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Journal articles on the topic 'Diabetes insípida - Gene AVP (Arginine vasopressin)'

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Published: 10 September 2021

Last updated: 29 July 2025

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1

Nagasaki, H., H. Yokoi, H. Arima, et al. "Overexpression of vasopressin in the rat transgenic for the metallothionein-vasopressin fusion gene." Journal of Endocrinology 173, no. 1 (2002): 35–44. http://dx.doi.org/10.1677/joe.0.1730035.

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Arginine vasopressin (AVP) is a major antidiuretic hormone, the overproduction of which causes diluting hyponatremia in humans and is called the syndrome of inappropriate antidiuresis (SIAD). To study physiological changes resulting from AVP overproduction and to develop an animal model of hyponatremia, the human AVP gene was expressed under the control of the metallothionein promoter in transgenic (Tg) rats. Analyses of AVP immunoreactivity (irAVP) in the tissues revealed that the transgene is expressed mainly in the central nervous system. Gel filtration showed that irAVP in the brain and pl

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Kakiya, Satoshi, Hiroshi Arima, Hisashi Yokoi, Takashi Murase, Yuko Yambe, and Yutaka Oiso. "Effects of acute hypotensive stimuli on arginine vasopressin gene transcription in the rat hypothalamus." American Journal of Physiology-Endocrinology and Metabolism 279, no. 4 (2000): E886—E892. http://dx.doi.org/10.1152/ajpendo.2000.279.4.e886.

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We investigated the baroregulation of arginine vasopressin (AVP) gene transcription in the supraoptic (SON) and paraventricular nuclei (PVN) in conscious rats by use of intronic in situ hybridization. Hemorrhage of 16 ml/kg body wt decreased mean arterial pressure (MAP) by 57% and increased both plasma AVP (control, 1.2 ± 0.3 pg/ml; 16 ml/kg body wt, 38.9 ± 3.2 pg/ml) at 10 min and AVP heteronuclear (hn)RNA levels (SON, 150%; PVN, 140% of control values) at 20 min. On the other hand, hemorrhage of 7 ml/kg body wt had no significant effect on MAP, plasma AVP, or the AVP hnRNA levels. To better

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Feldkamp, Lara L. I., Elke Kaminsky, Tina Kienitz, and Marcus Quinkler. "Central Diabetes Insipidus Caused by Arginine Vasopressin Gene Mutation: Report of a Novel Mutation and Review of Literature." Hormone and Metabolic Research 52, no. 11 (2020): 796–802. http://dx.doi.org/10.1055/a-1175-1307.

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AbstractFamilial neurohypophyseal diabetes insipidus (FNDI) is an autosomal dominant hereditary disorder characterized by severe polydipsia and polyuria that usually presents in early childhood. In this study, we describe a new arginine vasopressin (AVP) gene mutation in an ethnic German family with FNDI and provide an overview of disease-associated AVP-gene mutations that are already described in literature. Three members of a German family with neurohypophyseal diabetes insipidus were studied. Isolated DNA from peripheral blood samples was used for mutation analysis by sequencing the whole c

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Nicholson, H. D., A. J. Smith, S. D. Birkett, P. A. Denning-Kendall, and B. T. Pickering. "Two vasopressin-like peptides in the pig testis?" Journal of Endocrinology 117, no. 3 (1988): 441–46. http://dx.doi.org/10.1677/joe.0.1170441.

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ABSTRACT Vasopressin (VP)-like immunoreactivity (IR) has been located in the testes of several species of mammal. There is evidence that most of this IR in the rat does not represent authentic arginine vasopressin (AVP) and that a second AVP-like peptide may exist. We have studied testis samples from the pig, which produces lysine vasopressin (LVP) in its pituitary, and have found both LVP- and AVP-like IR. High-performance liquid chromatography (HPLC) of testis extracts showed two peaks of VP-IR. The first peak co-eluted with authentic LVP and was recognized only by antisera which cross-react

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Kim, J. K., S. N. Summer, W. M. Wood, J. L. Brown, and R. W. Schrier. "Arginine vasopressin secretion with mutants of wild-type and Brattleboro rats AVP gene." Journal of the American Society of Nephrology 8, no. 12 (1997): 1863–69. http://dx.doi.org/10.1681/asn.v8121863.

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Defects in peptide processing are associated with several disorders, including central diabetes insipidus (CDI). In the Brattleboro (BB) rat with CDI, the mRNA and protein of arginine vasopressin (AVP) are present in the hypothalamus, but no circulating AVP is detectable, thus suggesting a processing defect. The present study examined AVP secretion in cultured COS cells transfected with various constructs from wild-type and mutated Brattleboro AVP gene precursors. The precursor contains three exons encoding for vasopressin (VP), neurophysin (NP), and glycopeptide (GP). The Brattleboro rat has

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Marzocchi, Carlotta, Silvia Cantara, Alfonso Sagnella, Maria Grazia Castagna, and Marco Capezzone. "Autosomal dominant familial neurohypophyseal diabetes insipidus caused by a novel missense mutation in AVP gene in a large Italian kindred." Endocrine 74, no. 1 (2021): 188–92. http://dx.doi.org/10.1007/s12020-021-02830-x.

