Importance of Melanocortin Signaling in Refeeding-Induced Neuronal Activation and Satiety

Singru, Praful S.; Sánchez, Edith; Fekete, Csaba; Lechan, Ronald M.

doi:10.1210/en.2006-1233

Cited by 65 publications

(59 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These results are in agreement with data previously described, which show that refeeding activates ARC and PVN neurons, indicating that these nuclei also are implicated in the responses associated with satiety (39). Activation of parvocellular PVN in response to food intake is likely to involve vagal innervation, since vagotomy abolishes the activation of this region induced by feeding (47).…”

Section: Discussionsupporting

confidence: 93%

“…It was previously shown that ARC neurons participate in the regulation of food intake during the early phase of refeeding (39). 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.…”

Section: Discussionmentioning

confidence: 78%

“…Responses associated with satiety also involve hypothalamic pathways, such as PVN and the arcuate nucleus (ARC), as demonstrated by their activation following food intake (39). These nuclei have been implicated in the control of energy homeostasis and express orexigenic and anorexigenic peptides (38).…”

mentioning

confidence: 99%

See 2 more Smart Citations

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

View full text Add to dashboard Cite

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...

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 78%

See 1 more Smart Citation

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

View full text Add to dashboard Cite

show abstract

“…The PVN is one of the major sites of neuronal activation upon feeding (37), and a selective role in food intake has been demonstrated here for the MC4R (11,18,19). Therefore, we examined neuronal activation in PVN under different physiological states in both wild-type and Nckx4 mutant mice, using c-Fos expression as a marker.…”

Section: Mc4r-dependent and Ca 2ϩ -Sensitive Hyperactivation Of Pvn Nsupporting

confidence: 52%

An Essential Role for the K+-dependent Na+/Ca2+-exchanger, NCKX4, in Melanocortin-4-receptor-dependent Satiety

Lytton

2014

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background:The melanocortin-4 receptor, MC4R, regulates satiety, but the signaling mechanism is unknown. Results: K ϩ -dependent Na ϩ /Ca 2ϩ -exchanger, NCKX4, knock-out mice are lean and hypophagic and display MC4R-dependent, Ca 2ϩ -sensitive, constitutive activation of paraventricular nucleus neurons. Conclusion: Ca 2ϩ signaling is required for MC4R action, and its dysregulation in Nckx4 Ϫ/Ϫ mice leads to anorexia.

show abstract

“…The brains were post-fixed in the same fixative overnight, cryoprotected in 30% sucrose solution, embedded, and serially sectioned on a cryostat (Leica) at 20 mm thickness in the coronal plane and collected in PBS. Sections were processed for CART immunolabeling using the streptavidin-biotin-peroxidase method described earlier (Singru et al, 2007). Briefly, sections were incubated in mouse monoclonal primary antibodies against CART (54-102) diluted in 1% bovine serum albumin (Sigma) containing 0.3% Triton X-100 and 0.09% sodium azide at 1 : 5000 dilution for 2 days at 41C.…”

Section: Immunocytochemistrymentioning

confidence: 99%

Importance of Cocaine- and Amphetamine-Regulated Transcript Peptide in the Central Nucleus of Amygdala in Anxiogenic Responses Induced by Ethanol Withdrawal

Dandekar

Singru

Kokare

et al. 2007

Neuropsychopharmacol

View full text Add to dashboard Cite

We studied the involvement of cocaine-and amphetamine-regulated transcript peptide (CART) in the central nucleus of amygdala (CeA), lateral bed nucleus of the stria terminalis (BNSTl) and nucleus accumbens shell (AcbSh) in generation of ethanol withdrawal symptoms, with particular focus on anxiety-like behavior using a social interaction test. Administration of CART (54-102) into the lateral ventricle (50 and 100 ng) and bilaterally in the CeA (10 and 20 ng) caused a significant reduction in social interaction, suggesting an anxiogenic action of the peptide. Chronic ethanol treatment for 15 days followed by withdrawal precipitated an anxiogenic response at 24 h that was attenuated by intracerebroventricular (5 ml) and intra-CeA (1 ml) administration of antibodies against CART (1 : 500 dilution). An immunocytochemistry protocol was employed to study the response of the endogenous CART system in the CeA following chronic ethanol withdrawal. At 0 h ethanol withdrawal, CART immunoreactivity was apparent in few fibers and the profile was similar to that in the pair-fed control rats. Twenty-four hours following ethanol withdrawal, a highly significant increase (Po0.001) in CART immunoreactivity was noticed in the CeA, which returned to normal 48 and 72 h post-withdrawal. Similar doses of CART or CART antibody injected bilaterally into the BNSTl or AcbSh produced no response in the social interaction test. Furthermore, the CART immunoreactivity profile did not change at the post-withdrawal time points in each of these brain sites. We suggest that CART may mediate the early signs of anxiety-like behavior induced by ethanol withdrawal within the neuroanatomical framework of the CeA.

show abstract

Importance of Melanocortin Signaling in Refeeding-Induced Neuronal Activation and Satiety

Cited by 65 publications

References 55 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

An Essential Role for the K+-dependent Na+/Ca2+-exchanger, NCKX4, in Melanocortin-4-receptor-dependent Satiety

Importance of Cocaine- and Amphetamine-Regulated Transcript Peptide in the Central Nucleus of Amygdala in Anxiogenic Responses Induced by Ethanol Withdrawal

Contact Info

Product

Resources

About