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Distinct Firing Activities of the Hypothalamic Arcuate Nucleus Neurons to Appetite HormonesNa, Junewoo, Park, Byong Seo, Jang, Doohyeong, Kim, Donggue, Tu, Thai Hien, Ryu, Youngjae, Ha, Chang Man, Koch, Marco, Yang, Sungchil, Kim, Jae Geun, Yang, Sunggu 18 January 2024 (has links)
The hypothalamic arcuate nucleus (Arc) is a central unit that controls the appetite through
the integration of metabolic, hormonal, and neuronal afferent inputs. Agouti-related protein (AgRP),
proopiomelanocortin (POMC), and dopaminergic neurons in the Arc differentially regulate feeding
behaviors in response to hunger, satiety, and appetite, respectively. At the time of writing, the anatomical
and electrophysiological characterization of these three neurons has not yet been intensively
explored. Here, we interrogated the overall characterization of AgRP, POMC, and dopaminergic
neurons using genetic mouse models, immunohistochemistry, and whole-cell patch recordings.
We identified the distinct geographical location and intrinsic properties of each neuron in the Arc
with the transgenic lines labelled with cell-specific reporter proteins. Moreover, AgRP, POMC, and
dopaminergic neurons had different firing activities to ghrelin and leptin treatments. Ghrelin led to
the increased firing rate of dopaminergic and AgRP neurons, and the decreased firing rate of POMC.
In sharp contrast, leptin resulted in the decreased firing rate of AgRP neurons and the increased
firing rate of POMC neurons, while it did not change the firing rate of dopaminergic neurons in Arc.
These findings demonstrate the anatomical and physiological uniqueness of three hypothalamic Arc
neurons to appetite control.
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CYSTIC FIBROSIS IN MICE ELICITS MULTIPLE CHANGES IN PITUITARY GLAND FUNCTIONRosenberg, Lewis A. January 2006 (has links)
No description available.
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A fully functional proopiomelanocortin/melanocortin-1 receptor system regulates the differentiation of human scalp hair follicle melanocytes.Kauser, Sobia, Thody, Anthony J., Schallreuter, Karin U., Gummer, C.L., Tobin, Desmond J. January 2005 (has links)
No / The proopiomelanocortin (POMC)-derived peptides, ACTH and alpha-MSH, are the principal mediators of human skin pigmentation via their action at the melanocortin-1 receptor (MC-1R). Recent data have demonstrated the existence of a functionally active beta-endorphin/mu-opiate receptor system in both epidermal and hair follicle melanocytes, whereby beta-endorphin can regulate melanogenesis, dendricity, and proliferation in these cells. However, a role for ACTH and alpha-MSH in the regulation of the human follicular pigmentary unit has not been determined. This study was designed to examine the involvement of ACTH and the alpha-MSH/MC-1R system in human follicular melanocyte biology. To address this question we employed RT-PCR and immunohisto/cytochemistry, and a functional role for these POMC peptides was assessed in follicular melanocyte cultures. Human scalp hair follicle melanocytes synthesized and processed POMC. ACTH and alpha-MSH in association with their processing enzymes and MC-1R are expressed in human follicular melanocytes at the message level in vitro and at the protein level both in situ and in vitro. The expression of the POMC/MC-1R receptor system was confined only to subpopulations of poorly and moderately differentiated melanocytes. In addition, functional studies revealed that ACTH and alpha-MSH are able to promote follicular melanocyte differentiation by up-regulating melanogenesis, dendricity, and proliferation in less differentiated melanocyte subpopulations. Thus, these findings suggest a role for these POMC peptides in regulating human hair follicle melanocyte differentiation.
