Mechanisms by which the orexigen NPY regulates anorexigenic α-MSH and TRH

Cyr, Nicole E.; Toorie, Anika M.; Steger, Jennifer S.; Sochat, Matthew; Hyner, Samantha; Perelló, Mario; Stuart, Ronald C.; Nillni, Eduardo A.

doi:10.1152/ajpendo.00448.2012

Cited by 39 publications

(23 citation statements)

References 71 publications

(91 reference statements)

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“…The importance of these GABAergic stimuli in the control of energy balance has been substantially demonstrated (Horvath et al 1997, Wu et al 2009, Wu & Palmiter 2011, and conditional deletion of the vesicular GABA transporter in AgRP neurons blunts the inhibitory tone onto postsynaptic POMC neurons, leading to an enhanced melanocortigenic output and a lean phenotype (Tong et al 2008). Moreover, AGRP and NPY directly hyperpolarize POMC neurons and decrease the production and release of a-MSH, further inhibiting the activity of this population of neurons , Cyr et al 2013. Thus, AgRP neurons are able to negatively modulate the anorexigenic effects of POMC neurons by direct (GABAergic synapsis) and indirect (MCR antagonism) mechanisms (Fig.…”

Section: Arc Neuronal Circuits: Pomc Agrp and Ripcre Neuronsmentioning

confidence: 99%

Hypothalamic and brainstem neuronal circuits controlling homeostatic energy balance

Schneeberger¹,

Gomis²,

Claret³

2014

Journal of Endocrinology

234

199

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Alterations in adequate energy balance maintenance result in serious metabolic disturbances such as obesity. In mammals, this complex process is orchestrated by multiple and distributed neuronal circuits. Hypothalamic and brainstem neuronal circuits are critically involved in the sensing of circulating and local factors conveying information about the energy status of the organism. The integration of these signals culminates in the generation of specific and coordinated physiological responses aimed at regulating energy balance through the modulation of appetite and energy expenditure. In this article, we review current knowledge on the homeostatic regulation of energy balance, emphasizing recent advances in mouse genetics, electrophysiology, and optogenetic techniques that have greatly contributed to improving our understanding of this central process.

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Section: Arc Neuronal Circuits: Pomc Agrp and Ripcre Neuronsmentioning

confidence: 99%

Hypothalamic and brainstem neuronal circuits controlling homeostatic energy balance

Schneeberger¹,

Gomis²,

Claret³

2014

Journal of Endocrinology

234

199

View full text Add to dashboard Cite

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“…Human and animal studies suggest that adiposity-induced leptin increase and subsequent leptin resistance would affect these transmitters, causing or worsening asthma symptoms. This relates both to orexigenic neuropeptides such as neuropeptide Y (114)(115)(116)(117)(118)(119)(120) , endocannabinoids (121,122) , endogenous opioids (123)(124)(125)(126) ; and anorexigenic neuropeptides such as tachykinins and its most studied members substance P (127)(128)(129)(130)(131)(132) , α-melanocyte-stimulating hormone (133)(134)(135) , corticotropin-releasing factor (136)(137)(138)(139)(140)(141) and serotonin (142)(143)(144)(145)(146)(147)(148)(149)(150) . Altogether, it suggests that these peptides can modulate asthmatic inflammation among obese patients.…”

Section: Possible Linksmentioning

confidence: 99%

Association between obesity and asthma – epidemiology, pathophysiology and clinical profile

