The APS Journal Legacy Content is the corpus of 100 years of historical scientific research from the American Physiological Society research journals. This package goes back to the first issue of each of the APS journals including the American Journal of Physiology, first published in 1898. The full text scanned images of the printed pages are easily searchable. Downloads quickly in PDF format.

Administration of gold thioglucose led to the development of hyperphagia and obesity in mice; this confirmed findings by previous investigators. By employing neutron activation analysis and radioautography, it was observed that this syndrome was associated with focal accumulation of gold in the hypothalamus. Animals treated with gold thiomalate failed to show any hypothalamic localization of gold radioautographically or any evidence of the syndrome of hyperphagia and obesity. In addition, other foci of gold localization were found in gold thioglucose-treated but not in the gold thiomalate-treated animals. Gamma spectroscopy studies made possible quantitative measurements of the gold content in the brains of both treated groups. Gold thioglucose-treated as well as gold thiomalate-treated animals had appreciable quantities of gold in the brain proper. Phosphorus 32 generated by neutron activation of the sulfur moiety of gold thioglucose proved to be insignificant in its contribution to the radioautographic findings. Implication of the above findings for the glucostatic theory of appetite regulation is discussed.

Thyrotropin (TSH), 1 MU/ml and N6, O2'-dibutyryl adenosine 3',5-cyclic monophosphoric acid (dbcAMP) greatly enhanced the release of thyroxine (T4) and triiodothyronine (T3) from mouse thyroids incubated in vitro. L-Epinephrine (E) and L-norepinephrine (NE) strongly inhibited the TSH and dbcAMP-stimulated release of thyroid hormones; L-isoproterenol (IPNE) exerted a relatively weak inhibition. The inhibition by catecholamines was prevented by the alpha-adrenergic blocker, phentolamine; L-propranolol, a beta-adrenergic blocker, had no effect on the inhibition. The TSH-induced release of thyroid hormones was not affected by adrenergic blockers. Epinephrine did not affect the increase in thyroidal cAMP content induced by TSH. These results indicate that catecholamines act by way of an alpha-adrenergic receptor to suppress TSH-stimulated release of thyroid hormones at a point beyond cAMP formation.

Gold thioglucose (GTG)-treated hyperphagic obese mice exhibit a pronounced anorexia upon adrenalectomy which is reversed by the systemic administration of adrenal glucocorticoids. To determine whether the return of hyperphagia was mediated by an action of the hormones on the central nervous system, food intake and body weight were monitored in anorexic GTG-treated obese adrenalectomized mice which received a single intracerebroventricular (icv) injection of very small amounts of adrenal glucocorticoids, including cortisone, corticosterone, and dexamethasone. The responses of untreated controls and adrenalectomized control mice were also studied. To rule out possible systemic effects of icv injections of adrenal glucocorticoids, food intake and body weight were also monitored in similar mice given a single ip injection of the hormones. We found that hyperphagia was restored and weight loss abolished in anorexic GTG-treated obese adrenalectomized mice after a single icv injection of adrenal glucocorticoids; the dose of cortisone required was found to be 1/60th of that previously shown to be needed systemically to restore hyperphagia. A single ip injection of these adrenal hormones in the small amounts given icv failed to induce hyperphagia in these mice. The icv and ip injections of the adrenal glucocorticoids did not significantly affect food intake or body weight of untreated controls and adrenalectomized control mice. These findings indicate that adrenal glucocorticoids act via the central nervous system in restoring hyperphagia in anorexic GTG-treated obese adrenalectomized mice.