A reexamination of the effects of intracerebroventricular glucocorticoids in adrenalectomized rats.

Several investigators have reported that many of the behavioral and metabolic effects of ADX can be reversed by appropriate levels of glucocorticoids administered either peripherally or centrally. The present studies were conducted to offer a comparison of the effects of orally administered corticosterone (CORT) with ICV glucocorticoids [CORT, CORT acetate, or dexamethasone (DEX)]. Of particular interest were the effects of glucocorticoid treatment on body weight gain and on macronutrient self-selection. Adult male Sprague-Dawley rats were fitted with ICV cannulae and either bilaterally ADX or given sham operations. In the first experiment, ADX animals were initially treated systematically with CORT (20 micrograms/ml in their drinking water). After a wash-out period during which no steroids were administered, ADX rats were given daily ICV CORT injections (100 micrograms/day in 10 microliters). Systemic CORT treatment promotes weight gain and normal food choice patterns in ADX rats. ICV injections failed to promote weight gain in ADX rats, and daily injection of the vehicle promoted a weight loss in sham-operated controls. Four additional experiments were conducted. ADX, glucocorticoid-treated animals and ADX, vehicle-treated controls as well as sham-operated, vehicle-treated controls were used to assess the effects of both steroid and vehicle on body weight gain and dietary selection patterns. ADX ICV-glucocorticoid-treated animals typically failed to gain weight at the rate observed when ADX rats are treated with CORT systematically. Under one condition, ADX-CORT-treated animals gained weight at a rate comparable to untreated controls, but their ICV-injected control group failed to gain weight.(ABSTRACT TRUNCATED AT 250 WORDS)

Lack of specificity of polyunsaturated fats in the inhibition of rat liver glucose-6-phosphate dehydrogenase.

The mechanism of the effect of polyunsaturated fatty acids (PUFA) on glucose-6-phosphate dehydrogenase (EC 1.1.1.49) (G6PDH) was studied in young, male Wistar rats. Starvation-refeeding increased G6PDH level above that seen in ad libitum-fed animals (enzyme overshoot). A second episode of starvation-refeeding produced even higher levels of G6PDH activity (induction increment). Interposing a high fat diet (containing PUFA) between starvation and feeding the inducer diet abolished one-half to two-thirds of the overshoot. Feeding a high fat diet between the two starvations abolished the induction increment. Inhibitors of arachidonic acid metabolism were not able to reverse the PUFA effect. In another set of experiments it was shown that both linoleic and linolenic acid are equally effective in either reducing the overshoot or abolishing the induction increment. The evidence was interpreted as supporting a hypothesis that the PUFA effect does not require the formation of a specific end product of arachidonic metabolism in a direct way.