Nonalcoholic fatty liver disease is associated with lower hepatic and erythrocyte ratios of phosphatidylcholine to phosphatidylethanolamine

Arendt, Bianca M.; David, W. L.; Simons, Brigitte; Noureldin, Seham; Therapondos, George; Guindi, Maha; Sherman, Morris; Allard, Johane P.

doi:10.1139/apnm-2012-0261

Cited by 119 publications

(109 citation statements)

References 37 publications

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“…PC depletion has been implicated in the pathogenesis of NAFLD (17,18,43,44). The current studies demonstrate that alcohol consumption in the background of obesity can lead to depletion of PC.…”

Section: Obesity Increased Hepatic Ces and Dag Hepatic Cesupporting

confidence: 50%

Alcohol produces distinct hepatic lipidome and eicosanoid signature in lean and obese

Puri

Vihervaara

et al. 2016

Journal of Lipid Research

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Section: Obesity Increased Hepatic Ces and Dag Hepatic Cesupporting

confidence: 50%

Alcohol produces distinct hepatic lipidome and eicosanoid signature in lean and obese

Puri

Vihervaara

et al. 2016

Journal of Lipid Research

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“…Importantly, a decrease in the PC:PE ratio was also observed in liver biopsies from patients with nonalcoholic steatohepatitis (Arendt et al, 2013; Li et al, 2006). Thus, the maintenance of the PC:PE ratio in hepatocyte membranes is critical for the integrity of the cell although each individual phospholipid plays a different role in hepatic lipid metabolism.…”

Section: Pe and Diseasesmentioning

confidence: 85%

Phosphatidylethanolamine Metabolism in Health and Disease

Calzada

Onguka

Claypool

2016

International Review of Cell and Molecular Biology

298

200

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Phosphatidylethanolamine (PE) is the second most abundant glycerophospholipid in eukaryotic cells. The existence of four only partially redundant biochemical pathways that produce PE, highlights the importance of this essential phospholipid. The CDP-ethanolamine and phosphatidylserine decarboxylase pathways occur in different subcellular compartments and are the main sources of PE in cells. Mammalian development fails upon ablation of either pathway. Once made, PE has diverse cellular functions that include serving as a precursor for phosphatidylcholine and a substrate for important posttranslational modifications, influencing membrane topology, and promoting cell and organelle membrane fusion, oxidative phosphorylation, mitochondrial biogenesis, and autophagy. The importance of PE metabolism in mammalian health has recently emerged following its association with Alzheimer's disease, Parkinson's disease, nonalcoholic liver disease, and the virulence of certain pathogenic organisms.

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“…Experimental choline deficiency in lower fat diet formulations than those tested here causes a decreased ratio of total hepatic PC/PE [44,47–49] and hepatic mitochondrial dysfunction [38–40]. Furthermore, NAFLD patients have a reduction of the total hepatic PC/PE ratio and impaired hepatocyte membrane integrity [44,50]. Maintenance of mitochondrial function requires homeostatic membrane phospholipid composition to coordinate surface charge, stereoelectronic relationships, and membrane dynamics that each effect membrane function and structural integrity, critical determinants of mitochondrial electron transport and oxidative phosphorylation [51–53].…”

Section: Discussionmentioning

confidence: 99%

Role of Choline Deficiency in the Fatty Liver Phenotype of Mice Fed a Low Protein, Very Low Carbohydrate Ketogenic Diet

et al. 2013

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Though widely employed for clinical intervention in obesity, metabolic syndrome, seizure disorders and other neurodegenerative diseases, the mechanisms through which low carbohydrate ketogenic diets exert their ameliorative effects still remain to be elucidated. Rodent models have been used to identify the metabolic and physiologic alterations provoked by ketogenic diets. A commonly used rodent ketogenic diet (Bio-Serv F3666) that is very high in fat (~94% kcal), very low in carbohydrate (~1% kcal), low in protein (~5% kcal), and choline restricted (~300 mg/kg) provokes robust ketosis and weight loss in mice, but through unknown mechanisms, also causes significant hepatic steatosis, inflammation, and cellular injury. To understand the independent and synergistic roles of protein restriction and choline deficiency on the pleiotropic effects of rodent ketogenic diets, we studied four custom diets that differ only in protein (5% kcal vs. 10% kcal) and choline contents (300 mg/kg vs. 5 g/kg). C57BL/6J mice maintained on the two 5% kcal protein diets induced the most significant ketoses, which was only partially diminished by choline replacement. Choline restriction in the setting of 10% kcal protein also caused moderate ketosis and hepatic fat accumulation, which were again attenuated when choline was replete. Key effects of the 5% kcal protein diet – weight loss, hepatic fat accumulation, and mitochondrial ultrastructural disarray and bioenergetic dysfunction – were mitigated by choline repletion. These studies indicate that synergistic effects of protein restriction and choline deficiency influence integrated metabolism and hepatic pathology in mice when nutritional fat content is very high, and support the consideration of dietary choline content in ketogenic diet studies in rodents to limit hepatic mitochondrial dysfunction and fat accumulation.

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Nonalcoholic fatty liver disease is associated with lower hepatic and erythrocyte ratios of phosphatidylcholine to phosphatidylethanolamine

Cited by 119 publications

References 37 publications

Alcohol produces distinct hepatic lipidome and eicosanoid signature in lean and obese

Alcohol produces distinct hepatic lipidome and eicosanoid signature in lean and obese

Phosphatidylethanolamine Metabolism in Health and Disease

Role of Choline Deficiency in the Fatty Liver Phenotype of Mice Fed a Low Protein, Very Low Carbohydrate Ketogenic Diet

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