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This results in a temporary state of adrenal insufficiency characterized by very low cortisol levels necessitating treatment with steroids to maintain a normal cortisol effect on body tissuesand to limit the onset of secondary adrenal insufficiency leading to the early stages of the metabolic syndrome in the adrenal cortex. In an animal model of adrenal insufficiency, cortisol levels in male rats were reduced by 20% after they were given a high fat diet for 4 days. Similarly, a rat model of adrenal insufficiency was developed whereby adrenal function was decreased by 20% for 4 days. When the animals were given a normal diet for 4 days, their adrenal glands did not differ in their levels of cortisol as measured by the immunofluorescence technique of a specific antibody. However, a rat model with no change in the adrenal glands showed decreased cortisol levels (p<0.05). The results indicate that the development of secondary adrenal insufficiency by a low glucocorticoid effect may be related to an increase in adrenal protein synthesis (Lanvall and Varma, 1998). 2. A very common occurrence in these situations is the development of chronic kidney diseases which involve several biochemical pathways. These include an overproduction of urea in the renal tubules resulting in increased secretion of cortisol and the resulting reduction in glomerular filtration rates (Grundy, 1991). 3. Some studies have revealed that cortisol levels may be enhanced in the liver of animals that had been sacrificed during late pregnancy. Since the cortisol levels in the plasma are not affected by dietary intake when they are given in a liquid form, that may in effect be giving the fetus a very large dose of cortisol, with possibly little or no effect on infant growth (Wagner, 1992). 4. These hormonal changes are particularly noteworthy because of their association with the onset of a number of conditions which can result in serious medical problems. 5. This phenomenon also has been shown to occur in children suffering from chronic fatigue syndrome and/or fibromyalgia (Lanvall and Varma, 1998). 6. In a study in the mid 1980's at the University College Hospital, London, the glucocorticoid effect was noted on the brain tissue of infants who were given oral corticosteroids in the first 2 weeks of life. The authors suggested that there was an adrenocortical decrease in metabolism in infancy caused by early exposure to glucocorticoids (Wagenmakers, 1987). 7. A paper with the title, "Corticotropin T releases glucocorticoid-like substances in Related Article: