scholarly journals Hypothesis and Theory: Evaluating the Co-Evolution of the Melanocortin-2 Receptor and the Accessory Protein MRAP1

2021 ◽  
Vol 12 ◽  
Author(s):  
Robert M. Dores ◽  
Emilia Chapa
Keyword(s):  
Anterior Pituitary ◽  
Gene Families ◽  
Cartilaginous Fish ◽  
Accessory Protein ◽  
Pituitary Hormone ◽  
Ligand Selectivity ◽  
Anterior Pituitary Hormone ◽  
Spontaneous Interaction ◽  
Potential Contact ◽  
Cartilaginous Fishes

The melanocortin receptors (MCRs) and the MRAP accessory proteins belong to distinct gene families that are unique to the chordates. During the radiation of the chordates, the melancortin-2 receptor paralog (MC2R) and the MRAP1 paralog (melanocortin-2 receptor accessory protein 1) have co-evolved to form a heterodimer interaction that can influence the ligand selectivity and trafficking properties of MC2R. This apparently spontaneous interaction may have begun with the ancestral gnathostomes and has persisted in both the cartilaginous fishes and the bony vertebrates. The ramifications of this interaction had profound effects on the hypothalamus/anterior pituitary/adrenal-interrenal axis of bony vertebrates resulting in MC2R orthologs that are exclusively selective for the anterior pituitary hormone, ACTH, and that are dependent on MRAP1 for trafficking to the plasma membrane. The functional motifs within the MRAP1 sequence and their potential contact sites with MC2R are discussed. The ramifications of the MC2R/MRAP1 interaction for cartilaginous fishes are also discussed, but currently the effects of this interaction on the hypothalamus/pituitary/interrenal axis is less clear. The cartilaginous fish MC2R orthologs have apparently retained the ability to be activated by either ACTH or MSH-sized ligands, and the effect of MRAP1 on trafficking varies by species. In this regard, the possible origin of the dichotomy between cartilaginous fish and bony vertebrate MC2R orthologs with respect to ligand selectivity and trafficking properties is discussed in light of the evolution of functional amino acid motifs within MRAP1.

scholarly journals THE HYPOPHYSIS AND SECRETION OF INSULIN

1942 ◽  
Vol 75 (5) ◽  
pp. 547-566 ◽  
Author(s):  
B. A. Houssay ◽  
V. G. Foglia ◽  
F. S. Smyth ◽  
C. T. Rietti ◽  
A. B. Houssay
Keyword(s):  
Insulin Secretion ◽  
B Cells ◽  
Blood Sugar ◽  
Anterior Pituitary ◽  
Blood Sugar Level ◽  
Pituitary Hormone ◽  
Pituitary Extract ◽  
Histological Changes ◽  
High Blood Sugar ◽  
Anterior Pituitary Hormone

The ability of the pancreas, from various types of dogs, to correct diabetic hyperglycemia has been studied (Table XI). The pancreas from one animal was united by a vascular union with the neck blood vessels of another dog which had been pancreatectomized for 20 hours. The time necessary to reduce the blood sugar level to 120 mg. per cent was determined. 1. Pancreas from 6 hypophysectomized dogs produced a normal insulin secretion, showing that an anterior pituitary hormone is not necessary for its production or maintenance. 2. In 14 of 17 normal dogs given anterior pituitary extract for 3 or more consecutive days and presenting diabetes (fasting blood sugar 150 mg. per cent or more) the pancreas showed diminished insulin production. 3. In animals which remained diabetic after discontinuing the injections of hypophyseal extract, the pancreas islands were markedly pathologic and the insulin secretion was practically nil. 4. When hyperglycemia existed on the 2nd to 5th day but fell later, the insulin secretion of 5 dogs was normal in 2, supernormal in 1, and less than normal in 2. Histologic examination showed a restoration of beta cells. 5. In 14 dogs resistant to the diabetogenic action of anterior pituitary extract, as shown by little or no change in blood sugar, the pancreatic secretion of insulin was normal in 6 cases, supernormal in 3, and subnormal in 5 cases. Clear signs of hyperfunction of B cells were observed. In 6 resistant animals a high blood sugar (150 mg. per cent) appeared shortly before transplanting, but insulin secretion was normal in 4, supernormal in 1, and subnormal in 1 case. 6. With one injection of extract and 1 day of hyperglycemia the capacity of the pancreas to secrete insulin was not altered. 7. A high blood sugar level lasting 4 days does not alter the islets. The hypophyseal extract acts, therefore, by some other mechanism. In normal dogs, the continuous intravenous infusion of glucose for 4 days maintained the blood sugar at levels as high as those after pituitary extract. In these animals the B cells were hyperplastic and insulin secretion normal. 8. Anterior hypophyseal hyperglycemia is due at first to extrapancreatic factors which are the most important, and last only during the injections of extracts. Pancreatic factors appear afterwards and are responsible for permanent diabetes. Hypophyseal extract produces histological changes in many tissues and damages the Langerhans islands. The coexistent high blood sugar probably exhausts the B cells and exaggerates their injury. 9. In all cases there is a relation between the cytology of the islet B cells and the insulin secreting capacity.

