Choline-deficiency fatty liver: relation of plasma phospholipids to liver triglycerides

Lombardi, Benito; Ugazio, G; An, Ru

doi:10.1152/ajplegacy.1966.210.1.31

Cited by 83 publications

(47 citation statements)

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“…Very early studies since the 1930s have shown that high-fat diet-induced hepatic steatosis in both healthy and diabetic animals could be prevented by ingestion of betaine or choline [22,23]. In the rat [24], hamster [25], dog [19] and monkey [26], choline deficiency results in liver dysfunction owing to accumulation of TG [27][28][29][30] and DAGs [31] within the hepatocyte. In rats, fatty liver begins within hours to days after initiation of a choline-deficient diet [32].…”

Section: Animal Studiesmentioning

confidence: 99%

“…Also, fatty liver induced by a high fat diet in rats could be reversed by daily administration of choline for only 12 days [33]. This may be explained by the impaired release of hepatic TGs in choline-deficiency fatty liver [27]. As previously mentioned, the active synthesis of PC derived from choline is essential for the hepatic synthesis and secretion of VLDL [30].…”

Section: Animal Studiesmentioning

confidence: 99%

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Phosphatidylcholine functional foods and nutraceuticals: A potential approach to prevent non‐alcoholic fatty liver disease

Duric

Sivanesan

Bakovic

2012

Euro J Lipid Sci & Tech

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Non‐alcoholic fatty liver disease (NAFLD) is the most common liver condition in the developed world and may progress to more severe forms of disease such as cirrhosis or liver cancer. Thus, steps taken to reduce its prevalence through preventative nutritional approaches such as functional foods and nutraceuticals (FFN) should be pursued. It is well known that certain lipotropic nutrients such as choline and metabolites betaine and phosphatidylcholine (PC; lecithin) could prevent or alleviate fatty liver through a variety of mechanisms, including increased hepatic VLDL secretion. Animal and human studies have demonstrated clear protective effects of choline, betaine and PC for NAFLD as well as possible roles in CVD prevention from epidemiological data. Currently, choline consumption is below dietary recommendations due in large part to a general lack of understanding regarding the importance of this nutrient for human health. As lecithin is commonly added (in small amounts) in many processed foods due to its functional capabilities, it is projected that increasing its abundance in the food supply and increasing consumer education and acceptance of lecithin‐based functional foods and nutraceuticals may represent a progressive step towards preventing liver and whole‐body metabolic pathologies in many areas of the world.

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Section: Animal Studiesmentioning

confidence: 99%

Section: Animal Studiesmentioning

confidence: 99%

Phosphatidylcholine functional foods and nutraceuticals: A potential approach to prevent non‐alcoholic fatty liver disease

Duric

Sivanesan

Bakovic

2012

Euro J Lipid Sci & Tech

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“…We also showed that EDI3 regulates cellular migration via the PKCa signaling pathway. Choline metabolism has been intensively discussed in relation to several diseases, including neurological disorders, 3 liver disease, 4,5 and tumor progression. [6][7][8][9][10] With respect to the latter, recent studies have suggested that elevated choline metabolism, including increased phosphocholine (PC) levels, is associated with worse prognosis.…”

Section: Introductionmentioning

confidence: 99%

EDI3 links choline metabolism to integrin expression, cell adhesion and spreading

Lesjak

Marchan

Stewart

et al. 2014

Cell Adhesion & Migration

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Endometrial carcinoma differential 3 (EDI3) was the first member of the glycerophosphodiesterase (GDE) protein family shown to be associated with cancer. Our initial work demonstrated that endometrial and ovarian cancer patients with primary tumors overexpressing EDI3 had a higher risk of developing metastasis and decreased survival. Further analysis indicated that EDI3 cleaves glycerophosphocholine to choline and glycerol-3-phosphate, increases the levels of active PKC, and enhances the migratory activity of tumor cells. Despite these initial findings, EDI3 remained mainly uncharacterized. Therefore, to obtain an overview of processes in which EDI3 may be involved, gene array analysis was performed using MCF-7 breast cancer cells after EDI3 knockdown compared with a non-targeting control siRNA. Several biological motifs were altered, including an enrichment of genes involved in integrin-mediated signaling. More specifically, silencing of EDI3 in MCF-7 and OVCAR-3 cells was associated with reduced expression of the key receptor subunit integrin b1, leading to decreased cell attachment and spreading accompanied by delayed formation of cell protrusions. To confirm these results, we stably overexpressed EDI3 in MCF-7 cells which led to elevated integrin b1 expression associated with enhanced cell attachment and spreading -two processes critical for metastasis. In conclusion, our data provide further insight into the role of EDI3 during cancer progression.

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“…Many patients with steatohepatitis develop some degree of fibrosis within the first years of follow-up (1)(2)(3). The pathogenesis of non-alcoholic fatty liver disease remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Repeated whiskey binges promote liver injury in rats fed a choline-deficient diet

Nieto

Rojkind

2007

Journal of Hepatology

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Choline-deficiency fatty liver: relation of plasma phospholipids to liver triglycerides

Cited by 83 publications

References 0 publications

Phosphatidylcholine functional foods and nutraceuticals: A potential approach to prevent non‐alcoholic fatty liver disease

Phosphatidylcholine functional foods and nutraceuticals: A potential approach to prevent non‐alcoholic fatty liver disease

EDI3 links choline metabolism to integrin expression, cell adhesion and spreading

Repeated whiskey binges promote liver injury in rats fed a choline-deficient diet

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