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J D Wilson

Publications and source records attributed to J D Wilson.

At least 433 records · Page 24Linked to original sources
PubMed1972

The relation between cholesterol absorption and cholesterol synthesis in the baboon.

To determine the relation between cholesterol absorption, total endogenous cholesterol synthesis, and hepatic cholesterol synthesis in a primate, cholesterol synthesis has been studied in biopsies of liver and ileum from normal baboons fed varying amounts of cholesterol and in biopsies of liver from baboons that had been subjected to ileal diversion. In addition, total cholesterol production rates, cholesterol absorption, and total endogenous cholesterol synthesis have been measured in these animals by a double isotope technique in which the animals were given a single injection of cholesterol-4-(14)C and fed constant amounts of cholesterol-1,2-(3)H for 4 months. From these studies, it has been concluded that on a low cholesterol intake cholesterol synthesis in the liver accounts for about three-fourths of total endogenous cholesterol production. The feeding of cholesterol produces complete inhibition of hepatic synthesis in the normal animal only when absorption approximates the amount synthesized by the liver when no cholesterol is fed, e.g., 400-500 mg/day. Finally, the intestine, which does not possess complete negative feedback control of cholesterol synthesis when cholesterol is fed, may be a significant site of nonhepatic cholesterol synthesis in these animals. In studies of four baboons subjected to ileal diversion, it was concluded that the regulation of cholesterol synthesis is distinctly different when the enterohepatic circulation is interrupted. These animals did not exhibit negative feedback of hepatic cholesterol synthesis when cholesterol was fed, despite the fact that cholesterol absorption approximated that of normal animals fed similar diets. The inference has been drawn that bile acids may be involved directly or indirectly in the regulation of hepatic cholesterol synthesis in this species or that the ileum itself may modulate the hepatic negative feedback.

Acetates↗
PubMed1972

Studies on the pathogenesis of the pseudohermaphroditism in the mouse with testicular feminization.

The pathogenesis of the male pseudohermaphroditism in the mouse with X-linked testicular feminization (Tfm) has been investigated by comparing testosterone formation, the effects of androgen administration, and the metabolism of testosterone-1,2-(3)H in normal mice and Tfm mice of varying ages. First, it was established that the adult Tfm animal, in contrast to the human with testicular feminization, has both a low serum testosterone and a low rate of testosterone formation as assessed in slices of testes utilizing a variety of precursors. However, the formation of testosterone from pregnenolone-7alpha-(3)H was shown to be normal in newborn Tfm testes, suggesting that a defect in testosterone synthesis may not be primary to this mutation. Second, to establish that the pseudohermaphroditic state is due to androgen resistance rather than to diminished androgen biosynthesis during fetal life, the effect of the administration of dihydrotestosterone to pregnant animals was studied in male, female, and Tfm offspring. Whereas normal and carrier female littermates demonstrated striking virilization of the internal genital tract after such treatment, there was no sign of virilization in the Tfm animals. This finding provides direct experimental evidence in support of the view that male pseudohermaphroditism in testicular feminization is the result of resistance to androgen action during androgen-mediated sexual differentiation in embryos. Third, the metabolism of testosterone-1,2-(3)H was investigated both in tissue slices and in functionally hepatectomized animals. Dihydrotestosterone formation in tissue slices of the fetal anlage of the male organs of accessory reproduction is normal in the Tfm animal, suggesting that the primary defect in this disorder involves an intracellular event subsequent to this step and that the deficient dihydrotestosterone formation observed in the adult genital tract of the Tfm mouse is secondary to the failure of differentiation in these tissues. Finally, deficient binding of testosterone in the nuclei of the submandibular gland of adult Tfm animals, a known testosterone target tissue, was demonstrated in functionally hepatectomized mice. This finding could either be a manifestation of the primary genetic defect in this disorder or might reflect another acquired abnormality due to incomplete differentiation of adrogen-sensitive cell lines.

Androgen-Insensitivity Syndrome↗