OBJECTIVE: Based on the inhibitory effects of teasaponin on pancreatic lipase activity in vitro, this study was performed to clarify whether teasaponin prevented obesity induced in mice by a high-fat diet for 11 weeks. DESIGN: For in vitro experiments, assay for the inhibitory effects of teasaponin on pancreatic lipase activity was performed by measuring the rate of release of oleic acid from triolein in an assay system using triolein emulsified with lecithin, gum arabic, Triton X-100 or 4-methylumbelliferyloleate. For in vivo experiments, female ICR mice were fed a high-fat diet with or without 0.5% teasaponin for 11 weeks. RESULTS: Teasaponin competitively inhibited the hydrolysis of triolein emulsified with lecithin, gum arabic, Triton X-100 or 4-methylumbelliferyloleate. Teasaponin inhibited the elevations of plasma triacylglycerol levels 3, 4 and 5 h after oral administration of lipid emulsion containing corn oil. Teasaponin suppressed the increases in body, parametrial adipose tissue weights and diameter in adipose cell size induced by a high-fat diet. Furthermore, feeding a high-fat diet plus teasaponin had no effect on stool frequency and content, but significantly increased triacylglycerol contents in feces as compared to feeding a high-fat diet. CONCLUSIONS: The anti-obesity effects of teasaponin in high-fat diet-treated mice may be partly mediated through delaying the intestinal absorption of dietary fat by inhibiting pancreatic lipase activity.

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In the hen, the preoptic area, medial basal hypothalamus, and anterior lobe of the pituitary showed a greater uptake of [3H]estradiol-17 beta (E2) in vivo than other tissues. This uptake was decreased when unlabeled diethylstilbestrol was injected together with the [3H]E2 or when unlabeled E2 was injected before the [3H]E2 injection. A specific estrogen binding component having properties of a receptor was found in vitro in both soluble and insoluble fractions of these tissues in a hypotonic buffer solution. The administration of E2 in vivo caused a marked decrease in the estrogen receptor binding in the soluble fraction with a concomitant increase in binding in the insoluble fraction; as a result, total binding (sum of the bindings in soluble and insoluble fraction) did not change.

The binding affinity and capacity of arginine vasotocin (AVT) receptor in the hen uterus changed during a period before and after oviposition. Three hours before oviposition, the binding capacity of the AVT receptor increased. An injection of prostaglandin (PG) F2 alpha caused an increase in the AVT receptor Bmax in the uterus, and indomethacin blocked the normal rise in the AVT receptor Bmax and PGF content prior to oviposition. However, just prior to oviposition, the binding affinity increased with a decrease in the binding capacity. A progesterone injection caused an increase in binding affinity and a decrease in binding capacity of the AVT receptor. The specific binding of the progesterone receptor in the uterus increased 2 h before oviposition and remained high until oviposition. Serum AVT levels increased at oviposition. An injection of AVT caused an increase in the affinity of the AVT receptor with a decrease in the capacity. The change in the affinity and capacity of AVT receptor at oviposition may result from the action of progesterone via increased progesterone receptor binding, and the action of AVT on its own receptors.

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