Strategies to Counter Saturated Fatty Acid (SFA)-Mediated Lipointoxication

Bâcle, Amélie; Ferreira, Thierry

doi:10.1016/b978-0-12-811297-7.00027-5

Cited by 3 publications

(7 citation statements)

References 90 publications

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“…However, whereas levels of TG are high in cells exposed to MUFA, SFA generally poorly accumulate within TG [12] . Instead, SFA preferentially accumulate within other lipid species, including membrane PL, ceramides, or diacylglycerol (DAG), an intermediate in TG synthesis [ 12 , 13 ].…”

Section: Fatty Acid Homeostasis: General Principlesmentioning

confidence: 99%

“…Indeed, under persistent lipointoxication, the ER tends to swell, and loses its ability to form a diffuse network through the cytoplasm to rather appear as stacks [ 17 , 65 , 69 ]. Under these circumstances, the UPR switches from anti- to pro-apoptotic leading to cell death in virtually all cell types (for review see [13] ). Importantly, apoptosis as an important mechanism for airway epithelial cell loss in CF airways is recognized [ 77 , 78 ].…”

Section: The Impacts Of Lipointoxication On the Physiology Of Cfmentioning

confidence: 99%

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Glued in lipids: Lipointoxication in cystic fibrosis

Vandebrouck

Ferreira

2020

EBioMedicine

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Cystic Fibrosis (CF) is an autosomal recessive disease caused by mutations in the CF transmembrane regulator (CFTR) gene, which encodes a chloride channel located at the apical surface of epithelial cells. Unsaturated Fatty Acid (UFA) deficiency has been a persistent observation in tissues from patients with CF. However, the impacts of such deficiencies on the etiology of the disease have been the object of intense debates. The aim of the present review is first to highlight the general consensus on fatty acid dysregulations that emerges from, sometimes apparently contradictory, studies. In a second step, a unifying mechanism for the potential impacts of these fatty acid dysregulations in CF cells, based on alterations of membrane biophysical properties (known as lipointoxication), is proposed. Finally, the contribution of lipointoxication to the progression of the CF disease and how it could affect the efficacy of current treatments is also discussed.

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Section: Fatty Acid Homeostasis: General Principlesmentioning

confidence: 99%

Section: The Impacts Of Lipointoxication On the Physiology Of Cfmentioning

confidence: 99%

Glued in lipids: Lipointoxication in cystic fibrosis

Vandebrouck

Ferreira

2020

EBioMedicine

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“…Maintaining the equilibrium between SFA, Mono- and Poly-Unsaturated Fatty Acids (UFA) within membrane PL is crucial to sustain the optimal membrane biophysical properties, compatible with selective organelle based processes, including vesicular budding or membrane-protein trafficking and function ( 6 ). As a corrolary, impaired balances within SFA and UFA have been demonstrated to result in dramatic cellular dysfunctions in cells relevant of the metabolic syndrome (for review, see ( 7 )). As examples, altered insulin secretion in pancreatic β-cells or impairment in Glucose disposal in muscle and liver cells have been reported in response to SFA overload ( 7 ).…”

Section: Introductionmentioning

confidence: 99%

“…As a corrolary, impaired balances within SFA and UFA have been demonstrated to result in dramatic cellular dysfunctions in cells relevant of the metabolic syndrome (for review, see ( 7 )). As examples, altered insulin secretion in pancreatic β-cells or impairment in Glucose disposal in muscle and liver cells have been reported in response to SFA overload ( 7 ). This process, which is referred to as lipotoxicity, ultimately leads to cell death by apoptosis in all the cellular systems tested ( 7 ).…”

Section: Introductionmentioning

confidence: 99%

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A comprehensive study of Phospholipid fatty acid rearrangements in the early onset of the metabolic syndrome: correlations to organ dysfunction

Bâcle

Kadri

Khoury

et al. 2019

Preprint

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1The balance within phospholipids (PL) between Saturated Fatty Acids (SFA) and mono-or poly-2 Unsaturated Fatty Acids (UFA), is known to regulate the biophysical properties of cellular membranes. 3As a consequence, perturbating this balance alters crucial cellular processes in many cell types, such 4 as vesicular budding and the trafficking/function of membrane-anchored proteins. The worldwide 5 spreading of the Western-diet, which is specifically enriched in saturated fats, has been clearly 6 correlated with the emergence of a complex syndrome, known as the Metabolic Syndrome (MetS), 7 which is defined as a cluster of risk factors for cardiovascular diseases, type 2 diabetes and hepatic 8 steatosis. However, no clear correlations between diet-induced fatty acid redistribution within cellular 9 PL, the severity/chronology of the symptoms associated to MetS and the function of the targeted 10 organs, particularly in the early onset of the disease, have been established. In an attempt to fill this 11 gap, we analyzed in the present study PL remodeling in rats exposed during 15 weeks to a High Fat/High 12 Fructose diet (HFHF) in several organs, including known MetS targets. We show that fatty acids from 13 the diet can distribute within PL in a very selective way, with PhosphatidylCholine being the preferred 14 sink for this distribution. Moreover, in the HFHF rat model, most organs are protected from this 15 redistribution, at least during the early onset of MetS, at the exception of the liver and skeletal muscles. 16Interestingly, such a redistribution correlates with clear-cut alterations in the function of these organs. 17 18

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A comprehensive study of phospholipid fatty acid rearrangements in metabolic syndrome: correlations with organ dysfunction

Bâcle

Kadri

Khoury

et al. 2020

Disease Models &Amp; Mechanisms

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The balance within phospholipids (PL) between Saturated Fatty Acids (SFA) and mono-or poly-Unsaturated Fatty Acids (UFA), is known to regulate the biophysical properties of cellular membranes. As a consequence, perturbating this balance alters crucial cellular processes in many cell types, such as vesicular budding and the trafficking/function of membrane-anchored proteins. The worldwide spreading of the Western-diet, which is specifically enriched in saturated fats, has been clearly correlated with the emergence of a complex syndrome, known as the Metabolic Syndrome (MetS), which is defined as a cluster of risk factors for cardiovascular diseases, type 2 diabetes and hepatic steatosis. However, no clear correlations between diet-induced fatty acid redistribution within cellular PL, the severity/chronology of the symptoms associated to MetS and the function of the targeted organs have been established. In an attempt to fill this gap, we analyzed in the present study PL remodeling in rats exposed during 15 weeks to a High Fat/High Fructose diet (HFHF) in several organs, including known MetS targets. We show that fatty acids from the diet can distribute within PL in a very selective way, with PhosphatidylCholine being the preferred sink for this distribution. Moreover, in the HFHF rat model, most organs are protected from this redistribution, at least during the early onset of MetS, at the exception of the liver and skeletal muscles. Interestingly, such a redistribution correlates with clear-cut alterations in the function of these organs.

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Strategies to Counter Saturated Fatty Acid (SFA)-Mediated Lipointoxication

Cited by 3 publications

References 90 publications

Glued in lipids: Lipointoxication in cystic fibrosis

Glued in lipids: Lipointoxication in cystic fibrosis

A comprehensive study of Phospholipid fatty acid rearrangements in the early onset of the metabolic syndrome: correlations to organ dysfunction

A comprehensive study of phospholipid fatty acid rearrangements in metabolic syndrome: correlations with organ dysfunction

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