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Abstract Purpose Familial neurohypophysial diabetes insipidus (FNDI), commonly caused by autosomal dominant arginine vasopressin (AVP) mutations, is a rare condition in which vasopressin fails in regulating body’s level of water with final polyuria and polydipsia. Genetic testing in familial cases of FNDI should be carry out to ensure adequate treatments and avoid disease manifestations especially in infants. Methods In this study, we investigated three-generations of a large Italian family with clinical diagnosis of familial central diabetes insipidus for the presence of potential pathogenic

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Melo, Maria Edna de, Suemi Marui, Vinícius Nahime de Brito, Marcio Corrêa Mancini, Berenice B. Mendonca, and Mirta Knoepfelmacher. "Autosomal dominant familial neurohypophyseal diabetes insipidus caused by a novel mutation in arginine-vasopressin gene in a Brazilian family." Arquivos Brasileiros de Endocrinologia & Metabologia 52, no. 8 (2008): 1272–76. http://dx.doi.org/10.1590/s0004-27302008000800011.

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Autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI) is a rare autosomal dominant disorder characterized by polyuria and polydipsia due to deficiency of arginine vasopressin (AVP). More than 50 mutations causing adFNDI have been already reported in the AVP gene. The aim of the present study is to analyze the AVP gene in four generations of one Brazilian kindred with adFNDI. The proband was a 31-year old female with huge hypotonic polyuria (10 L/day) dated from childhood. Molecular analysis included amplification of all exons and exon-intron regions of the AVP gene by PCR an

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Ma, X.-M., A. Levy, and S. L. Lightman. "Rapid changes in heteronuclear RNA for corticotrophin-releasing hormone and arginine vasopressin in response to acute stress." Journal of Endocrinology 152, no. 1 (1997): 81–89. http://dx.doi.org/10.1677/joe.0.1520081.

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Abstract The rapid detection of gene activation is important for our understanding of gene regulation. We have therefore studied heteronuclear (i.e. nascent) RNA (hnRNA) by using 35S-labelled corticotrophin-releasing hormone (CRH) riboprobes and arginine vasopressin (AVP) oligonucleotide probes directed against intronic and exonic sequences of both CRH and AVP transcripts for in situ hybridization studies of transcriptional changes during acute stress. CRH and AVP intronic signals (found in newly synthesized transcripts) were confined to the nuclei of the parvocellular cells in the paraventric

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9

Vargas-Poussou, R., L. Forestier, M. D. Dautzenberg, P. Niaudet, M. Déchaux, and C. Antignac. "Mutations in the vasopressin V2 receptor and aquaporin-2 genes in 12 families with congenital nephrogenic diabetes insipidus." Journal of the American Society of Nephrology 8, no. 12 (1997): 1855–62. http://dx.doi.org/10.1681/asn.v8121855.

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Congenital nephrogenic diabetes insipidus (CNDI) is a rare inherited disorder characterized by renal tubular insensitivity to the antidiuretic effect of arginine vasopressin (AVP). In a large majority of the cases, nephrogenic diabetes insipidus is an X-linked recessive disorder caused by mutations in the AVP V2 receptor gene (AVPR2). In the remaining cases, the disease is autosomal recessive or dominant and, for these patients, mutations in the aquaporin 2 gene (AQP2) have been reported. Fourteen probands belonging to 12 families were analyzed by single-strand conformational polymorphism and

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Pak, Toni R., Wilson C. J. Chung, Laura R. Hinds та Robert J. Handa. "Arginine vasopressin regulation in pre- and postpubertal male rats by the androgen metabolite 3β-diol". American Journal of Physiology-Endocrinology and Metabolism 296, № 6 (2009): E1409—E1413. http://dx.doi.org/10.1152/ajpendo.00037.2009.

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Arginine vasopressin (AVP) is a nonapeptide expressed in several brain regions. In addition to its well-characterized role in osmoregulation, AVP regulates paternal behavior, aggression, circadian rhythms, and the stress response. In the bed nucleus of the stria terminalis (BST), AVP gene expression is tightly regulated by gonadal steroid hormones. However, the degree by which AVP is regulated by gonadal steroid hormones in the suprachiasmatic nucleus (SCN) and medial amygdala (MeA) is unclear. Previous studies have shown that AVP expression in the brain of gonadectomized rats is restored with

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11

de Fost, M., A. S. P. van Trotsenburg, H. M. van Santen, et al. "Familial neurohypophyseal diabetes insipidus due to a novel mutation in the arginine vasopressin–neurophysin II gene." European Journal of Endocrinology 165, no. 1 (2011): 161–65. http://dx.doi.org/10.1530/eje-11-0048.

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BackgroundFamilial neurohypophyseal (central) diabetes insipidus (DI) is caused by mutations in the arginine vasopressin–neurophysin II (AVP–NPII) gene. The majority of cases is inherited in an autosomal dominant way. In this study, we present the clinical features of a mother and her son with autosomal dominant neurohypophyseal DI caused by a novel mutation.CaseA thirty-four-year-old woman and her three-year-old son were evaluated because of polyuria and polydipsia since the age of 1.5 years onwards. Both patients were subjected to a water deprivation test confirming the diagnosis of central

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Kondo, Noriko, Hiroshi Arima, Ryouichi Banno, Shinobu Kuwahara, Ikuko Sato, and Yutaka Oiso. "Osmoregulation of vasopressin release and gene transcription under acute and chronic hypovolemia in rats." American Journal of Physiology-Endocrinology and Metabolism 286, no. 3 (2004): E337—E346. http://dx.doi.org/10.1152/ajpendo.00328.2003.

