hypervitaminosis a/triglyceride

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Fatty liver in hypervitaminosis A: synthesis and release of hepatic triglycerides.

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Feeding large doses (30,000 IU/100 g body wt per day) of vitamin A to young rats for 2 days produced fatty liver, caused a stimulation of oxidation and esterification of [1-14C]palmitate by liver slices, and increased the activity of hepatic palmitoyl-CoA synthetase. Under similar conditions,

ALTERATIONS IN THE LIPIDS OF BONE CAUSED BY HYPERVITAMINOSIS A AND D.

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1. The total lipid, phospholipid, total and free fatty acid, free and esterified cholesterol contents of the long bones of normal, hypervitaminotic A, D and A plus D rats were determined. 2. Toxic amounts of vitamin A decreased the total fatty content, whereas toxic amounts of vitamin D increased

Implications of hypervitaminosis A on the calcium-phosphate metabolism and on blood lipids in hemodialysis.

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Serum levels of vitamin A (VA) were measured in 71 hemodialysis (HD) patients and in 30 normal controls. 65 of the 71 patients were taking multivitamin preparations (MP) containing VA. The HD patients had significantly greater values: 7.81 +/- 2.86 mumol/l (224 +/- 82 micrograms/dl) versus 3.97 +/-

Hydroxypropylcyclodextrins in parenteral use. II: Effects on transport and disposition of lipids in rabbit and humans.

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Hydroxypropyl ethers of cyclodextrins, after parenteral administration, come into contact with lipids in tissues and in circulation and form water-soluble inclusion complexes with these lipids. A single intravenous administration of hydroxypropyl-beta-cyclodextrin to a hereditary hyperlipidemic

[Forestier disease and metabolism disorders. A prospective controlled study of 25 cases].

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Metabolic disorders including diabetes mellitus, glucose intolerance, dyslipidemias, hyperuricemia, and hypervitaminosis A have often been mentioned in association with diffuse idiopathic skeletal hyperostosis (DISH). Production of bone under the influence of insulin or retinol has been suggested as

[Chronic fatal vitamin A poisoning with hemolytic anemia].

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A case of chronic, lethal vitamin A intoxication is reported, the diagnosis of which was not established intra vitam. The patient presented with chronic mixed prehepatic and hepatic icterus and hypersplenism with hemolytic anemia. On post mortem histological examination, abundant deposits of neutral

True deficiency of antioxidant vitamins E and A in dialysis patients. Relationship with clinical patterns of atherosclerosis.

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Atherosclerosis is an important cause of morbidity and mortality in peritoneal dialysis (PD) patients. Oxidative stress plays a role in the pathogenesis of uremic atherosclerosis. Although antioxidant substances (vitamins A and E) are elevated in the plasma of dialysis patients, intracellular and

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