Nutritional lipid-induced oxidative stress leads to mitochondrial dysfunction followed by necrotic death in FaO hepatocytes

Tirosh, Oren; Erez, Ilan; Anavi, Sarit; Ramadori, Giuliano; Madar, Zecharia

doi:10.1016/j.nut.2008.07.023

Cited by 17 publications

(6 citation statements)

References 43 publications

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“…We postulate that an increased intracellular ROS level likely precedes the loss of ∆ ΨM and mitochondria dysfunction. As this oxidative stress condition continues to worsen after birth, perhaps induced by nutritional lipid as previously indicated ( Tirosh et al, 2009 ), reduced ∆ ΨM and ATP production ultimately ensue. This is in agreement with a previous report of a similar mitochondrial disorder associated with the dysfunctional respiratory chain components ( Lebiedzinska et al, 2010 ).…”

Section: Discussionmentioning

confidence: 77%

Glucocorticoid receptor-PPARα axis in fetal mouse liver prepares neonates for milk lipid catabolism

Rando

Tan

Khaled

et al. 2016

eLife

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In mammals, hepatic lipid catabolism is essential for the newborns to efficiently use milk fat as an energy source. However, it is unclear how this critical trait is acquired and regulated. We demonstrate that under the control of PPARα, the genes required for lipid catabolism are transcribed before birth so that the neonatal liver has a prompt capacity to extract energy from milk upon suckling. The mechanism involves a fetal glucocorticoid receptor (GR)-PPARα axis in which GR directly regulates the transcriptional activation of PPARα by binding to its promoter. Certain PPARα target genes such as Fgf21 remain repressed in the fetal liver and become PPARα responsive after birth following an epigenetic switch triggered by β-hydroxybutyrate-mediated inhibition of HDAC3. This study identifies an endocrine developmental axis in which fetal GR primes the activity of PPARα in anticipation of the sudden shifts in postnatal nutrient source and metabolic demands.DOI: http://dx.doi.org/10.7554/eLife.11853.001

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Section: Discussionmentioning

confidence: 77%

Glucocorticoid receptor-PPARα axis in fetal mouse liver prepares neonates for milk lipid catabolism

Rando

Tan

Khaled

et al. 2016

eLife

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“…8-hydroxydeoxyguanosine (8-OHdG) content was measured by using a competitive enzyme-linked immunosorbent assay (ELISA) kit (Elabscience) according to the manufacturer’s instructions. ROS content was measured following the method described by Tirosh et al [38] with slight modification. CuZnSOD and MnSOD activities were determined according to the method of Lambertucci et al [39].…”

Section: Methodsmentioning

confidence: 99%

A Comparative Study on Antioxidant System in Fish Hepatopancreas and Intestine Affected by Choline Deficiency: Different Change Patterns of Varied Antioxidant Enzyme Genes and Nrf2 Signaling Factors

