The effects of dietary magnesium (Mg) depletion on thyroid function were studied in young male rats. The rats were fed a semipurified diet containing either 12 ppm Mg (deficient rats) or 662 ppm Mg (control rats) for 14 to 28 days. Results showed that the Mg-deficient rats had decreased body weight gain, lowered concentrations of plasma thyroxine (T4) and Mg, but increased weight of the thyroid gland when expressed in proportion to the body weight (milligrams/100 g). There was no difference in the accumulation (uptake) of 131I, 24 hours after Na131I injection, between the Mg-deficient and Mg-supplemented rats. The protein-bound 131I (PB131I) level and the ratio of PB131I to total 131I in plasma was significantly reduced in Mg-deficient rats. Serum thyroid-stimulating hormone (TSH) levels after thyrotropin-releasing hormone injection (TRH, 50 ng/100 g body weight) increased fivefold at 30 minutes, but declined to near the basal level at 2 hours in both groups. No consistent difference in TSH response was observed between the two treatments. Serum T4 response to TRH challenge was significantly reduced in Mg-deficient as compared to Mg-adequate rats at all time intervals. The reduction of T4 level could be due to an impaired T4 synthesis or release in Mg-deficient rats.

No abstract

Plasma concentrations of immunoreactive growth hormone (GH) and of 17-hydroxycorticosteroids (17OH-CS) were measured during electrical stimulation of hypothalamus or hippocampus in 6 conscious monkeys adapted to chronic restraint in primate chairs. Plasma GH and 17OH-CS increased during 13/14 hypothalamic stimulation experiments. During hippocampal stimulation, however, changes of plasma GH and 17OH-CS were variable. In 6 of 12 hippocampal experiments the qualitative change of plasma 17OH-CS differed from that of GH. These dissociated hormonal changes during hippocampal stimulation are evidence that the central neurological control systems for GH and ACTH are functionally distinct. When the GH and 17OH-CS changes were correlated with the behavior elicited by brain stimulation rather than with the site of stimulation, peak increases of GH, but not of 17OH-CS, were significantly greater during behavior characterized by pupillary dilatation or vigorous attempts to escape from the primate chair than during simple ‘alerting’ behavior. This suggests that plasma GH may reflect the intensity of the central excitatory state better than plasma 17OH-CS.