scholarly journals Paediatric Langerhans Cell Histiocytosis Disease: Long-Term Sequelae in the Hypothalamic Endocrine System

2021 ◽  
pp. 1-9
Author(s):  
Elisa Vaiani ◽  
Guido Felizzia ◽  
Fabiana Lubieniecki ◽  
Jorge Braier ◽  
Alicia Belgorosky
Keyword(s):  
Anterior Pituitary ◽  
Langerhans Cell Histiocytosis ◽  
Endocrine System ◽  
Langerhans Cell ◽  
Hormone Deficiency ◽  
Bone Lesions ◽  
Pituitary Hormone ◽  
Multisystem Disease ◽  
Anterior Pituitary Hormone

Langerhans cell histiocytosis (LCH) is a disorder of the mononuclear phagocyte system that can affect almost any organ and system. The most common central nervous system (CNS) manifestation in LCH is the infiltration of the hypothalamic-pituitary region leading to destruction and neurodegeneration of CNS tissue. The latter causes the most frequent endocrinological manifestation, that is, central diabetes insipidus (CDI), and less often anterior pituitary hormone deficiency (APD). The reported incidence of CDI is estimated between 11.5 and 24% and is considered a risk factor for neurodegenerative disease and APD. Three risk factors for development of CDI are recognized in the majority of the studies: (1) multisystem disease, (2) the occurrence of reactivations or active disease for a prolonged period, and (3) the presence of craniofacial bone lesions. Since CDI may occur as the first manifestation of LCH, differential diagnosis of malignant diseases like germ cell tumours must be made. APD is almost always associated with CDI and can appear several years after the diagnosis of CDI. Growth hormone is the most commonly affected anterior pituitary hormone. Despite significant advances in the knowledge of LCH in recent years, little progress has been made in preventing long-term sequelae such as those affecting the hypothalamic-pituitary system.

Anterior Pituitary Hormone Abnormalities following Traumatic Brain Injury

2005 ◽  
Vol 22 (9) ◽  
pp. 937-946 ◽  
Author(s):  
Manfred Schneider ◽  
Harald Jörn Schneider ◽  
Günter Karl Stalla
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Anterior Pituitary ◽  
Pituitary Hormone ◽  
Anterior Pituitary Hormone

Vasopressin as a neuroendocrine regulator of anterior pituitary hormone secretion

1993 ◽  
Vol 129 (6) ◽  
pp. 489-496 ◽  
Author(s):  
Andreas Kjær
Keyword(s):  
Arginine Vasopressin ◽  
Mode Of Action ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
Pituitary Hormones ◽  
Pituitary Hormone ◽  
Anterior Pituitary Hormones ◽  
Anterior Pituitary Hormone

Secretion of the anterior pituitary hormones adrenocorticotropin (ACTH), β-endorphin and prolactin (PRL) is complex and involves a variety of factors. This review focuses on the involvement of arginine-vasopressin (AVP) in neuroendocrine regulation of these anterior pituitary hormones with special reference to receptor involvement, mode of action and origin of AVP. Arginine-vasopressin may act via at least two types of receptors: V1− and V2−receptors, where the pituitary V1−receptor is designated V1b. The mode of action of AVP may be mediating, i.e. anterior pituitary hormone secretion is transmitted via release of AVP, or the mode of action may be permissive, i.e. the presence of AVP at a low and constant level is required for anterior pituitary hormones to be stimulated. Under in vivo conditions, the AVP-induced release of ACTH and β-endorphin is mainly mediated via activation of hypothalamic V1− receptors, which subsequently leads to the release of corticotropin-releasing hormone. Under in vitro conditions, the AVP-stimulated release of ACTH and β-endorphin is mediated via pituitary V1b− receptors. The mode of action of AVP in the ACTH and β-endorphin response to stress and to histamine, which is involved in stress-induced secretion of anterior pituitary hormones, is mediating (utilizing V1− receptors) as well as permissive (utilizing mainly V1− but also V2−receptors). The AVP-induced release of PRL under in vivo conditions is conveyed mainly via activation of V1−receptors but V2−receptors and probably additional receptor(s) may also play a role. In stress- and histamine induced PRL secretion the role of AVP is both mediating (utilizing V1 −receptors) and permissive (utilizing both V1− and V2− receptors). Arginine-vasopressin may be a candidate for the PRL-releasing factor recently identified in the posterior pituitary gland. Arginine-vasopressin of both magno- and parvocellular origin may be involved in the regulation of anterior pituitary hormone secretion and may reach the corticotrophs and the lactotrophs via three main routes: the peripheral circulation, the long pituitary portal vessels or the short pituitary portal vessels.

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