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Although acute decreases in plasma volume are known to enhance the osmotically induced arginine vasopressin (AVP) release, it is unclear whether there is also such interaction at the level of gene transcription. It also remains to be established how sustained changes in plasma volume affect the osmoregulation. In this study, we examined how acute and chronic decreases in blood volume affected the osmoregulation of AVP release and gene transcription in rats. Acute hypovolemia was induced by intraperitoneal injection of polyethylene glycol (PEG), and chronic hypovolemia was induced by 3 days of

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13

Makretskaya, N. A., U. S. Nanzanova, I. R. Hamaganova, E. R. Eremina, and A. N. Tiulpakov. "Clinical and laboratory characteristics of arginine vasopressin resistance, caused by a new homozygous mutation p.R113C in AQP2." Problems of Endocrinology 69, no. 2 (2023): 75–79. http://dx.doi.org/10.14341/probl13188.

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Congenital nephrogenic diabetes insipidus (CNDI, arginine vasopressin resistance) is a rare inherited disorder characterized by insensitivity of the kidney to the antidiuretic effect of vasopressin. NDI is clinically characterized by polyuria with hyposthenuria and nocturia and polydipsia. In the majority of cases, about 90%, nephrogenic diabetes insipidus is an X-linked recessive disorder caused by mutations in the AVP V2 receptor gene (AVPR2). In the remaining cases, about 10%, the disease is autosomal recessive or dominant and, for these patients, mutations in the aquaporin 2 gene (AQP2) ha

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Yambe, Yuko, Yasuko Watanabe-Tomita, Satoshi Kakiya, et al. "Analysis of the vasopressin system and water regulation in genetically polydipsic mice." American Journal of Physiology-Endocrinology and Metabolism 278, no. 2 (2000): E189—E194. http://dx.doi.org/10.1152/ajpendo.2000.278.2.e189.

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Polydipsic mice, STR/N, which show extreme polydipsia and polyuria, were discovered in 1958. In the STR/N, urine outputs are much higher than in control mice. The possibility of an abnormal regulation of the arginine vasopressin (AVP) system, or an abnormality in the renal susceptibility to AVP, should be considered. In this study we investigated the AVP system and water regulation in STR/N. We sequenced the AVP and the AVP V2-receptor genes of the STR/N by direct sequencing. No mutation was found in either of them. AVP gene expression examined by in situ hybridization and plasma sodium in 8-w

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Fuller, P. J., J. A. Clements, G. W. Tregear, I. Nikolaidis, P. L. Whitfeld, and J. W. Funder. "Vasopressin-neurophysin II gene expression in the ovary: studies in Sprague–Dawley, Long–Evans and Brattleboro rats." Journal of Endocrinology 105, no. 3 (1985): 317–21. http://dx.doi.org/10.1677/joe.0.1050317.

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ABSTRACT The neurohypophysial hormones oxytocin and arginine vasopressin (AVP) have been identified on immunological criteria in the ovary. Confirmation of extraneuronal synthesis requires the demonstration in the tissue of the specific messenger RNA (mRNA) for the preprohormone. Using a synthetic pentadecamer nucleotide probe, highly specific for the 5′ region of rat neurophysin II (NPII), we have demonstrated the presence of AVP-NPII mRNA in the ovary of Sprague–Dawley, Long–Evans and Brattleboro rats, with an apparent molecular weight identical to that seen for hypothalamus. These findings,

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Yokoi, H., H. Nagasaki, K. Tachikawa, et al. "Adaptation to sustained high plasma vasopressin in water and electrolyte homeostasis in the rat transgenic for the metallothionein-vasopressin fusion gene." Journal of Endocrinology 173, no. 1 (2002): 23–33. http://dx.doi.org/10.1677/joe.0.1730023.

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Prolonged exposure of tissues to a receptor agonist often leads to adaptive changes that limit the subsequent responsiveness of the tissue to the same agonist. Recently, we have generated rats transgenic for the metallothionein I-human arginine vasopressin (AVP) fusion gene (Tg), which produced high plasma AVP with relatively preserved renal water excretion, suggesting that there might be adaptive mechanism(s) for maintaining water and electrolyte homeostasis against chronic AVP oversecretion from the earliest stage of life. In this study, to investigate whether down-regulation of AVP V2 recep

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Batista, Sergio L., Ayrton C. Moreira, Jose Antunes-Rodrigues, Margaret de Castro, Lucila L. K. Elias, and Paula C. L. Elias. "Clinical features and molecular analysis of arginine-vasopressin neurophysin II gene in long-term follow-up patients with idiopathic central diabetes insipidus." Arquivos Brasileiros de Endocrinologia & Metabologia 54, no. 3 (2010): 269–73. http://dx.doi.org/10.1590/s0004-27302010000300004.

