Abstract
Choline (Ch) is an important nutrient that is involved in many physiological functions. Deprivation of Ch (CD) may lead to hepatocellular modifications and/or even hepatic tumorigenesis and it can be a frequent problem in clinical settings; it can accompany various common pathological (alcoholism and malnutrition) or physiological states (pregnancy and lactation). The aim of this review is to provide an up-to-date overview of the major metabolic pathways involved in the hepatic response toward the experimentally or clinically induced CD, and to shed more light on the implicated (and probably interrelated) mechanisms responsible for the observed hepatocellular modifications and/or carcinogenesis.
Acknowledgements
This work was supported by the State Scholarships Foundation of the Hellenic Republic (in terms of a scholarship to Dr. Hussam Al-Humadi), as well as by the National and Kapodistrian University of Athens.
Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
Notes
1The ingredients of CDD used in our experiments are [Citation13]: casein 10%, α-protein 10%, sucrose 51%, alphacel 5%, lard 20%, manganese sulfate H2O 150 mg kg-1, zinc chloride 20 mg kg-1, chromium potassium sulfate 12H2O 55 mg kg-1, sodium selenite 1 mg kg-1, and salt mixture Wesson 4% (calcium carbonate 21%, copper sulfate 5H2O 0.0039%, ferric phosphate 1.470%, manganese sulfate H2O 0.02%, magnesium sulfate 7H2O 9%, potassium aluminum sulfate 0.009%, potassium chloride 12%, potassium dihydrogen phosphate 31%, potassium iodide 0.005%, sodium chloride 10.5%, sodium fluoride 0.057%, tricalcium phosphate 14.9%, plus ICN vitamin diet fortification mixture except Ch chloride). An experimentally suitably matched MCDD would be an isocaloric diet that would also be deprived of Met. Readers should bear in mind that diets differ from reference to reference, depending upon the manufacturers' formulas.