{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,25]],"date-time":"2026-08-25T14:48:59Z","timestamp":1787669339773,"version":"build-2736575974"},"reference-count":50,"publisher":"Cambridge University Press (CUP)","issue":"3","license":[{"start":{"date-parts":[[2009,6,4]],"date-time":"2009-06-04T00:00:00Z","timestamp":1244073600000},"content-version":"unspecified","delay-in-days":9896,"URL":"https:\/\/www.cambridge.org\/core\/terms"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Br J Nutr"],"published-print":{"date-parts":[[1982,5]]},"abstract":"<jats:p>1. Rats were given a purified folate-deficient diet containing 5 g succinylsulphathiazole\/kg for 4\u20135 months in two experiments. Control rats were supplemented with folic acid in the drinking-water.<\/jats:p><jats:p>2. Weight gain was much below normal in the folate-deprived rats after the first month. Very low folate levels were recorded in blood, liver and peripheral nerve (12\u201333% of control). In Ihe central nervous system, including the cerebrospinal fluid, the folate depletion was less conspicuous (50\u201380% of control). Only marginal signs of anaemia were found and no signs of neurological dysfunction were detected, using nerve conduction velocity measurement and co-ordination tests.<\/jats:p><jats:p>3. Light and electron microscopy of the folate deficient liver revealed fatty infiltration, and enlargement of liver parenchymal cells, nuclei and nucleoli. There was often a considerable amount of bile ductular cells in the lobuli but no cirrhosis. The morphological changes resembled those observed in choline deficiency.<\/jats:p><jats:p>4. Phospholipid N-methylation in liver was depressed in folate deficiency. This was probably due to a decreased availability of S-adenosylmethionine caused by the low concentrations of methylated folate in liver. Intraperitoneal administration of methionine did not normalize phospholipid methylation.<\/jats:p><jats:p>5. In folate deficiency the proportion of ethanolamine phosphoglyceride in liver was increased at the expense of choline phosphoglyceride, which is consistent with a decreased phospholipid methylation. Also an increase in liver triacylglycerol was noted, in accordance with the morphological observations. Brain lipid composition was unchanged.<\/jats:p><jats:p>6. After the injection of labelled ethanolamine, isotope accumulated in liver phosphoethanolamine in folate deficiency, probably due to an impairment of the CTP: ethanolaminephosphate cytidylyltransferase(<jats:italic>EC<\/jats:italic>2.7.7.14) reaction. The mechanism of this impairment is discussed.<\/jats:p><jats:p>7. Although the low concentrations of folate was the main nutritional change in the deprived animals, changes with respect to vitamin B<jats:sup>12<\/jats:sup>and maybe also choline cannot be excluded. We conclude that some of the changes in folate deficiency, i.e. fatty liver and decreased biosynthesis of liver phospholipids may be due to a precipitated deficiency of lipotropic agents, whereas other differences may be specific for deficiency of folate<jats:italic>per se<\/jats:italic>, such as changes in liver phospholipid fatty acids and some of the morphological aberrations.<\/jats:p>","DOI":"10.1079\/bjn19820063","type":"journal-article","created":{"date-parts":[[2005,5,24]],"date-time":"2005-05-24T23:20:35Z","timestamp":1116976835000},"page":"505-520","source":"Crossref","is-referenced-by-count":39,"title":["Effect of experimental folate deficiency on lipid metabolism in liver and brain"],"prefix":"10.1017","volume":"47","author":[{"given":"B.","family":"\u00c5kesson","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C.","family":"Fehling","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"J\u00e4gerstad","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"U.","family":"Stenram","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"56","published-online":{"date-parts":[[2009,6,4]]},"reference":[{"key":"S0007114582001421_ref050","doi-asserted-by":"publisher","DOI":"10.1139\/o79-071"},{"key":"S0007114582001421_ref020","first-page":"50","volume":"70","author":"Grisham","year":"1960","journal-title":"Archs Path."},{"key":"S0007114582001421_ref014","first-page":"517","volume-title":"Folic Acid in Neurology, Psychiatry, and Internal Medicine","author":"Fehling","year":"1979"},{"key":"S0007114582001421_ref032","doi-asserted-by":"publisher","DOI":"10.1016\/0041-008X(65)90093-1"},{"key":"S0007114582001421_ref025","first-page":"191","volume":"51","author":"Haltia","year":"1970","journal-title":"Br. 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