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Biomedical subjects

E Ginter

Publications and source records attributed to E Ginter.

At least 55 records · Page 3Linked to original sources

Hypocholesterolemic effect of ascorbic acid in maturity-onset diabetes mellitus.

A significantly lower vitamin C concentration has been found in the blood and particularly in the leukocytes of hypercholesterolemic diabetic patients than of healthy blood donors. Ascorbic acid administered in a dose of 500 mg per day for 12 months to metabolically stabilized hypercholesterolemic subjects with maturity-onset diabetes mellitus (diabetic diet without insulin or diabetic drugs) brought about a striking decline of cholesterolemia and a moderate decline of triglyceridemia. The serum lipid level in the control group given placebo remained unaltered. A daily administration of 500 mg of ascorbic acid for six months failed to affect the fasting level of serum immunoreactive insulin. It is assumed that the long-term administration of ascorbic acid to maturity-onset diabetics removed the tissue ascorbate deficiency and improved the liver ability to compensate the increased endogenous synthesis of cholesterol by its enhanced transformation to bile acids.

Ascorbic Acid

Effect of chronic physical exercise on cholesterol biosynthesis in meal-fed rats.

Chronic physical exercise (in a rotating drum) influenced liver cholesterologenesis (from acetate-l-14C) in vivo in meal-fed rats (for 2 hours daily) in close temporary correlation with the time of realimentation. If always performed just prior to feeding physical exercise blocks the development of adaptive hyperchloesterologenesis as a metabolic response to infrequent feeding. If it is performed 3 and a half hours after realimentation, the stimulating effect of infrequent feeding on liver cholesterologenesis is not modified.

Animals

Reduction of gallstone formation by ascorbic acid in hamsters.

The addition of 0.5% of ascorbic acid to the lithogenic diet of golden hamsters whose body pool was labelled with 26-14C-cholesterol, lowered the formation of gallstones, the cholesterol concentration and half-life in blood plasma and in the liver, and accelerated cholesterol transformation to bile acids.

Animals

Localization of the interference of ascorbic acid deficiency with bile acid biogenesis.

The catabolism of 26-14C-cholesterol and of 26-14C-7alpha-hydroxycholesterol, the first stage in the transformation of cholesterol to bile acids, was studied in guinea-pigs with chronic latent vitamin C deficiency. Vitamin C deficiency markedly inhibited the oxidation of 26-14C-cholesterol to 14CO2, but did not significantly affect the catabolism of 26-14C-7alpha-hydroxycholesterol. The distribution of 14C in the tissues and body fluids of control and vitamin-deficient guinea pigs injected with labelled 7alpha-hydroxycholesterol was likewise the same. Ascorbic acids is probably needed only for 7alpha-hydroxylation of cholesterol, while the other stages of bile acid biogenesis are independent of vitamin C.

Animals

Determination of cholesterol turnover rate by a one-and two-pool kinetic analysis.

The cholesterol turnover rate in rabbits with alimentary cholesterol atherosclerosis and in guinea-pigs with chronic vitamin C deficiency was studied by a one- and two-pool kinetic analysis. The one-pool analysis yielded exaggeraged values for the turnover rate, but the turnover rate differences between the control and experimental groups in the one- and the two-pool analysis were very similar. One-pool analysis can be used in initial studies to obtain preliminary data on the effect of nutritional, pharmacological and other factors on cholesterol turnover rate.

Animals

Effect of ascorbic acid on plasma cholesterol in humans in a long-term experiment.

During the period of a low vitamin C intake (approximately equal to 20 mg per day) ascorbic acid in a dose of 2 x 500 mg per day was administered to 82 men and women aged 50-75 years. A correlation of plasma cholesterol levels determined before and after a three months' administration of ascorbic acid showed the effect of vitamin C to be dependent on the starting concentration of plasma cholesterol: the higher the initial cholesterolemia, the greater the hypocholesterolemic effect of ascorbic acid. On restricting the experimental group to subjects with an initial cholesterolemia above 230 mg%, the effect of the same dose of ascorbic acid on cholesterolemia was followed in three-month periods for a further 9 months. In all these time intervals, ascorbic acid was found significantly to depress cholesterolemia and its effects persisted 6 weeks after termination of the experiment. The administration of 2 x 500 mg ascorbic acid daily during one year resulted in an abrupt increase of ascorbemia and a marked accumulation of ascorbic acid in the leucocytes. Six weeks following interruption of ascorbic acid intake, vitamin C concentration in the leucocytes significantly declined but still continued to be twice higher than in the control receiving no ascorbic acid supplement.

Aged

Ascorbic acid synthesis in certain guinea pigs.

Three guinea pigs fed a vitamin C-free diet manifested no symptoms of scurvy even after 4-8 months, normally increased in body weight and excreted quantities of ascorbic acid in urine far exceeding the total body pool of ascorbic acid. The course of healing subsequent to experimental trauma in one of these animals proved to be entirely normal and vitamin C concentration in its liver after 8 months of a scorbutogenic regimen was found to be more than twice that in guinea pigs with a daily intake of 10 mg ascorbic acid. It is evident that certain guinea pigs are capable to synthesize ascorbic acid that fully covers the needs of the organism. However, the freqency of occurence of such guinea pigs appears to be extremely small.

Animals

Ascorbic acid in cholesterol and bile acid metabolism.

Latent chronic ascorbic acid deficiency provokes in guinea pigs a metabolic disorder in the liver, causing an impaired cholesterol transformation to its principal catabolic product, bile acids. This metabolic disorder induces hypercholesterolemia and accumulation of cholesterol in the liver and slows the release of cholesterol from the circulation. Ascorbic acid probably intervenes into the biosynthesis of bile acids at the stage of 7 alpha-hydroxylation of the cholesterol nucleus. High doses of ascorbic acid significantly stimulate cholesterol transformation to bile acids in guinea pigs and decrease plasma cholesterol concentration in humans.

Aged