Effects of adrenalectomy and corticosterone administration on hypothalamic obesity in rats

Bruce, Brendan; King, Bruce M.; Phelps, Glenn R.; Veitia, Marie

doi:10.1152/ajpendo.1982.243.2.e152

Cited by 43 publications

(20 citation statements)

References 21 publications

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“…These hormones regulate the expression of similar neuropeptides in brain regions involved in feeding behavior and body weight regulation. Glucocorticoids have a permissive effect on obesity, as evidenced by the ability of adrenalectomy to ameliorate obesity (156)(157)(158). Conversely, hypercortisolism leads to abnormalities of adipose distribution (159).…”

Section: The Physiological Role Of Leptin In Energy Homeostasis Leptimentioning

confidence: 99%

Leptin

Ahima

Flier

2000

Annu. Rev. Physiol.

1,530

1,136

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The discovery of the adipose-derived hormone leptin has generated enormous interest in the interaction between peripheral signals and brain targets involved in the regulation of feeding and energy balance. Plasma leptin levels correlate with fat stores and respond to changes in energy balance. It was initially proposed that leptin serves a primary role as an anti-obesity hormone, but this role is commonly thwarted by leptin resistance. Leptin also serves as a mediator of the adaptation to fasting, and this role may be the primary function for which the molecule evolved. There is increasing evidence that leptin has systemic effects apart from those related to energy homeostasis, including regulation of neuroendocrine and immune function and a role in development.

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Section: The Physiological Role Of Leptin In Energy Homeostasis Leptimentioning

confidence: 99%

Leptin

Ahima

Flier

2000

Annu. Rev. Physiol.

1,530

1,136

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“…Lesions of the ventromedial hypothalamus (VMH) and genetic obesity in rodents cause hyperactivity in the HPA system, hyperinsulinemia, decreased activity in the sympathetic nervous system, obesity, loss of circadian rhythms in food intake and frequently, hyperphagia [re viewed in [14][15][16], Bilateral adrenalectomy and loss of cor ticosteroid secretion reverses or ameliorates the hyperin sulinemia, hyperphagia and obesity in rats with VMH lesions [17] or genetic obesity [18. 19] and corticosteroid treatment restores them [17][18][19][20][21].…”

Section: Introductionmentioning

confidence: 99%

“…19] and corticosteroid treatment restores them [17][18][19][20][21]. Moreover, treatment of obese rats with RU 38486, a glucocorticoid receptor antagonist, also ameliorates the obesity syndrome [22], Thus, it is clear that activity of the HPA system stimulat ed by lesions of the VMH or genetic lesions is required for the obesity syndrome to occur.…”

Section: Introductionmentioning

confidence: 99%

Ventromedial Hypothalamic Lesions Inhibit Corticosteroid Feedback Regulation of Basal ACTH during the Trough of the Circadian Rhythm

et al. 1995

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We have determined the effects of bilateral electrolytic lesions of the ventromedial hypothalamus (VMH) on activity in the hypothalamo-pituitary-adrenal (HPA) system. Acutely, during the first 5 days, lesions of the anterior-medial VMH caused loss of the diurnal rhythms in food intake and plasma corticosterone (B) levels. Plasma B concentrations were elevated during the time of the normal trough of the basal diurnal rhythm in HPA axis activity and the diurnal rhythm in food intake was abolished, in agreement with the results of others. Consistent with hyperactivity in the HPA axis, lesioned rats had increased adrenal weight, decreased thymus and body weights and decreased plasma transcortin concentrations. To determine how lesions of the VMH provoke these increases in activity of the HPA system, the sensitivity of ACTH in adrenalectomized, lesioned rats to replacement with exogenous B was determined under basal conditions during the trough (morning – AM) and peak (evening -PM) of the diurnal rhythm in HPA axis activity. ACTH in lesioned rats in the AM was insensitive to feedback over the very low range of plasma B of 1-4 µg/dl, whereas sham-lesioned controls exhibited the normal, high sensitivity of ACTH to B at this time of day. There was no difference between the sensitivity of ACTH to this low range of B in the PM in VMH- and sham-lesioned rats. Two to 5 weeks after VMH lesions, as found by others, mean daily plasma B levels did not differ from sham-lesioned controls; however, plasma B during the AM was still mildly elevated in these rats. Inhibition of plasma B in the PM by dexamethasone was less effective in lesioned rats. Although HPA system responses to hypoglycemia, corticotropin-releasing factor and ACTH were normal, the lesioned rats exhibited obesity, hyperinsulinemia, hyperglycemia, hypertension and tachycardia, all signs consistent with mild hyperactivity of the PHA axis. Occupancy of type I, high-affinity corticosteroid receptors is known to control basal activity of the HPA system during the trough of the diurnal rhythm and to interact with glucocorticoid receptors to affect basal activity during the peak of the diurnal rhythm and during AM stress. We conclude that VMH lesions disrupt transmission of inhibitory signals, mediated by occupancy of type I corticosteroid receptors, that are initiated by a B feedback site.

