Adrenalectomy decreases neuropeptide Y mRNA levels in the arcuate nucleus

Bd, White; Rg, Dean; Rj, Martin

doi:10.1016/0361-9230(90)90047-4

Cited by 84 publications

(37 citation statements)

References 32 publications

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“…NPY in the ARC is known to increase food intake; thus we can predict that NPY neurons would not be activated in the ADX group. In fact, previous studies demonstrated that adrenalectomy decreases NPY mRNA expression in the ARC (41,50). ␣-melanocyte-stimulating hormone, derived from proopiomelanocortin (POMC) cleavage in the ARC, has well-established anorexigenic effects (38); thus we can speculate that the phenotype of Fos-expressing neurons in the ARC could be POMC neurons.…”

Section: Discussionmentioning

confidence: 92%

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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Section: Discussionmentioning

confidence: 92%

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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show abstract

“…It has been suggested that plasma corticosterone is implicated in the hypothalamic NPY expression. [18][19][20][21] Taken together, it is concluded that a chronic increase in plasma corticosterone in MS/RF rats during the repeated fasting/RF cycles might have contributed to a tonic increase in NPY expression, and the increased plasma corticosterone and NPY expression by repeated fasting/RF cycles may partly be in charge of the sustained compensatory hyperphagia in the MS/RF group. Previous reports have suggested that elevated plasma corticosterone may be necessary for fasting-induced increase in NPY mRNA expression.…”

Section: Discussionmentioning

confidence: 99%

“…13,14 NPY, a potent orexic peptide, stimulates feeding. [15][16][17] Several results suggest that glucocorticoids regulate the hypothalamic NPY expression: adrenalectomy downregulates the expression of NPY gene in the hypothalamus; 18 NPY neurons in the hypothalamic arcuate nucleus contain glucocorticoid receptors 19 and elevated plasma corticosterone appears to be necessary for fastinginduced increase in NPY mRNA expression. 20,21 These reports led us to hypothesize that neonatal MS may lead to development of eating disorders in the offspring later in life, possibly, due to altered HPA axis characteristics modulating the hypothalamic expression of feeding peptides.…”

Section: Introductionmentioning

confidence: 99%

Sustained hyperphagia in adolescent rats that experienced neonatal maternal separation

et al. 2008

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Objective: To examine the neurobiological basis of bingeing-related eating disorders using an animal model system. Design: Sprague-Dawley pups were separated from dam for 3 h daily during the first two weeks of birth (maternal separation (MS)), or left undisturbed (non-handled (NH)). Pups were subjected to repeated fasting/refeeding (RF) cycles; that is, 24 h food deprivation and 24 h RF (NH/RF or MS/RF), or had free access to food and water (NH/fed control (FC) or MS/FC) from postnatal day (PND) 28-40. Measurements: Body weight gain and food intake were recorded. The arcuate expression of neuropeptide Y (NPY) and plasma corticosterone levels were analyzed on PND 29 and 40. Results: Decrease in weight gain by repeated fasting/RF cycles was smaller in MS pups than in NH. Interestingly, weight changes responding to fasting or RF increased in MS/RF compared with NH/RF. Compensatory hyperphagia was diminished in NH/RF after the third fasting trial, but persisted in MS/RF throughout the experimental period. The arcuate expression of NPY mRNA responding to food deprivation was blunted, but elevation of plasma corticosterone exaggerated, in the MS group, compared to the NH group, on PND 29 after the first fasting session. However, both the arcuate NPY mRNA and plasma corticosterone levels were increased in MS/RF, but not in NH/RF, on PND 40 after the six sets of fasting/RF cycles, compared to the free FC groups. Conclusion: Experience of neonatal MS may lead to an exaggerated feeding response to repeated fasting/RF challenges at adolescence, perhaps, due to increased responsiveness of the hypothalamic-pituitary-adrenal gland axis. Additionally, the results suggested that an increased action of the hypothalamic NPY may not be necessary to induce compensatory hyperphagia following food deprivation.

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“…There is considerable evidence indicating a positive effect of CORT, as well as type I1 receptor stimulation, on the synthesis or turnover of NPY and NE, in the ARC or hypothalamus as well as the locus coeruleus (52,215,(221)(222)(223)(224)(225)(226). This positive relation between CORT and NPY gene expression is not evident, however, in all NPY-producing neurons, including those of the brainstem, cortex or PVN itself (215,222,227). Daily rhythms of CORT, neurochemical activity, and feeding.…”

Section: Interactions Between Cort Insulin and Hypothalamic Neurochementioning

confidence: 99%

Adrenal Steroid Receptors: Interactions with Brain Neuropeptide Systems in Relation to Nutrient Intake and Metabolism

Tempel

Leibowitz

1994

J Neuroendocrinology

194

127

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The glucocorticoid, corticosterone (CORT), is believed to have an important function in modulating nutrient ingestion and metabolism. Recent evidence described in this review suggests that the effects of this adrenal hormone are mediated through two steroid receptor subtypes, the type I mineralocorticoid receptor and the type II glucocorticoid receptor. These receptors, which have different affinities for CORT, respond to different levels of circulating hormone. They mediate distinct effects of the steroid, which can be distinguished by the specific nutrient ingested and by the particular period of the circadian cycle.Under normal physiological conditions, the type I receptor is tonically activated, either by low basal levels of circulating CORT (0.5-2 pg%) normally available across the circadian cycle or possibly by the mineralocorticoid aldosterone. This type I activation is required for the maintenance of fat ingestion and fat deposition that occurs during most meals of the feeding cycle. In contrast, the type II receptor is phasically activated by moderate levels of CORT (2-1 0 pg%) normally reached during the circadian peak. Activation of this receptor is required for the natural surge in carbohydrate ingestion and metabolism that is essential at the onset of the active feeding cycle when the body's glycogen stores are at their nadir, and gluconeogenesis is needed to maintain blood glucose levels. This receptor is also activated during periods of increased energy requirements, such as, after exercise and food restriction, when CORT levels rise further ( > 10 pg%) and when its catabolic effects on fat and protein stores predominate to provide additional substrates for glucose homeostasis. These functions of CORT on fat and carbohydrate balance are mediated, in part, by type I and type II receptors located within the hypothalamic paraventricular nucleus, which is known to have key functions in controlling nutrient intake and metabolism, as well as circulating CORT levels. Moreover, the type II receptors within this nucleus, in addition to the arcuate nucleus, may interact positively with the peptide, neuropeptide Y, and the catecholamine, norepinephrine, both of which act to enhance natural carbohydrate feeding and CORT release at the onset of the natural feeding cycle.Thus, under normal conditions, endogenous CORT has a primary function in controlling nutrient ingestion and metabolism over the natural circadian cycle, through the coordinated action of the type I and type II steroid receptor systems. Through this action, CORT has impact on total caloric intake and body weight gain over the long term. Moreover, under conditions of obesity, diabetes and food restriction, steroid receptor function is greatly disturbed in association with chronic high circulating levels of CORT and abnormal glucose homeostasis. These disturbances in steroid action, along with dysfunction in brain neurochemical processes, very possibly contribute to the maintenance of hyperphagia and body weight gain in obese and diabetic ...

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Adrenalectomy decreases neuropeptide Y mRNA levels in the arcuate nucleus

Cited by 84 publications

References 32 publications

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

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

Sustained hyperphagia in adolescent rats that experienced neonatal maternal separation

Adrenal Steroid Receptors: Interactions with Brain Neuropeptide Systems in Relation to Nutrient Intake and Metabolism

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