result indicated that FLHS continues to be the major cause of mortality in commercial caged laying hens kept in either controlled environment sheds or naturally ventilated sheds. As part of the epidemiological study, a questionnaire was circulated among farms and the responses revealed that there is a general lack of knowledge of FLHS in the industry.The study of the pathogenesis of FLHS is very difficult as it occurs sporadically and over an extended period of time in the field. In the studies in Chapter 6, an oestradiol (E 2 ) hen model was used to study the condition. The administration of exogenous E 2 reproduced the disease in 30 wk old laying hens, and was associated with significant changes in E 2 plasma levels and metabolic iv profiles, increased liver weights, and macroscopic (fat depositions, haemorrhages and haematomas) and microscopic alterations. Hens exposed to E 2 and fed ad libitum diet experienced severe FLHS and had a higher incidence of FLHS than hens that had their feed intake restricted by 10%. One interesting observation from this study (not reported from other investigators) was the alteration of total leukocyte n...

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“…LPS has been shown to modulate SREBP expression in macrophages, while also subduing liver PGC1α expression [29,42,43], and thus being associated with an abnormal Sirt1-regulation of basal adipocyte cell functioning [27,44]. The LPS-facilitated "blockage" of the elimination of cholesterol from macrophages has been demonstrated to serve as an important factor in the cholesterol-rich lipoprotein intercommunication network [45][46][47], thus impacting on LPS neutralization in metabolic diseases, with focus on diabetes [48][49][50].…”

Section: Lps Modulation Of Sirt1/p53 Interactions Is Coupled To Fat Imentioning

confidence: 99%

“…IFγ has also been shown to affect genes, like Sirt1 and p53 apoptosis coupled genes, whose role are being "dissociated" in dysfunctional stages of metabolism [45][46][47][48][49][50][51][52][53]. The impact of IFγ on chromatin modeling stimulates macrophages, controlling gene transcription, thus regulating inflammatory cytokine production in activated macrophages [46,47].…”

Section: Lps Modulation Of Sirt1/p53 Interactions Is Coupled To Fat Imentioning

confidence: 99%

“…An interest in the nutritional modulation of obesity, with or without concomitant diabetes, has increased due to the effects of feeding patterns on Sirt1 and p53, being involved in the reciprocal nuclear-mitochondrial interactions, emerging mutations, as well as apoptosis (cell death) and/or responses encompassing permanent cellular senescence [35][36][37][38][39][40][41]. Sirt1 and its posttranscriptional impact on p53 [42,43] is heavily involved in the differentiation of adipocytes, as well as lipid metabolism in general [44][45][46][47][48], with their implications for abnormal Sirt1 deacetylation of p53, linked to lipid metabolism with its characteristic transformation of adipocytes and ensuing liver disease. Interestingly, both Sirt1 and p53 knockout mice develop NAFLD [49][50][51][52], which alludes to a close connections between adipocyte phenotype "switch" involving Sirt 1 and/or p53 impact on mitochondrial functioning [53][54][55][56].…”

Section: Food Restriction Organ Crosstalk In Obese/diabetic "Mice Andmentioning

confidence: 99%

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Introductory Chapter: Obesity—“OMICS” and Endocrinology

Gordeladze¹

2017

Adiposity - Omics and Molecular Understanding

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Involvement of lipid droplets in hepatic responses to lipopolysaccharide treatment in mice

Cited by 15 publications

References 47 publications

Low Levels of Blood Lipids Are Associated with Etiology and Lethal Outcome in Acute Liver Failure

Low Levels of Blood Lipids Are Associated with Etiology and Lethal Outcome in Acute Liver Failure

Fatty Liver Haemorrhagic Syndrome in Laying Hens: Field and Experimental Investigations

Introductory Chapter: Obesity—“OMICS” and Endocrinology

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