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INTRODUCTION: Central diabetes insipidus (DI) characterized by polyuria, polydipsia and inability to concentrate urine, has different etiologies including genetic, autoimmune, post-traumatic, among other causes. Autosomal dominant central DI presents the clinical feature of a progressive decline of arginine-vasopressin (AVP) secretion. OBJECTIVE: In this study, we characterized the clinical features and sequenced the AVP-NPII gene of seven long-term follow-up patients with idiopathic central DI in an attempt to determine whether a genetic cause would be involved. METHODS: The diagnosis of cent

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Gupta, S., T. D. Cheetham, H. J. Lambert, et al. "Thirst perception and arginine vasopressin production in a kindred with an activating mutation of the type 2 vasopressin receptor: the pathophysiology of nephrogenic syndrome of inappropriate antidiuresis." European Journal of Endocrinology 161, no. 3 (2009): 503–8. http://dx.doi.org/10.1530/eje-09-0246.

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BackgroundActivating mutations of the vasopressin receptor gene on the X chromosome cause the nephrogenic syndrome of inappropriate antidiuresis (NSIAD). We describe a male child who presented with persistent hyponatraemia and whose mother was also found to be hyponatraemic. She had learnt to avoid excess fluid consumption because of associated malaise. Both individuals had a subnormal ability to excrete a water load with mother also demonstrating a heightened sense of thirst at low serum osmolalities.ResultsMother and child were found to have the previously characterised activating mutation (

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Perrotta, Silverio, Natascia Di Iorgi, Fulvio Della Ragione, et al. "Early-onset central diabetes insipidus is associated with de novo arginine vasopressin–neurophysin II or Wolfram syndrome 1 gene mutations." European Journal of Endocrinology 172, no. 4 (2015): 461–72. http://dx.doi.org/10.1530/eje-14-0942.

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ObjectiveIdiopathic early-onset central diabetes insipidus (CDI) might be due to mutations of arginine vasopressin–neurophysin II (AVP–NPII (AVP)) or wolframin (WFS1) genes.Design and methodsSequencing of AVP and WFS1 genes was performed in nine children with CDI, aged between 9 and 68 months, and negative family history for polyuria and polydipsia.ResultsTwo patients carried a mutation in the AVP gene: a heterozygous G-to-T transition at nucleotide position 322 of exon 2 (c.322G>T) resulting in a stop codon at position 108 (p.Glu108X), and a novel deletion from nucleotide 52 to 54 (c.52_54

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Patti, Giuseppa, Saverio Scianguetta, Domenico Roberti, et al. "Familial neurohypophyseal diabetes insipidus in 13 kindreds and 2 novel mutations in the vasopressin gene." European Journal of Endocrinology 181, no. 3 (2019): 233–44. http://dx.doi.org/10.1530/eje-19-0299.

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Background Autosomal dominant neurohypophyseal diabetes insipidus (adNDI) is caused by arginine vasopressin (AVP) deficiency resulting from mutations in the AVP-NPII gene encoding the AVP preprohormone. Aim To describe the clinical and molecular features of Italian unrelated families with central diabetes insipidus. Patients and methods We analyzed AVP-NPII gene in 13 families in whom diabetes insipidus appeared to be segregating. Results Twenty-two patients were found to carry a pathogenic AVP-NPII gene mutation. Two novel c.173 G>C (p.Cys58Ser) and c.215 C>A (p.Ala72Glu) missense mutat

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Ye, Lei, Xiaoying Li, Ying Chen, et al. "Autosomal Dominant Neurohypophyseal Diabetes Insipidus with Linkage to Chromosome 20p13 but without Mutations in the AVP-NPII Gene." Journal of Clinical Endocrinology & Metabolism 90, no. 7 (2005): 4388–93. http://dx.doi.org/10.1210/jc.2004-2000.

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Abstract Context: Autosomal dominant neurohypophyseal diabetes insipidus (ADNDI) has been known as a rare disorder transmitted as an autosomal dominant trait, characterized by polyuria and polydipsia, and caused by deficient neurosecretion of arginine vasopressin precursor (AVP-NPII). We reported an ADNDI family with linkage to chromosome 20p13 but without mutations in the AVP-NPII gene. Objective: The objective of this study was to identify the corresponding locus responsible for ADNDI in a family without AVP-NP II gene mutations. Subjects and Methods: Two families with ADNDI were diagnosed b

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Hayashi, Masayuki, Hiroshi Arima, Noriyuki Ozaki, et al. "Progressive polyuria without vasopressin neuron loss in a mouse model for familial neurohypophysial diabetes insipidus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 5 (2009): R1641—R1649. http://dx.doi.org/10.1152/ajpregu.00034.2009.

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Familial neurohypophysial diabetes insipidus (FNDI), an autosomal dominant disorder, is mostly caused by mutations in the gene of neurophysin II (NPII), the carrier protein of arginine vasopressin (AVP). Previous studies suggest that loss of AVP neurons might be the cause of polyuria in FNDI. Here we analyzed knockin mice expressing mutant NPII that causes FNDI in humans. The heterozygous mice manifested progressive polyuria as do patients with FNDI. Immunohistochemical analyses revealed that inclusion bodies that were not immunostained with antibodies for mutant NPII, normal NPII, or AVP were

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Hayashi, Masayuki, Hiroshi Arima, Motomitsu Goto, et al. "Vasopressin gene transcription increases in response to decreases in plasma volume, but not to increases in plasma osmolality, in chronically dehydrated rats." American Journal of Physiology-Endocrinology and Metabolism 290, no. 2 (2006): E213—E217. http://dx.doi.org/10.1152/ajpendo.00158.2005.

