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The association of DM.HT and JRA has not been previously recorded.The purpose of this comnunication Is to report our preliminary findings In a 14 year old Haitian girl who developed In sulln-dependent DM at age 6 yrs. goiter at 9 yrs. and polyarticular JRA at 12 yrs.No evidence of lridocyclitis was present.Fo1 lowing thyroid and gold therapy the goiter regressed and the arthritis improved.There was a family history of DM and goiter i the mother and of DM in maternal relatives.lnvestlgations reveal

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ExtractPregnant Sprague-Dawley rats from the 18th to the 21st day of gestation were fasted for 16 hr and anesthetized, and a constant infusion of uniformly labeled glucose-14 C and of glucose-2-3 H was started. The purpose was to see if the regulation of fetal blood glucose concentration differed from the maternal during fasting. The results are given in Figures 2 and 3. During the course of the infusions, the specific activity of glucose was, at all points measured, two to four times lower in the fetal than in the maternal serum. The higher fetal than maternal supply of blood glucose could be derived either frcm gluconeogenesis or from glycogenolysis in the fetus.In vitro studies indicate that the fetal rat liver is unable to perform gluconecgenesis. Therefore, the placenta was investigated for the presence of a gluconeogenetic pathway. Placenta slices showed no ability to convert pyruvate into glucose (Fig. 8). No phosphoenolpyruvate carboxykinase (EG. 4.1.1.32) activity could be found in placenta homogenates.The possibility of the presence of gluconeogenesis in the rat fetus has been investigated in vivo. Intraperitoneal injections of pyruvate-2-l4 C and glycerol-1 ,3-14 C were given to 1-day-old newborns, prematures (fetuses which were delivered 1 day prior to term), and fetuses in situ. The 1-day-old newborns do convert both substrates to glucose, with averages of 50 and 70%, respectively, of serum radioactivity being due to glucosel4 C, thus proving the validity of this way of investigating gluconeogenesis in vivo. The prematures did not synthesize glucose from pyruvate, but glucose synthesis occurred from glycerol, an average of 70% of serum radioactivity being due to glucose-14 C. The fetuses which were injected in situ did not synthesize glucose frcm either one of the two substrates. These experiments would seem to exclude fetal gluconeogenesis as the source of fetal blood glucose in the constant infusion experiments mentioned above.Fetal hepatic glycogenolysis can account only in part for the higher dilution of the specific activity of glucose in the fetus after a 16-hr fast. The data in Table I show that at the time when the constant infusions were started (after a 16-hr fast) the fetal liver glycogen concentration had diminished from 111 zt 5 to 82 ± 10 mg/g wet weight, as compared to the fed state. This decrease is too small to account for the higher fetal than maternal dilution of blood glucose specific activity, or for the maintenance of unchanged blood glucose levels in the fetus after a 16-hr fast (86 ± 8 and 92 ± 11 mg/100 ml, respectively).An unknown mechanism leading to the privileged situation of the fetus with regard to blood glucose levels during a fasting state must be postulated. SpeculationGluconeogenesis is inactive in the rat fetus, as investigated by in vivo and in vitro methods. Fetal hepatic glycogenolysis cannot be the only source of fetal blood glucose during fasting. The factors leading to the privileged situation of the fetus with regard to blood glucose levels during a fasting...

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