For the study of biosynthetic pathways and their alterations under various experimental conditions, the method of in vivo conversion is more suitable than in vitro incubation experiments. In rats, in vivo conversion of radioactive progesterone to corticosterone and aldosterone and of corticosterone to aldosterone was demonstrated. The conversion of progesterone and corticosterone to aldosterone occurred only in the presence of the adrenals, while a minimum extra-adrenal conversion of progesterone to corticosterone was observed.
After the administration of ACTH for 9 to 25 days, the adrenals became hypertrophied, and an increased conversion rate from progesterone to corticosterone was demonstrated. Simultaneously, the conversion rate of corticosterone to aldosterone was decreased. Such a change in the biosynthetic pathway of aldosterone may at least in part be responsible for the reduced production of aldosterone from endogenous precursors, observed after repeated administration of ACTH.
Both the NZW and NZB mice exhibit an elevated fasting blood sugar level when compared to Swiss white mice. The NZB/NZW F1 hybrid mouse shows still a higher fasting serum glucose level than either of its parental strains. The elevated glucose level is noted very early in the animals' life, long before definitive signs or symptoms of pathology are evident, and remains elevated at least until the fortieth week of life, the last testing period in our series before sacrificing the aminals. There are two major peaking periods for the glucose levels, namely at 4-10 weeks of age and then again at 31-40 weeks of age. These age periods correspond to the very young animal and to the animal that is beyond its prime and most likely sick and near the end of its lifespan due to the animals' inherent disease processes. The NZB and NZB/NZW F1 hybrid succumb to their disease processes at approximately 8-10 months of age. The NZW usually lives until 18 months. The questions are raised: does the altered immunologic state in the NZB and/or the NZB/NZW F1 hybrid produce the elevated blood sugar levels and the pancreatic histopathology or is it the early hyperglycemic condition coupled with pancreatic pathology which are in some measure instrumental in producing the lesions discussed and observed, in the beginning of the three to four month period of age, in the various organs? Is there a relationship between the hyperglycemic condition and the immune state or are these independent phenomena in a genetically "mixed up" mouse?
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