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The synthesis of arginine vasopressin (AVP) in the magnocellular neurons of the supraoptic (SON) and paraventricular nuclei (PVN) is physiologically regulated by plasma osmolality and volume. To clarify how the regulation of AVP gene transcription is affected by chronic dehydration, we examined changes in the transcriptional activities of AVP gene by plasma osmolality and volume in both euhydrated and dehydrated conditions. Euhydrated rats had free access to water, whereas dehydrated rats had been deprived of water for 3 days before experiments. Rats in both conditions were subjected to acute

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Abu Libdeh, Abdulsalam, Floris Levy-Khademi, Maha Abdulhadi-Atwan, et al. "Autosomal recessive familial neurohypophyseal diabetes insipidus: onset in early infancy." European Journal of Endocrinology 162, no. 2 (2010): 221–26. http://dx.doi.org/10.1530/eje-09-0772.

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BackgroundFamilial neurohypophyseal diabetes insipidus (FNDI), usually an autosomal dominant disorder, is caused by mutations in the arginine vasopressin (AVP)–neurophysin II preprohormone leading to aberrant preprohormone processing and gradual destruction of AVP-secreting cells. Patients typically present between 1 and 6 years of age with polyuria and polydipsia.ObjectiveClinical, biochemical, and genetic studies of three new cases of autosomal recessive FNDI presenting in early infancy.PatientsThree Palestinian cousins presented with failure to thrive, vomiting, irritability, and fever. The

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Kageyama, Kazunori, Komaki Hanada, Yasumasa Iwasaki, et al. "Pituitary adenylate cyclase-activating polypeptide stimulates corticotropin-releasing factor, vasopressin and interleukin-6 gene transcription in hypothalamic 4B cells." Journal of Endocrinology 195, no. 2 (2007): 199–211. http://dx.doi.org/10.1677/joe-07-0125.

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Corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) are the two major regulatory peptides in the hypothalamic–pituitary–adrenal axis. CRF, produced in the hypothalamic paraventricular nucleus (PVN) in response to stress, is secreted into the pituitary portal circulation, resulting in the release of adrenocorticotropic hormone from the anterior pituitary. AVP is synthesized in the PVN and supraoptic nucleus by various stressors. Hypothalamic 4B cells coexpress CRF and AVP. In 4B cells transfected with either a CRF or an AVP promoter-luciferase construct, forskolin increased the

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García-Castaño, Alejandro, Leire Madariaga, Gustavo Pérez de Nanclares, et al. "Forty-One Individuals With Mutations in the AVP-NPII Gene Associated With Familial Neurohypophyseal Diabetes Insipidus." Journal of Clinical Endocrinology & Metabolism 105, no. 4 (2020): 1112–18. http://dx.doi.org/10.1210/clinem/dgaa069.

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Abstract Context Familial neurohypophyseal diabetes insipidus is a rare disease produced by a deficiency in the secretion of antidiuretic hormone and is caused by mutations in the arginine vasopressin gene. Objective Clinical, biochemical, and genetic characterization of a group of patients clinically diagnosed with familial neurohypophyseal diabetes insipidus, 1 of the largest cohorts of patients with protein neurophysin II (AVP-NPII) gene alterations studied so far. Design The AVP-NPII gene was screened for mutations by PCR followed by direct Sanger sequencing in 15 different unrelated famil

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Vaid, Sonal, Juvianee Estrada-Veras, William A. Gahl, et al. "Clinical, Laboratory, and Imaging Features Associated with Arginine Vasopressin Deficiency (Central Diabetes Insipidus) in Erdheim–Chester Disease (ECD)." Cancers 17, no. 5 (2025): 824. https://doi.org/10.3390/cancers17050824.

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Purpose: Erdheim–Chester disease (ECD) is an L Group Langerhans histiocytosis associated with pathogenic variants within the MAPK pathways, most commonly the BRAF gene. We analyzed prevalence, genetic, biochemical, and pituitary imaging features associated with arginine vasopressin deficiency (AVP-D), one of the most common endocrinopathies in ECD. Methods: A cross-sectional descriptive study of 61 subjects with ECD was conducted at a clinical research center from January 2011 to December 2018, with molecular genetics, baseline biochemical and pituitary endocrine function studies, and dedicate

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Heppner, Christina, Jörg Kotzka, Catharina Bullmann, Wilhelm Krone, and Dirk Müller-Wieland. "Identification of Mutations of the Arginine Vasopressin-Neurophysin II Gene in Two Kindreds with Familial Central Diabetes Insipidus." Journal of Clinical Endocrinology & Metabolism 83, no. 2 (1998): 693–96. http://dx.doi.org/10.1210/jcem.83.2.4571.

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Familial central diabetes insipidus is transmitted as an autosomal dominant trait with almost complete penetrance. Twenty-three different mutations of the arginine vasopressin-neurophysin II gene have been reported to date, located within the signal peptide-, the arginine vasopressin-, or the neurophysin II-coding region. In the present study two kindreds with familial central diabetes insipidus were examined. The entire coding region of the arginine vasopressin-neurophysin II gene of one affected subject of each family was amplified by PCR and subcloned into a pUC 18 plasmid, and six positive

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Færch, Mia, Jane H. Christensen, Søren Rittig, et al. "Diverse vasopressin V2 receptor functionality underlying partial congenital nephrogenic diabetes insipidus." American Journal of Physiology-Renal Physiology 297, no. 6 (2009): F1518—F1525. http://dx.doi.org/10.1152/ajprenal.00331.2009.