2016

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Obesity is a risk factor for asthma, and obese asthmatics have lower disease control and increased symptom severity. Several putative links have been proposed, including genetics, mechanical restriction of the chest and the intake of corticosteroids. The most consistent evidence, however, comes from studies of cytokines produced by the adipose tissue called adipokines. Adipokine imbalance is associated with both proinflammatory status and asthma. Although reverse causation has been proposed, it is now acknowledged that obesity precedes asthma symptoms. Nevertheless, prenatal origins of both conditions complicate the search for causality. There is a confirmed role of neuro-immune cross-talk mediating obesityinduced asthma, with leptin playing a key role in these processes. Obesity-induced asthma is now considered a distinct asthma phenotype. In fact, it is one of the most important determinants of asthma phenotypes. Two main subphenotypes have been distinguished. The first phenotype, which affects adult women, is characterised by later onset and is more likely to be non-atopic. The childhood obesity-induced asthma phenotype is characterised by primary and predominantly atopic asthma. In obesity-induced asthma, the immune responses are shifted towards T helper (Th) 1 polarisation rather than the typical atopic Th2 immunological profile. Moreover, obese asthmatics might respond differently to environmental triggers. The high cost of treatment of obesity-related asthma, and the burden it causes for the patients and their families call for urgent intervention. Phenotype-specific approaches seem to be crucial for the success of prevention and treatment.

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“…NPY has been implicated in inhibiting post-translational processing of POMC to yield a-MSH by decreasing prohormone convertase 2 (PC2) protein; this effect is associated with downregulation of early growth response protein 1 (EGR-1) and is likely occurring via NPY1R, as blocking NPY1R is able to restore PC2 activity and a-MSH release. 2 After ICV injection, NPY decreased the phosphorylation of CREB, an effect normally caused by a-MSH, and NPY also decreased the amount of a-MSH in the PVN. 2 When co-injected, a-MSH overpowers the orexigenic effect of NPY, 180 but when promoting positive energy balance NPY signals to decrease the amount of a-MSH in the hypothalamus.…”

Section: Communication Between A-msh and Npymentioning

confidence: 94%

“…2 After ICV injection, NPY decreased the phosphorylation of CREB, an effect normally caused by a-MSH, and NPY also decreased the amount of a-MSH in the PVN. 2 When co-injected, a-MSH overpowers the orexigenic effect of NPY, 180 but when promoting positive energy balance NPY signals to decrease the amount of a-MSH in the hypothalamus. Figure 2.…”

Section: Communication Between A-msh and Npymentioning

confidence: 94%

“…The two peptides are also associated with each other, with the NPY system acting to regulate the activity of a-MSH in the hypothalamus by decreasing its phosphorylation capacity and amount present in the paraventricular nucleus (PVN). 2 Both peptides also affect adipose physiology; NPY mainly affects adipogenesis, while a-MSH primarily affects lipolysis.…”

Section: Introductionmentioning

confidence: 99%

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Recent advances in the understanding of how neuropeptide Y andα-melanocyte stimulating hormone function in adipose physiology

2016

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Communication between the brain and the adipose tissue has been the focus of many studies in recent years, with the "brain-fat axis" identified as a system that orchestrates the assimilation and usage of energy to maintain body mass and adequate fat stores. It is now well-known that appetiteregulating peptides that were studied as neurotransmitters in the central nervous system can act both on the hypothalamus to regulate feeding behavior and also on the adipose tissue to modulate the storage of energy. Energy balance is thus partly controlled by factors that can alter both energy intake and storage/expenditure. Two such factors involved in these processes are neuropeptide Y (NPY) and a-melanocyte stimulating hormone (a-MSH). NPY, an orexigenic factor, is associated with promoting adipogenesis in both mammals and chickens, while a-MSH, an anorexigenic factor, stimulates lipolysis in rodents. There is also evidence of interaction between the 2 peptides. This review aims to summarize recent advances in the study of NPY and a-MSH regarding their role in adipose tissue physiology, with an emphasis on the cellular and molecular mechanisms. A greater understanding of the brain-fat axis and regulation of adiposity by bioactive peptides may provide insights on strategies to prevent or treat obesity and also enhance nutrient utilization efficiency in agriculturally-important species.

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Mechanisms by which the orexigen NPY regulates anorexigenic α-MSH and TRH

Cited by 39 publications

References 71 publications

Hypothalamic and brainstem neuronal circuits controlling homeostatic energy balance

Hypothalamic and brainstem neuronal circuits controlling homeostatic energy balance

Association between obesity and asthma – epidemiology, pathophysiology and clinical profile

Recent advances in the understanding of how neuropeptide Y andα-melanocyte stimulating hormone function in adipose physiology

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