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Beschreibung drei neuer endokrinologischer SyndromeKrude, Heiko 03 August 2004 (has links)
In den letzten fünf Jahren gelang es, drei neue genetische Krankheitsbilder aus dem Kreis der pädiatrischen Endokrinologie klinisch zu beschreiben und deren genetische Grundlage aufzuklären. Hierbei waren vor allem die klinischen Erscheinungsbilder ungewöhnlicher Patienten, die neben bekannten hormonellen Ausfällen durch assoziierte Defekte auffielen, für die gezielte Suche nach genetischen Defekten ausschlaggebend. In allen drei Fällen konnten die assoziierten Symptome durch den primären genetischen Defekt molekular geklärt werden. Mittlerweile ist bei weiteren Patienten ein Mutationsnachweis gelungen und der zuerst von uns beschriebene Phänotyp konnte jeweils bestätigt werden. Bei den beschriebenen defekten handelt es sich um den POMC Gendefekt (klinisches Bild: Adipositas, rote Haarfarbe und Hypocortisolismus), den LHX3 gendefekt (klinisches Bild: Hypopituitarismus und Enschränkung der Haslrotation) und den NKX2.1 Gendefekt (klinisches Bild: Angeborene Hypothyreose und Choreoathetose). / In the last few years'' three new genetic syndromes were described which affect diseases within the field of paediatric endocrinology. The clinical picture of uncommon patients, which are affected beside known endocrine defects by additional associated symptoms, led to the molecular differential diagnosis which resulted in the description of new mutations. In all three cases the additional symptoms could be explained by the identified genetic defect. Meanwhile additional patients were identified with mutations in the affected genes, which confirmed the initial description of the new clinical diseases. The identified syndromes are: POMC gene defect (clinical picture: obesity, red hair, hypocortisolism), LHX3 gene defect (clinical picture: hypopituitarism and decreased neck movement) and NKX2.1 gene defect (clinical picture: congenital hypothyroidism and choreoathetosis).
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Effects of ACTH Mutations on POMC-induced Melanoma Suppression and SteroidgenesisHung, Chia-Chun 08 September 2009 (has links)
Proopiomelanocortin (POMC) is a 241 amino acids precursor protein, which encodes various neuropeptides including corticotropin (ACTH), a-melanocyte-stimulating hormone (a-MSH), and b-endorphin (b-EP). POMC plays an important role in stress response, metabolism, energy homeostasis and anti-inflammation. Recent studies demonstrated that systemic POMC gene delivery potently suppresses the tumor growth and metastasis of B16-F10 melanoma in vitro and in vivo via inhibition of NF-£eB/COX2 pathway. However, systemic POMC expression also led to elevated urine excretion and water intake in mice. This was attributed to enhanced steroidgenesis as evidence by elevated plasma corticosteroids levels in animals and increased cortisol production in adrenal H295R cells after POMC gene delivery. Since corticosteroids are also potent anti-inflammatory agents, it remains unclear whether the ACTH-mediated cortisol synthesis also contributed to the POMC-induced tumor suppression. To address this issue, we generated a series of adenovirus vectors encoding POMC genes with mutation or deletion in ACTH domain including ACTH (K15A/R17A). Unlike the wild type POMC, gene delivery of ACTH (K15A/R17A) resulted in significantly lower cortisol production, CYP11B1 mRNA level, and glucocorticoid responsive element (GRE)-driven luciferase activities in H295R cells. ACTH (K15A/R17A) gene delivery did not affect the urination and water intake in mice. Above all, ACTH (K15A/R17A) gene delivery remained capable of inhibiting the colonies formation and invasiveness of B16-F10 melanoma cells. In summary, steroidgenesis is not essential to POMC-mediated melanoma suppression. In addition, ACTH (K15A/R17A) gene delivery may provide a better alternative for melanoma control.
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The Processing of β-Endorphin in Morphine Treated Rats Using SELDI-TOF Mass SpectrometryEdwards, Jennifer Y. 18 December 2007 (has links)
No description available.
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EFFECT OF GUT PEPTIDES ON HYPOTHALAMIC mRNA CONCENTRATION AND DRY MATTER INTAKE IN RUMINANTSRelling, Alejandro Enrique 22 July 2009 (has links)
No description available.
