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- Author: N. L. WRIGHT x
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SUMMARY
A case report is presented giving details of a patient who showed the unusual combination of secondary hypothyroidism associated with primary testicular disease; the latter was probably prepubertal in origin, and there was evidence of eunuchoidism. Reference is made to previous reports of the co-existence of deficiency in both thyroid and testis, and to possible mechanisms involved in the relationships which may exist between these conditions.
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SUMMARY
Renal excretion in intact, sham-operated and neurohypophysectomized ducks was studied. Neurohypophysectomy produced immediate and profound polydipsia and polyuria. These conditions steadily diminished during the first 2 weeks after the operation and by the 14th day they had stabilized at levels which were approximately three times higher than the corresponding values in sham-operated birds. The stabilized levels of polydipsia and polyuria persisted throughout the remainder of the 60–90 day experimental period. The rates of excretion of Na+, Cl− and total osmotically active material were also increased when compared with intact or sham-operated birds. No change in the rate of K+ excretion was observed.
The i.m. administration of vasopressin reduced the rate of urine flow to that observed in the control birds but the rates of electrolyte excretion were not restored to normal. Synthetic oxytocin had no antidiuretic effect in the neurohypophysectomized birds. Arginine vasotocin treatment restored the rates of both water and ion excretion to values very close to those observed in intact and sham-operated birds.
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The aim of this study was to validate the role of estrogen receptor α (ERα) signaling in the regulation of glucose metabolism, and to compare the molecular events upon treatment with the ERα-selective agonist propyl pyrazole triol (PPT) or 17β-estradiol (E2) in ob/ob mice. Female ob/ob mice were treated with PPT, E2 or vehicle for 7 or 30 days. Intraperitoneal glucose and insulin tolerance tests were performed, and insulin secretion was determined from isolated islets. Glucose uptake was assayed in isolated skeletal muscle and adipocytes. Gene expression profiling in the liver was performed using Affymetrix microarrays, and the expression of selected genes was studied by real-time PCR analysis. PPT and E2 treatment improved glucose tolerance and insulin sensitivity. Fasting blood glucose levels decreased after 30 days of PPT and E2 treatment. However, PPT and E2 had no effect on insulin secretion from isolated islets. Basal and insulin-stimulated glucose uptake in skeletal muscle and adipose tissue were similar in PPT and vehicle-treated ob/ob mice. Hepatic lipid content was decreased after E2 treatment. In the liver, treatment with E2 and PPT increased and decreased the respective expression levels of the transcription factor signal transducer and activator of transcription 3, and of glucose-6-phosphatase. In summary, our data demonstrate that PPT exerts anti-diabetic effects, and these effects are mediated via ERα.
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