Inhibitory effects of specific apolipoprotein C-III isoforms on the binding of triglyceride-rich lipoproteins to the lipolysis-stimulated receptor.

ApoC-III overexpression in mice results in severe hypertriglyceridemia due primarily to a delay in the clearance of triglyceride-rich lipoproteins. We have, in primary cultures of rat hepatocytes, characterized a lipolysis-stimulated receptor (LSR). The apparent number of LSR that are available on rat liver plasma membranes is negatively correlated with plasma triglyceride concentrations measured in the fed state.

Identification of a lipolysis-stimulated receptor that is distinct from the LDL receptor and the LDL receptor-related protein.

This paper provides further characterization of a receptor that, in cells lacking the LDL receptor (FH fibroblasts), mediates lipoprotein binding, uptake, and degradation when incubated with oleate at concentrations not exceeding albumin binding capacity. This oleate-activated receptor is genetically distinct from the LDL receptor and is hereafter referred to as the lipolysis-stimulated receptor (LSR). Its apparent affinity was higher for triglyceride-rich lipoproteins (chylomicrons, VLDL) and for lipid emulsions supplemented with recombinant apoE, than for LDL which contains solely apoB.

[Induction of fetal thymidine kinase by phyto-estrogens in the immature rat uterus].

Administration of phytooestrogens to immature female rats leads to a large increase in uterine thymidine kinase activity. That increase concerns to a large extent the fetal isoenzyme of thymidine kinase. These results confirm the estrogenic properties of phytoestrogens and allow to specify their physiological effects.

[Demonstration of fetal-type thymidine kinase in cancer of the breast].

Seventy five human breast cancers were examined in order to search for the presence of thymidine kinase of the fetal-type (TK-F). The presence of TK-F was evidenced in all tumors. Its activity varied from one to another tumor, but it was evident that the increased TK activity observed in mammary cancers could exclusively be related to high TK-F activity.

Estrogen and progesterone receptors in mammary tumors induced in rats by simultaneous administration of 17 beta-estradiol and progesterone.

Mammary tumors were promoted in male rats of the Wistar WAG strain by continuous and simultaneous administration of 17 beta-estradiol and progesterone. Tumor induction and growth were dependent on estradiol and on progesterone. Their histological features were comparable with those of human breast cancers.