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The redox - biochemistry of human hair pigmentation.Schallreuter, Karin U., Salem, Mohamed M.A., Hasse, Sybille, Rokos, Hartmut 10 1900 (has links)
No / The biochemistry of hair pigmentation is a complex field involving a plethora of protein and peptide mechanisms. The in loco factory for melanin formation is the hair follicle melanocyte, but it is common knowledge that melanogenesis results from a fine tuned concerted interaction between the cells of the entire dermal papilla in the anagen hair follicle. The key enzyme is tyrosinase to initiate the active pigmentation machinery. Hence, an intricate understanding from transcription of mRNA to enzyme activity, including enzyme kinetics, substrate supply, optimal pH, cAMP signaling, is a must. Moreover, the role of reactive oxygen species on enzyme regulation and functionality needs to be taken into account. So far our knowledge on the entire hair cycle relies on the murine model of the C57BL/6 mouse. Whether this data can be translated into humans still needs to be shown. This article aims to focus on the effect of H2O2-redox homeostasis on hair follicle pigmentation via tyrosinase, its substrate supply and signal transduction as well as the role of methionine sulfoxide repair via methionine sulfoxide reductases A and B (MSRA and B).
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Pleiotropic Effects of Proopiomelanocortin and VGF Nerve Growth Factor Inducible Neuropeptides for the Long-Term Regulation of Energy BalanceHelfer, Gisela, Stevenson, T.J. 2020 May 1927 (has links)
Yes / Seasonal rhythms in energy balance are well documented across temperate and equatorial zones animals. The long-term regulated changes in seasonal physiology consists of a rheostatic system that is essential to successful time annual cycles in reproduction, hibernation, torpor, and migration. Most animals use the annual change in photoperiod as a reliable and robust environmental cue to entrain endogenous (i.e. circannual) rhythms. Research over the past few decades has predominantly examined the role of first order neuroendocrine peptides for the rheostatic changes in energy balance. These anorexigenic and orexigenic neuropeptides in the arcuate nucleus include neuropeptide y (Npy), agouti-related peptide (Agrp), cocaine and amphetamine related transcript (Cart) and pro-opiomelanocortin (Pomc). Recent studies also indicate that VGF nerve growth factor inducible (Vgf) in the arcuate nucleus is involved in the seasonal regulation of energy balance. In situ hybridization, qPCR and RNA-sequencing studies have identified that Pomc expression across fish, avian and mammalian species, is a neuroendocrine marker that reflects seasonal energetic states. Here we highlight that long-term changes in arcuate Pomc and Vgf expression is conserved across species and may provide rheostatic regulation of seasonal energy balance. / Academy of Medical Sciences, Leverhulme Trust
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Génomique fonctionnelle des cellules corticotropes hypophysaires : contrôle génétique de la gestion systémique des stressLanglais, David 08 1900 (has links)
L'axe hypothalamo-hypophyso-surrénalien (HPA) permet de maintenir l'homéostasie de l'organisme face à divers stress. Qu'ils soient de nature psychologique,
physique ou inflammatoire/infectieux, les stress provoquent la synthèse et la libération
de CRH par l'hypothalamus. Les cellules corticotropes hypophysaires perçoivent ce
signal et en réaction, produisent et sécrètent l'ACTH. Ceci induit la synthèse des
glucocorticoïdes (Gc) par le cortex surrénalien; ces stéroïdes mettent le système
métabolique en état d’alerte pour la réponse au stress et à l’agression. Les Gc ont le rôle
essentiel de contrôler les défenses de l'organisme, en plus d'exercer une rétro-inhibition
sur l'axe HPA.
L'ACTH est une petite hormone peptidique produite par le clivage d'un
précurseur: la pro-opiomélanocortine (POMC). À cause de sa position critique dans la
normalisation de l'homéostasie, le contrôle transcriptionnel du gène Pomc a fait l'objet
d'études approfondies au cours des dernières décennies. Nous savons maintenant que la
région promotrice du gène Pomc permet une expression ciblée dans les cellules POMC
hypophysaires. L'étude du locus Pomc par des technologies génomiques m'a permis de
découvrir un nouvel élément de régulation qui est conservé à travers l'évolution des
mammifères. La caractérisation de cet enhancer a démontré qu'il dirige une expression
restreinte à l'hypophyse, et plus particulièrement dans les cellules corticotropes. De
façon intéressante, l'activité de cet élément dépend d'un nouveau site de liaison recrutant
un homodimère du facteur de transcription Tpit, dont l'expression est également limitée
aux cellules POMC de l'hypophyse. La découverte de cet enhancer ajoute une toute
nouvelle dimension à la régulation de l'expression de POMC.