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X-linked congenital nephrogenic diabetes insipidus (CNDI) is characterized by a defective renal response to the antidiuretic hormone (AVP) due to variations in the arginine vasopressin receptor 2 ( AVPR2) gene. In a unique group of patients, the renal insensitivity to the effects of AVP is incomplete resulting in a partial phenotype. To investigate the molecular defects, two previously published variations in the AVPR2 gene, known to cause a partial CNDI phenotype, were expressed in transiently transfected human embryonic kidney cells. One variation (p.Arg104Cys) is located in the first extrac

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Toustrup, Lise Bols, Helene Kvistgaard, Johan Palmfeldt, et al. "The Novel Ser18del AVP Variant Causes Inherited Neurohypophyseal Diabetes Insipidus by Mechanisms Shared with Other Signal Peptide Variants." Neuroendocrinology 106, no. 2 (2017): 167–86. http://dx.doi.org/10.1159/000477246.

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Background/Aim: Variability in the severity and age at onset of autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI) may be associated with certain types of variants in the arginine vasopressin (AVP) gene. In this study, we aimed to describe a large family with an apparent predominant female occurrence of polyuria and polydipsia and to determine the underlying cause. Methods: The family members reported their family demography and symptoms. Two subjects were diagnosed by fluid deprivation and dDAVP challenge tests. Eight subjects were tested genetically. The identified vari

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Makedonskaia, Sofiia, and Arkhip Makedonskiy. "Genetic factors in polyuria: exploring diabetes insipidus and primary polydipsia." Current Research, no. 38-1 (220) (September 20, 2024): 23–29. https://doi.org/10.5281/zenodo.13800087.

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<em>Polyuria, characterized by excessive urine output, is a clinical indicator of various underlying conditions, most notably diabetes insipidus (DI) and primary polydipsia (PP). This article investigates the genetic and non-genetic factors contributing to polyuria, with a specific focus on DI and PP. DI results from the kidneys' inability to concentrate urine due to a deficiency in antidiuretic hormone (ADH) or resistance to its action, often driven by mutations in the arginine vasopressin (AVP) gene. PP, on the other hand, involves excessive water intake, frequently linked to psychiatric dis

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Priou, Anne, Charles Oliver, and Michel Grino. "In situ hybridization of arginine vasopressin (AVP) heteronuclear ribonucleic acid reveals increased AVP gene transcription in the rat hypothalamic paraventricular nucleus in response to emotional stress." Acta Endocrinologica 128, no. 5 (1993): 466–72. http://dx.doi.org/10.1530/acta.0.1280466.

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The regulation of anterior pituitary adrenocorticotropin hormone (ACTH) secretion during stress involves several hypothalamic neurohormones, including arginine vasopressin (AVP). In situ hybridization techniques have been used to study the regulation of neuropeptide messenger ribonucleic acids in the hypothalamus. Owing to the relatively slow time course of the changes in cytoplasmic messenger ribonucleic acid concentrations, rapid alterations in the level of neuropeptide gene transcription could not be detected. Because of its rapid processing, the nuclear level of the heteronuclear ribonucle

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Christensen, Jane H., Charlotte Siggaard, Thomas J. Corydon, et al. "Differential Cellular Handling of Defective Arginine Vasopressin (AVP) Prohormones in Cells Expressing Mutations of the AVP Gene Associated with Autosomal Dominant and Recessive Familial Neurohypophyseal Diabetes Insipidus." Journal of Clinical Endocrinology & Metabolism 89, no. 9 (2004): 4521–31. http://dx.doi.org/10.1210/jc.2003-031813.

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An unusual mutation in the arginine vasopressin (AVP) gene, predicting a P26L amino acid substitution of the AVP prohormone, is associated with autosomal recessive familial neurohypophyseal diabetes insipidus (FNDI). To investigate whether the cellular handling of the P26L prohormone differed from that of the Y21H prohormone associated with autosomal dominant inheritance of FNDI, the mutations were examined by heterologous expression in cell lines. Immunoprecipitation demonstrated retarded processing and secretion of the Y21H prohormone, whereas the secretion of the P26L prohormone seemed to b

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Kvistgaard, Helene, Jane H. Christensen, Jan-Ove Johansson, et al. "A Novel Synonymous Variant in the AVP Gene Associated with Autosomal Dominant Familial Neurohypophyseal Diabetes Insipidus Causes Partial RNA Missplicing." Neuroendocrinology 107, no. 2 (2018): 167–80. http://dx.doi.org/10.1159/000491579.

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Objective: Autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI) is characterized by severe polyuria and polydipsia and is caused by variations in the gene encoding the AVP prohormone. This study aimed to ascertain a correct diagnosis, to identify the underlying genetic cause of adFNDI in a Swedish family, and to test the hypothesis that the identified synonymous exonic variant in the AVP gene (c.324G>A) causes missplicing and endoplasmic reticulum (ER) retention of the prohormone. Design/Patients: Three affected family members were admitted for fluid deprivation test and

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Wahlstrom, Justin T., Michael J. Fowler, Wendell E. Nicholson, and William J. Kovacs. "A Novel Mutation in the Preprovasopressin Gene Identified in a Kindred with Autosomal Dominant Neurohypophyseal Diabetes Insipidus." Journal of Clinical Endocrinology & Metabolism 89, no. 4 (2004): 1963–68. http://dx.doi.org/10.1210/jc.2003-031542.

