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Biomedical subjects

U Keup

Publications and source records attributed to U Keup.

9 recordsLinked to original sources
PubMed1982

Reduction of carbohydrate-induced hypertriglyceridemia in (fa,fa) "Zucker" rats by the alpha-glucosidase inhibitor acarbose (BAY g 5421).

Inhibition of carbohydrate digestion by the alpha-glucosidase inhibitor acarbose (BAY g 5421)reduces carbohydrate-induced postprandial blood glucose increase and insulin secretion. As a consequence, in feeding experiments sucrose-induced hyperinsulinemia and hypertriglyceridemia in genetically obese (fa,fa) "Zucker" rats were dose-dependently reduced by addition of acarbose to the diet (15-80 mg/100 g feed). The body weight gain was dose-dependently reduced. In short-term experiments with a fat-free diet acarbose not only prevented serum triglyceride and free fatty acid increase in spite of lowered insulin concentrations but also decreased their concentrations below the values obtained on standard feed. Under these conditions there were no significant effects on body weight. Hypertriglyceridemia induced by i.v. injection of the lipoprotein lipase inhibitor Triton WR 1339 was reduced without affecting body weight in "Zucker" rats after 3 days on a fat-free diet supplemented with acarbose. The triglyceride increase was even lower than in animals kept on standard feed. The data demonstrate that acarbose reduces sucrose-induced hypertriglyceridemia in (fa,fa) "Zucker" rats by diminishing VLDL production and/or secretion rather than by increasing VLDL removal from the blood.

Acarbose↗
PubMed1982

Inhibition of disaccharide digestion in rat intestine by the alpha-glucosidase inhibitor acarbose (BAY g 5421).

Administration of the alpha-glucosidase inhibitor, acarbose (BAY g 5421), to rats together with a sucrose load results in a marked retardation of sucrose digestion. The carbohydrate content of the small intestine is dose dependently increased; the time needed for the absorption is doubled. In the large intestine significant amounts of carbohydrate can be found only after administration of high doses of acarbose (2-4 mg/kg p.o.). In oral sucrose and maltose loading tests the blood glucose increase is dose dependently reduced by acarbose (ED50, 1 or 12 mg/kg, respectively). In perfused jejunal loops of rats, acarbose inhibits the absorption of sucrose (4 g/l) and maltose (1 and 2 g/l), the IC50 values being 3.2, 36, and 57 micrograms/ml, respectively. The data indicate that acarbose effectively inhibits sucrose digestion. It is 10-20 times less effective with maltose as a substrate. Slight malabsorption is induced by acarbose only in doses higher than the ED50.

Acarbose↗
PubMed1976

Studies on the determination and induction of cholesterol 7alpha-hydroxylase.

To determine the activity of cholesterol 7alpha-hydroxylase, different fractions from rat liver homogenates are incubated with glucose-6-phosphate, glucose-6-phosphate dehydrogenase and NADP as well as with cholesterol-4-14C. The 7alpha-hydroxycholesterol-4-14C formed is separated from the extract of the incubation preparation by means of thin-layer chromatography and its radioactivity is calculated as a percentage (conversion figure) of the total radioactivity on the plate. The highest conversion is found in the 18 000 X g supernatant. It is of the order of 1--4%. This activity decreases to about one-half when the homogenate or the cell fraction is stored, while cooling, for two days. It can be shown that repeated pretreatment of rats with phenobarbital increases the activity of hepatic cholesterol 7alpha-hydroxylase by more than three times over the control values. 1-(2'-Hydroxyphenyl-acetyl)-4-methyl-1,2,3,6-tetrahydropyridine (Bay a 4798) a choleretically active drug also increases the activity of this enzyme in the rat more than twofold. This effect is confirmed by reduced biliary excretion of radioactive cholesterol and increased biliary excretion of radioactive bile acids following i.v. administration of DL-mevalolactone-2-14C and continuous intraduodenal infusion of Bay a 4798.

Animals↗
PubMed1975

Inhibition of sucrase by tris in rat and man, demonstrated by oral loading tests with sucrose.

In the course of work concerned with the inhibition of small intestinal carbohydrate digesting enzymes, experiments were performed on rats and two healthy volunteers using tris as a sucrase inhibitor. The following results were obtained: (1) Tris does not lower the blood glucose in fasting rats after oral or subcutaneous doses up to 500 mg/kg, when administered as neutral solution (pH 7.0). (2) Tris reduces reduces the glycemia in rats and human subjects after a sucrose load. In addition, the insulinemia caused by administration of sucrose is reduced in man. This smoothing effect on both curves is dose-dependent. A delay of gastric emptying by tris could be excluded. (3) After a glucose or matose load in rats, tris has no effect on the blood sugar curve. (4) The marked smoothing effect of tris is after sucrose loading is probably caused by its well-known in vitro inhibitory effect on intestinal sucrase activity of pigs and humans.

Administration, Oral↗