Les cytokines pro-inflammatoires IL6/LIF et les Gc sont connus pour leur
antagonisme sur la réaction inflammatoire et sur le promoteur Pomc via l'action des
facteurs de transcription Stat3 et GR respectivement. L'analyse génomique des sites liés
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par ces deux facteurs nous a révélé une interrelation complexe et a permis de définir un
code transcriptionnel entre ces voies de signalisation. En plus de leur action par
interaction directe avec l’ADN au niveau des séquences régulatrices, ces facteurs
interagissent directement entre eux avec des résultats transcriptionnels différents. Ainsi,
le recrutement de GR par contact protéine:protéine (tethering) sur Stat3 étant lié à
l'ADN provoque un antagonisme transcriptionnel. Inversement, le tethering de Stat3 sur
GR supporte une action synergique, tout comme leur co-recrutement à l'ADN sur des
sites contigus ou composites. Lors d'une activation soutenue, ce synergisme entre les
voies IL6/LIF et Gc induit une réponse innée de défense cellulaire. Ainsi lors d'un stress
majeur, ce mécanisme de défense est mis en branle dans toutes les cellules et tissus.
En somme, les travaux présentés dans cette thèse définissent les mécanismes
transcriptionnels engagés dans le combat de l'organisme contre les stress. Plus
particulièrement, ces mécanismes ont été décrits au niveau de la réponse globale des
corticotropes et du gène Pomc. Il est essentiel pour l'organisme d'induire adéquatement
ces mécanismes afin de faire face aux stress et d'éviter des dérèglements comme les
maladies inflammatoires et métaboliques. / The hypothalamo-pituitary-adrenal (HPA) axis regulates homeostasis in various
conditions of stress contributing to both the stress response and its termination.
Psychological, physical or inflammatory/infectious stresses all prompt the synthesis and
secretion of hypothalamic CRH. The pituitary corticotrope cells receive this signal and
in turn, secrete ACTH which triggers the synthesis of glucocorticoids (Gc) by the
adrenal cortex; these steroids induce a general state of alertness in order to fight or flight
aggressions and stresses. Glucocorticoids have the critical role to restrict the stress
response by exerting a negative feedback on the HPA axis.
ACTH is a small peptidic hormone produced after cleavage of a precursor
protein: pro-opiomelanocortin (POMC). Due to its critical role in homeostasis,
transcriptional control of the Pomc gene has been intensely studied during the last
decades. Previous investigations identified a promoter region that is sufficient for
expression of Pomc in the appropriate pituitary cells. Genome-wide studies of the Pomc
locus led me to discover a novel regulatory element that is conserved throughout
mammalian evolution. The activity of this enhancer is restricted to the pituitary, and
more precisely to the corticotrope lineage. Interestingly, its activity depends on a novel
transcription factor binding motif that binds homodimers of Tpit, a transcription factor
that is only found in pituitary POMC cells. The discovery of this enhancer adds a new
dimension in the control of pituitary Pomc expression.
The IL6/LIF pro-inflammatory cytokines and the glucocorticoids are well known
for their antagonism in control of the inflammatory response; at the Pomc promoter,
their action is mediated by the transcription factors Stat3 and GR, respectively. The
analysis of genomic sites bound by these two factors revealed a complex relationship
and led us to define a transcription regulatory code linking these signalling pathways. In
addition to their direct DNA interaction with cognate regulatory sequences, these factors
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interact with each other with different outcomes. Thus, the recruitment of GR on DNAbound
Stat3 through protein:protein contacts (tethering) results in transcriptional
antagonism. Conversely, Stat3 tethering to GR produces synergism; this is also the case
when the two factors are co-recruited to DNA on contiguous or composite binding sites.
Prolonged activation of the IL6/LIF and Gc pathways elicits a synergistic innate cell
defense response in all cells and tissues.
In summary, this doctoral work has defined transcriptional mechanisms that
mediate and control the stress response. In particular, pituitary components of the stress
response were defined at the level of the Pomc gene and as a global response of
corticotrope cells. This response is critical for appropriate organism defense during
stresses such as those produced in inflammatory and metabolic diseases.
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