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Abstract Autosomal dominant neurohypophyseal diabetes insipidus (ADNDI) is a defect in free water conservation caused by mutations in the single gene that encodes both vasopressin (VP) and its binding protein, neurophysin II (NP II). Most of the human mutations in this gene have been in the portion encoding the NP molecule; the resultant abnormal gene products are believed to cause cellular toxicity as improperly folded precursor molecules accumulate in the endoplasmic reticulum. We identified a new American kindred with ADNDI and found a novel mutation in the VP molecule. A 78-yr-old man was

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Morishita, Yoshiaki, Hiroshi Arima, Maiko Hiroi, et al. "Poly(A) Tail Length of Neurohypophysial Hormones Is Shortened Under Endoplasmic Reticulum Stress." Endocrinology 152, no. 12 (2011): 4846–55. http://dx.doi.org/10.1210/en.2011-1415.

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Familial neurohypophysial diabetes insipidus (FNDI) is caused by mutations in the gene locus of arginine vasopressin (AVP), an antidiuretic hormone. Although the carriers are normal at birth, polyuria and polydipsia appear several months or years later. Previously, we made mice possessing a mutation causing FNDI and reported that the mice manifested progressive polyuria as do the patients with FNDI. Here, we report that decreases in AVP mRNA expression in the supraoptic nucleus were accompanied by shortening of the AVP mRNA poly(A) tail length in the FNDI mice, a case in which aggregates accum

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Katoh, Akiko, Hiroaki Fujihara, Toyoaki Ohbuchi, et al. "Specific expression of an oxytocin-enhanced cyan fluorescent protein fusion transgene in the rat hypothalamus and posterior pituitary." Journal of Endocrinology 204, no. 3 (2009): 275–85. http://dx.doi.org/10.1677/joe-09-0289.

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We have generated rats bearing an oxytocin (OXT)-enhanced cyan fluorescent protein (eCFP) fusion transgene designed from a murine construct previously shown to be faithfully expressed in transgenic mice. In situ hybridisation histochemistry revealed that the Oxt–eCfp fusion gene was expressed in the supraoptic nucleus (SON) and the paraventricular nucleus (PVN) in these rats. The fluorescence emanating from eCFP was observed only in the SON, the PVN, the internal layer of the median eminence and the posterior pituitary (PP). In in vitro preparations, freshly dissociated cells from the SON and

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Bichet, Daniel G. "GENETICS IN ENDOCRINOLOGY Pathophysiology, diagnosis and treatment of familial nephrogenic diabetes insipidus." European Journal of Endocrinology 183, no. 2 (2020): R29—R40. http://dx.doi.org/10.1530/eje-20-0114.

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For an endocrinologist, nephrogenic diabetes insipidus (NDI) is an end-organ disease, that is the antidiuretic hormone, arginine-vasopressin (AVP) is normally produced but not recognized by the kidney with an inability to concentrate urine despite elevated plasma concentrations of AVP. Polyuria with hyposthenuria and polydipsia are the cardinal clinical manifestations of the disease. For a geneticist, hereditary NDI is a rare disease with a prevalence of five per million males secondary to loss of function of the vasopressin V2 receptor, an X-linked gene, or loss of function of the water chann

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Mortensen, Line A., Claus Bistrup, Boye L. Jensen, and Gitte R. Hinrichs. "A mini-review of pharmacological strategies used to ameliorate polyuria associated with X-linked nephrogenic diabetes insipidus." American Journal of Physiology-Renal Physiology 319, no. 5 (2020): F746—F753. http://dx.doi.org/10.1152/ajprenal.00339.2020.

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Nephrogenic diabetes insipidus (NDI) is characterized by renal resistance to the antidiuretic hormone arginine vasopressin (AVP), which leads to polyuria, plasma hyperosmolarity, polydipsia, and impaired quality of living. Inherited forms are caused by X-linked loss-of-function mutations in the gene encoding the vasopressin 2 receptor (V2R) or autosomal recessive/dominant mutations in the gene encoding aquaporin 2 (AQP2). A common acquired form is lithium-induced NDI. AVP facilitates reabsorption of water through increased abundance and insertion of AQP2 in the apical membrane of principal cel

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Hashimoto, Hirofumi, Susumu Hyodo, Makoto Kawasaki, et al. "Centrally administered adrenomedullin 2 activates hypothalamic oxytocin-secreting neurons, causing elevated plasma oxytocin level in rats." American Journal of Physiology-Endocrinology and Metabolism 289, no. 5 (2005): E753—E761. http://dx.doi.org/10.1152/ajpendo.00042.2005.

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We examined the effects of intracerebroventricular (ICV) administration of adrenomedullin 2 (AM2) on plasma oxytocin (OXT) and arginine vasopressin (AVP) levels in conscious rats. Plasma OXT levels were markedly increased 5 min after ICV administration of AM2 (1 nmol/rat) compared with vehicle and remained elevated in samples taken at 10, 15, 30, and 60 min. By contrast, plasma AVP levels were not significantly elevated in samples taken between 5 and 180 min after ICV administration of AM2 except at the 30-min time point. Fos-like immunoreactivity (Fos-LI) was observed in various brain areas,

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Leung, Mei Tik, Jacqueline K. K. Sit, Hoi Ning Cheung, Yan Ping Iu, Winnie K. Y. Chan, and Chi Chung Shek. "Contiguous gene deletion in a Chinese family with X-linked nephrogenic diabetes insipidus: challenges in early diagnosis and implications for affected families." Journal of Pediatric Endocrinology and Metabolism 32, no. 8 (2019): 915–20. http://dx.doi.org/10.1515/jpem-2019-0028.