Liu

Jiang

et al. 2017

PLoS ONE

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The liver and intestine are susceptible to the oxidative damage which could result in several diseases. Choline deficiency induced oxidative damage in rat liver cells. Thus, this study aimed to investigate the potential molecular mechanisms responsible for choline deficiency-induced oxidative damage. Juvenile Jian carp were fed diets differing in choline content [165 (deficient group), 310, 607, 896, 1167 and 1820 mg/kg diet] respectively for 65 days. Oxidative damage, antioxidant enzyme activities and related gene expressions in the hepatopancreas and intestine were measured. Choline deficiency decreased choline and phosphatidylcholine contents, and induced oxidative damage in both organs, as evidenced by increased levels of oxidative-stress markers (malondialdehyde, protein carbonyl and 8-hydroxydeoxyguanosine), coupled with decreased activities of antioxidant enzymes [Copper-zinc superoxide dismutase (CuZnSOD), manganese superoxide dismutase (MnSOD), glutathione peroxidase (GPx) and glutathione-S-transferase (GST)]. However, choline deficiency increased glutathione contents in the hepatopancreas and intestine. Furthermore, dietary choline deficiency downregulated mRNA levels of MnSOD, GPx1b, GST-rho, mGST3 and Kelch-like ECH associating protein 1 (Keap1b) in the hepatopancreas, MnSOD, GPx1b, GPx4a, GPx4b, GST-rho, GST-theta, GST-mu, GST-alpha, GST-pi and GST-kappa in the intestine, as well as intestinal Nrf2 protein levels. In contrast, choline deficiency upregulated the mRNA levels of GPx4a, GPx4b, mGST1, mGST2, GST-theta, GST-mu, Keap1a and PKC in the hepatopancreas, mGST3, nuclear factor erythoid 2-related factor 2 (Nrf2) and Keap1a in the intestine, as well as hepatopancreatic Nrf2 protein levels. This study provides new evidence that choline deficiency-induced oxidative damage is associated with changes in the transcription of antioxidant enzyme and Nrf2/Keap1 signaling molecules in the hepatopancreas and intestine. Additionally, this study firstly indicated that choline deficiency induced varied change patterns of different GPx and GST isoforms. Meanwhile, the changes of some GPx and GST isoforms caused by choline deficiency in the intestine were contrary to those in the hepatopancreas.

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“…In vitro studies indicated that cells treated with OA or olive oil were associated with less mitochondrial ROS production than cells treated with certain PUFA (e.g., DHA) or a soybean-oil-based LE [45, 46]. In a preclinical rodent study, lipid peroxidation was lower among mice administered OA or olive oil by gavage than among mice administered PUFA (i.e., LA or DHA) or fish oil [47].…”

Section: Evolution Of Parenteral Lipid Emulsionsmentioning

confidence: 99%

Lipid emulsions in parenteral nutrition of intensive care patients: current thinking and future directions

Calder

Jensen

Koletzko³

et al. 2010

Intensive Care Med

185

152

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BackgroundEnergy deficit is a common and serious problem in intensive care units and is associated with increased rates of complications, length of stay, and mortality. Parenteral nutrition (PN), either alone or in combination with enteral nutrition, can improve nutrient delivery to critically ill patients. Lipids provide a key source of calories within PN formulations, preventing or correcting energy deficits and improving outcomes.DiscussionIn this article, we review the role of parenteral lipid emulsions (LEs) in the management of critically ill patients and highlight important biologic activities associated with lipids. Soybean-oil-based LEs with high contents of polyunsaturated fatty acids (PUFA) were the first widely used formulations in the intensive care setting. However, they may be associated with increased rates of infection and lipid peroxidation, which can exacerbate oxidative stress. More recently developed parenteral LEs employ partial substitution of soybean oil with oils providing medium-chain triglycerides, ω-9 monounsaturated fatty acids or ω-3 PUFA. Many of these LEs have demonstrated reduced effects on oxidative stress, immune responses, and inflammation. However, the effects of these LEs on clinical outcomes have not been extensively evaluated.ConclusionsOngoing research using adequately designed and well-controlled studies that characterize the biologic properties of LEs should assist clinicians in selecting LEs within the critical care setting. Prescription of PN containing LEs should be based on available clinical data, while considering the individual patient’s physiologic profile and therapeutic requirements.

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Nutritional lipid-induced oxidative stress leads to mitochondrial dysfunction followed by necrotic death in FaO hepatocytes

Cited by 17 publications

References 43 publications

Glucocorticoid receptor-PPARα axis in fetal mouse liver prepares neonates for milk lipid catabolism

Glucocorticoid receptor-PPARα axis in fetal mouse liver prepares neonates for milk lipid catabolism

A Comparative Study on Antioxidant System in Fish Hepatopancreas and Intestine Affected by Choline Deficiency: Different Change Patterns of Varied Antioxidant Enzyme Genes and Nrf2 Signaling Factors

Lipid emulsions in parenteral nutrition of intensive care patients: current thinking and future directions

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