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Submitted on October 9, 2003
Accepted on February 5, 2004
Department of Physiology, School of Medicine, University of California, San Francisco, San Francisco, CA 94143-0444
* To whom correspondence should be addressed. E-mail: susanne{at}itsa.ucsf.edu.
Passive elevations in glucocorticoids result in increased insulin and abdominal obesity with peripheral wasting as observed in Cushing's syndrome, with little effect on chow intake. In the absence of insulin (streptozotocin-induced diabetes (STZ)), diabetic rats markedly increase their chow intake in proportion to glucocorticoids. Given a choice of lard or chow, diabetic rats first eat lard then reduce caloric intake to normal for 48 h before returning to hyperphagia on chow alone. We performed 3 experiments to determine the relationship of corticosterone (B) and insulin on lard intake, chow intake, body weight, hormones and fat depots. The results of these studies clarify the actions of both circulating glucocorticoids and insulin on caloric intake in adult male rats. Our experiments show that glucocorticoids provoke dose-related increases in total caloric intake which persist for days and weeks; the results also suggest that increasing insulin concentrations stimulated by glucocorticoids determine the amount of fat intake. Furthermore, we show that lard intake is associated with increasing insulin concentrations. Additionally, the results in adrenalectomized (ADX) and ADX-STZ rats strongly suggest that it is a combination of B and insulin that increases abdominal fat depot weight. Independently of the hormonally manipulated rats, the results also show that intact rats voluntarily eat a considerable and stable proportion of their daily calories as lard, when given a choice between lard and chow. These results suggest that some human obesities may result from elevated glucocorticoids and insulin increasing the proportional intake of high density calories.
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