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“…On the other hand, bilateral adrenalectomy (ADX) reduces food intake and body weight gain, and these effects are reversed by glucocorticoid replacement in rats (12). Furthermore, ADX reduces hyperphagia and obesity in different experimental models, whereas glucocorticoid replacement reverses these effects (4,8,52). Hypophagia induced by ADX has been associated with a decrease of mRNA expression of hypothalamic neuropeptide Y (NPY), a potent orexigenic neuropeptide (41).…”

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confidence: 99%

Hypophagia induced by glucocorticoid deficiency is associated with an increased activation of satiety-related responses

Uchôa¹,

Sabino²,

Ruginsk³

et al. 2009

Journal of Applied Physiology

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Uchoa ET, Sabino HA, Ruginsk SG, Antunes-Rodrigues J, Elias LL. Hypophagia induced by glucocorticoid deficiency is associated with an increased activation of satiety-related responses. J Appl Physiol 106: 596 -604, 2009. First published November 20, 2008 doi:10.1152/japplphysiol.90865.2008.-Glucocorticoids have major effects on food intake, demonstrated by the decrease of food intake following adrenalectomy. Satiety signals are relayed to the nucleus of the solitary tract (NTS), which has reciprocal projections with the arcuate nucleus (ARC) and paraventricular nucleus (PVN) of the hypothalamus. We evaluated the effects of glucocorticoids on the activation of hypothalamic and NTS neurons induced by food intake in rats subjected to adrenalectomy (ADX) or sham surgery 7 days before the experiments. One-half of ADX animals received corticosterone (ADXϩB) in the drinking water (B: 25 mg/l). Fos/tyrosine hydroxylase (TH), Fos/corticotrophin-releasing factor (CRF) and Fos immunoreactivity were assessed in the NTS, PVN, and ARC, respectively. Food intake and body weight were reduced in the ADX group compared with sham and ADXϩB groups. Fos and Fos/TH in the NTS, Fos, and Fos/CRF immunoreactive neurons in the PVN and Fos in the ARC were increased after refeeding, with higher number in the ADX group, compared with sham and ADXϩB groups. CCK administration showed no hypophagic effect on ADX group despite a similar increase of Fos/TH immunoreactive neurons in the NTS compared with sham and ADXϩB groups, suggesting that CCK alone cannot further increase the anorexigenic effect induced by glucocorticoid deficiency. The present data indicate that glucocorticoid withdrawal reduced food intake, which was associated with higher activation of ARC, CRF neurons of the PVN, and catecholaminergic neurons of the NTS. In the absence of glucocorticoids, satiety signals elicited during a meal lead to an augmented activation of brain stem and hypothalamic pathways. glucocorticoids; food intake; satiety signals; nucleus of the solitary tract; paraventricular nucleus of the hypothalamus; arcuate nucleus of the hypothalamus GLUCOCORTICOIDS PLAY AN IMPORTANT ROLE in the control of feeding behavior. Increased food intake and body weight gain are associated with glucocorticoid treatment in humans (46). On the other hand, bilateral adrenalectomy (ADX) reduces food intake and body weight gain, and these effects are reversed by glucocorticoid replacement in rats (12). Furthermore, ADX reduces hyperphagia and obesity in different experimental models, whereas glucocorticoid replacement reverses these effects (4,8,52). Hypophagia induced by ADX has been associated with a decrease of mRNA expression of hypothalamic neuropeptide Y (NPY), a potent orexigenic neuropeptide (41). ADX also may reduce food intake through the increase of corticotrophin-releasing factor (CRF) mRNA expression in the paraventricular nucleus (PVN), since CRF is a well-known anorexigenic peptide (1, 2). CRF neurons in the PVN receive projections from neurons of the nucleus of the...

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Effects of adrenalectomy and corticosterone administration on hypothalamic obesity in rats

Cited by 43 publications

References 21 publications

Leptin

Leptin

Ventromedial Hypothalamic Lesions Inhibit Corticosteroid Feedback Regulation of Basal ACTH during the Trough of the Circadian Rhythm

Hypophagia induced by glucocorticoid deficiency is associated with an increased activation of satiety-related responses

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