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Biomedical subjects

G R Phelps

Publications and source records attributed to G R Phelps.

5 recordsLinked to original sources

Tuberculosis in a captive colony of pinnipeds.

Tuberculosis was diagnosed in 10 of 16 otariid seals upon post mortem examination. The species involved were New Zealand fur seals (Arctocephalus forsteri), Australian sea lions (Neophoca cinerea) and an Australian fur seal (Arctocephalus pusillus doriferus). Five seals died, four as a direct result of mycobacterial infection. One seal died of unrelated disease. The remaining 10 animals were subsequently tuberculin tested and then killed and necropsied. Tuberculous lesions were seen in five. Gross pathological changes were most commonly seen in the respiratory system. However, a generalized infection, a case with lesions confined to the liver and draining lymph nodes, and a case with tuberculous meningitis also were seen. Histological lesions were characterized by spindle cell proliferation and necrosis without mineralization or giant cell formation. The mycobacteria isolated was identified as belonging to the Mycobacterium tuberculosis complex but it appeared to be unique. Intradermal tuberculin testing showed promise as a diagnostic aid; however, the results were not statistically significant. Circumstances suggest that the initial infection was present when the seals were captured from the wild.

Animals↗

Effects of adrenalectomy and corticosterone administration on hypothalamic obesity in rats.

The present experiment was designed to assess the role of adrenal hormones in hypothalamic hyperphagia and obesity. Ventromedial hypothalamic (VMH) or sham lesions were produced either 15 days before or after adrenalectomy (ADX) or sham adrenalectomy in rats in a completely counterbalanced design (experiment 1). Body weight and food intake were recorded for 30 days after the second surgery. Adrenalectomy in obese VMH animals eliminated all excess weight gain and decreased food intake to below the level of all control groups. VMH lesions in ADX animals did not produce the characteristic weight gain associated with ventromedial hypothalamic damage, and this group was not significantly different from animals with sham lesions in body weight or food intake. In experiment 2, the administration of corticosterone resulted in a marked increase in the rate of weight gain in ADX-VMH animals, and the withdrawal of the hormones was followed by weight loss. It is concluded that adrenal glucocorticoid hormones are necessary for the development and maintenance of VMH hyperphagia and obesity.

Adrenal Glands↗

Hypothalamic obesity in female rats in absence of vagally mediated hyperinsulinemia.

In order to assess the role of vagally mediated hyperinsulinemia in hypothalamic obesity, plasma insulin and glucose levels were assayed in vagotomized and sham-vagotomized female rats after a 6-h fast and after a measured glucose meal both before and 10-14 days after ventromedial hypothalamic (VMH) lesions. Both groups displayed similar gains in body weight in the first 10 days after VMH lesions, but only the sham-vagotomized VMH-lesioned animals displayed elevated fasting insulin levels. Fasting glucose levels did not differ either before or after the lesion. The insulin response to oral glucose was increased in VMH rats, both in vagotomized and sham-vagotomized animals, and it is concluded that the hyperresponsiveness to oral glucose is independent of vagal mediation. Vagotomy markedly exaggerated the glucose and insulin response to oral glucose loading in both intact rats and rats with VMH lesions, probably as a result of more rapid absorption of glucose from the intestine. It is concluded that the fasting hyperinsulinemia that is characteristic of VMH animals is under vagal control and that its elimination does not prevent the development of obesity.

Animals↗