Hypothalamic corticotropin-releasing hormone is a mediator of the anorexigenic effect of leptin.

Uehara, Yutaka; Shimizu, Hiroyuki; Ohtani, Ken-Ichi; Sato, Nobuaki; Mori, Masataka

doi:10.2337/diabetes.47.6.890

Cited by 171 publications

(87 citation statements)

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“…Both in vivo and in vitro studies have shown that leptin increases expression of CRF in the hypothalamus [12,28,43,54]. In fact, simultaneous injection of leptin and a non-specific CRF receptor antagonist confirmed that a ligand for CRF receptor contributes to leptin's anorectic effect [21,59].…”

Section: Discussionmentioning

confidence: 96%

Regulation of corticotropin-releasing factor and urocortin 2/3 mRNA by leptin in hypothalamic N39 cells

et al. 2013

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Corticotropin-releasing factor (CRF) activates the pituitary-adrenal axis during stress, and shows anorectic effects via CRF type 1 receptors in the hypothalamus.Both urocortin (Ucn) 2 and Ucn3 also act as anorectic neuropeptides via CRF type 2 receptors. Leptin, a product of the obesity gene secreted mainly from adipose tissue, reduces food intake and increases energy expenditure. A possible interaction between leptin and CRF/Ucns has been suggested, as leptin can regulate expression and activation of CRF and Ucns in the hypothalamus. This study aimed to explore the possible function of leptin in the hypothalamus, and its effects in regulating CRF and Ucns. The study identified mRNA expression of the leptin receptor (Ob-R) and its subtypes, CRF, and Ucn2/3 in mouse hypothalamic N39 cells. Leptin stimulated signal transducer and activators of transcription type 3 (STAT3) phosphorylation, directly increased the mRNA levels of both CRF and Ucn2/3 in hypothalamic cells, and increased Ob-Rb mRNA levels. A Janus kinase inhibitor inhibited the leptin-mediated increase in STAT3 phosphorylation, and then the increases in CRF and Ucn2/3 mRNA levels. Leptin may contribute to a stress response or anorectic effect via the regulation 2 of CRF and Ucn2/3 in the hypothalamus.

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Section: Discussionmentioning

confidence: 96%

Regulation of corticotropin-releasing factor and urocortin 2/3 mRNA by leptin in hypothalamic N39 cells

et al. 2013

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“…CRH has also been shown to mediate the anorexigenic effects of leptin (32). Besides having anorexigenic effects, CRH has been shown to increase sympathetic nerve activity in brown adipose tissue involved in the control of thermogenesis (6) and also to mediate leptin actions on the expression of uncoupling protein mRNA in this tissue (33).…”

Section: Discussionmentioning

confidence: 99%

Estradiol-induced hypophagia is associated with the differential mRNA expression of hypothalamic neuropeptides

Silva

Castro

Amaral

et al. 2010

Braz J Med Biol Res

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“…When delivered icv, urocortin (177) and urocortin II (144) produce greater intake suppression and fewer stress-related responses than does CRH. The contemporary model has assigned a role for CRH in the mediation of leptin effects (156,188,192). Thus, CRH 2a -R mRNA, CRH mRNA, and peptide level are increased after icv leptin administration (132,145,192), and treatment with a CRH-R antagonist attenuates the intake suppression that otherwise follows icv leptin administration (64,188).…”

Section: Crh/urocortinmentioning

confidence: 99%

“…The contemporary model has assigned a role for CRH in the mediation of leptin effects (156,188,192). Thus, CRH 2a -R mRNA, CRH mRNA, and peptide level are increased after icv leptin administration (132,145,192), and treatment with a CRH-R antagonist attenuates the intake suppression that otherwise follows icv leptin administration (64,188). The mediating mechanisms for these actions (with possibilities involving, for example, Ob-Rb on CRH neurons and projections to PVN from arcuate neurons containing POMC, CART, AgRP, and NPY (e.g., 85,42) are yet to be established.…”

Section: Crh/urocortinmentioning

confidence: 99%

“…It will be important to then build models of the brainstem circuitry and test hypotheses about downstream mediation. Taking a lead from the hypothalamic work, for example, one can ask whether brainstem application of MC3/4-R or CRH-R antagonists reverses effects that arise from brainstem leptin administration (64,164,188). It is also timely to evaluate changes in peptide and peptide receptor expression as functions of physiological manipulations such as deprivation and overfeeding, asking whether similar effects are obtained in brainstem and hypothalamus (see, e.g., 206).…”

Section: Crh/urocortinmentioning

confidence: 99%

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The Neuroanatomical Axis for Control of Energy Balance

Grill

Kaplan

2002

Frontiers in Neuroendocrinology

351

219

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The hypothalamic feeding-center model, articulated in the 1950s, held that the hypothalamus contains the interoceptors sensitive to blood-borne correlates of available or stored fuels as well as the integrative substrates that process metabolic and visceral afferent signals and issue commands to brainstem mechanisms for the production of ingestive behavior. A number of findings reviewed here, however, indicate that sensory and integrative functions are distributed across a central control axis that includes critical substrates in the basal forebrain as well as in the caudal brainstem. First, the interoceptors relevant to energy balance are distributed more widely than had been previously thought, with a prominent brainstem complement of leptin and insulin receptors, glucose-sensing mechanisms, and neuropeptide mediators. The physiological relevance of this multiple representation is suggested by the demonstration that similar behavioral effects can be obtained independently by stimulation of respective forebrain and brainstem subpopulations of the same receptor types (e.g., leptin, CRH, and melanocortin). The classical hypothalamic model is also challenged by the integrative achievements of the chronically maintained, supracollicular decerebrate rat. Decerebrate and neurologically intact rats show similar discriminative responses to taste stimuli and are similarly sensitive to intake-inhibitory feedback from the gut. Thus, the caudal brainstem, in neural isolation from forebrain influence, is sufficient to mediate ingestive responses to a range of visceral afferent signals. The decerebrate rat, however, does not show a hyperphagic response to food deprivation, suggesting that interactions between forebrain and brainstem are necessary for the behavioral response to systemic/ metabolic correlates of deprivation in the neurologically intact rat. At the same time, however, there is evidence suggesting that hypothalamic-neuroendocrine responses to fasting depend on pathways ascending from brainstem. Results reviewed are consistent with a distributionist (as opposed to hierarchical) model for the control of energy balance that emphasizes: (i) control mechanisms endemic to hypothalamus and brainstem that drive their unique effector systems on the basis of local interoceptive, and in the brainstem case, visceral, afferent inputs and (ii) a set of uni-and bidirectional interactions that coordinate adaptive neuroendocrine, autonomic, and behavioral responses to changes in metabolic status. KEY WORDS: feeding behavior; leptin; glucose sensing; decerebrate; neuropeptide; hypothalamic model; caudal brainstem; energy balance.

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Hypothalamic corticotropin-releasing hormone is a mediator of the anorexigenic effect of leptin.

Cited by 171 publications

References 0 publications

Regulation of corticotropin-releasing factor and urocortin 2/3 mRNA by leptin in hypothalamic N39 cells

Regulation of corticotropin-releasing factor and urocortin 2/3 mRNA by leptin in hypothalamic N39 cells

Estradiol-induced hypophagia is associated with the differential mRNA expression of hypothalamic neuropeptides

The Neuroanatomical Axis for Control of Energy Balance

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