Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003969 (vitamin C deficiency)
 625 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cholesterol lithogenesis is the end result of hepatic microsomal enzymatic alterations which determine an increase in cholesterol synthesis (HMG CoA reductase) and a decrease in its transformation into bile salts (7 alpha hydroxylase). Therefore biliary cholesterol excretion is increased while bile salt excretion is diminished. Ascorbic Acid (A.A.) seems capable of reversing those enzymatic derrangements in scorbutic animals. Since hamsters are able to synthesize A.A., we evaluated its effect used in high doses during diet induced lithogenesis. Two groups of 6 weeks old, male hamsters, were fed with a lithogenic diet for 30 days. Group A received the usual amount of A.A. contained in the diet (0.25 mg/day/manster) while group B had supplementary A.A. added to drinking water (5 mg/day/hamster). Thirteen out of twenty of group A (65%) and 5 out of 20 of group B (25%) developed cholesterol calculi (p 0.05). Less stones were found in the gallbladders of hamsters fed with supplementary A.A. It is concluded that A.A. in this model, has an inhibitory effect on lithogenesis. The possible mechanism seems to be related to A.A. influence on the microsomal enzymes involved in lithogenesis. These findings, plus the lack of undesirable secondary effects of supplementary A.A. suggest a potential therapeutic role in human cholelithiasis.
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PMID:[Prevention of cholelithiasis with ascorbic acid. Experimental study in hamsters]. 53 39

Chronic vitamin C deficiency was induced in guinea pigs by restricting their vitamin C intake to 0.5 mg daily. This was just sufficient to prevent rapidly fatal scurvy and 55 per cent of the animals survived. In 16 weeks their serum ascorbic acid (SAA) fell to 0.16 +/- 0.06 mg/dl as compared to 0.73 +/- 0.11 in control animals receiving 5 mg vitamin C daily. There was a marked increase in serum cholesterol, LDL-cholesterol, VLDL-cholesterol, triglycerides and total lipids. HDL-cholesterol was, however, decreased resulting in a shift of the LDL/HDL ratio from 1.13 +/- 0.16 in the control to 5.91 +/- 1.70 in the low vitamin C group. Cholesterol feeding (100 mg/day) by itself lowered the SAA significantly, besides producing hyperlipidemia. When the vitamin C intake was reduced to only 0.5 mg/day, the effects of cholesterol feeding were exaggerated; the magnitude of hyperlipidemia was now significantly greater than with simple cholesterol feeding. The LDL/HDL ratio rose to 19.02 +/- 3.32 from 1.13 +/- 0.16 in the normal guinea pigs. Chronic vitamin C deficiency seems to affect the blood lipid profile unfavourably which could promote atherogenesis.
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PMID:Aggravation of cholesterol induced hyperlipidemia by chronic vitamin C deficiency: experimental study in guinea pigs. 325 10

Cholesterol accumulates in the blood serum and in the liver of guinea pigs with chronic latent vitamin C deficiency. The reason for this is the decreased rate of transformation of cholesterol to bile acids in the liver of animals deficient in vitamin C. A significant direct correlation exists between the vitamin C concentration in the liver and the rate of cholesterol transformation to bile acids.
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PMID:Cholesterol: vitamin C controls its transformation to bile acids. 468 43