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Abstract Nephrogenic diabetes insipidus (NDI) is a rare disorder of the renal collecting tubules, characterized by an inability to concentrate urine due to an impaired response to arginine vasopressin (AVP), resulting in dilute urine and polyuria. Causes of NDI are heterogeneous and diagnosing congenital NDI (cNDI) in young infants is clinically challenging, as typical symptoms are often unappreciated or inconspicuous. Instead, young infants may present with non-specific signs such as vomiting, poor feeding, failure to thrive, unexplained fevers, irritability, constipation or diarrhea. We repo

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Otsubo, Hiroki, Susumu Hyodo, Hirofumi Hashimoto, et al. "Centrally administered adrenomedullin 5 activates oxytocin-secreting neurons in the hypothalamus and elevates plasma oxytocin level in rats." Journal of Endocrinology 202, no. 2 (2009): 237–47. http://dx.doi.org/10.1677/joe-09-0009.

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We examined the effects of i.c.v. administration of adrenomedullin 5 (AM5) on the brain of conscious rats. We used porcine AM5 in the present study because rat AM5 has not been detected. We observed Fos-like immunoreactivity (LI) in the hypothalamus and brainstem of conscious rats after i.c.v. administration of AM5 (2 nmol/rat). Fos-LI, measured at 90 min post-AM5 injection, was observed in various brain areas, including the supraoptic (SON) and the paraventricular nuclei (PVN). Dual immunostaining for Fos/oxytocin (OXT) and Fos/arginine vasopressin (AVP) revealed that OXT-LI neurones predomin

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Itoh, Shuji, Sakiko Yamada, Toyoki Mori, et al. "Attenuated stress-induced catecholamine release in mice lacking the vasopressin V1b receptor." American Journal of Physiology-Endocrinology and Metabolism 291, no. 1 (2006): E147—E151. http://dx.doi.org/10.1152/ajpendo.00005.2006.

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Vasopressin V1b receptor is specifically expressed in the pituitary and mediates adrenocorticotropin release, thereby regulating stress responses via its corticotropin releasing factor-like action. In the present study we examined catecholamine release in response to two types of stress in mice lacking the V1b receptor gene (V1bR−/− mice) vs. wild-type mice. There were no significant differences in the basal plasma levels of catecholamines between the two genotypes. In response to stress induced by forced swimming, norepinephrine (NE), but not epinephrine (E) or dopamine (DA), was increased in

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Atmis, Bahriye, Aysun Karabay Bayazit, Engin Melek, Atil Bisgin, and Ali Anarat. "From infancy to adulthood: challenges in congenital nephrogenic diabetes insipidus." Journal of Pediatric Endocrinology and Metabolism 33, no. 8 (2020): 1019–25. http://dx.doi.org/10.1515/jpem-2019-0529.

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AbstractObjectivesCongenital nephrogenic diabetes insipidus (NDI) is a rare hereditary disorder which is characterized by unresponsiveness to arginine vasopressin (AVP) in collecting ducts and leads to polyuria and polydipsia. The wide clinical spectrum of congenital NDI can cause difficulties in early diagnosis. We aimed to evaluate clinical prognosis of children with congenital NDI in long-term period.MethodsNineteen children with congenital NDI followed up in Pediatric Nephrology Department were enrolled to the study. This study is a single-center retrospective study, which reports clinical

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Tocci, Vera, Maria Mirabelli, Stefania Giuliano, et al. "A Partial Phenotype of adFNDI Related to the Signal Peptide c.55G>A Variant of the AVP Gene." Endocrines 2, no. 1 (2021): 37–43. http://dx.doi.org/10.3390/endocrines2010004.

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The autosomal dominant familial form of neurohypophyseal diabetes insipidus (adFNDI) is a rare inherited endocrine disorder characterized by hypotonic polyuria, severe thirst and polydipsia, which results from a deficient neurosecretion of the antidiuretic hormone, also known as arginine vasopressin (AVP). To date, adFNDI has been linked to more than 70 different heterozygous point mutations of the 2.5 kb AVP gene, encoding the composite precursor protein of AVP. A minority of disease-causing mutations, such as the common c.55G>A variant, are predicted to affect amino acid residues close to

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Ala, Y., D. Morin, B. Mouillac, et al. "Functional studies of twelve mutant V2 vasopressin receptors related to nephrogenic diabetes insipidus: molecular basis of a mild clinical phenotype." Journal of the American Society of Nephrology 9, no. 10 (1998): 1861–72. http://dx.doi.org/10.1681/asn.v9101861.

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X-linked nephrogenic diabetes insipidus (NDI) is a rare disease with defective renal and extrarenal arginine vasopressin V2 receptor responses due to mutations in the AVPR2 gene in Xq28. To study the cause of loss of function of mutant V2 receptors, we expressed 12 mutations (N55H, L59P, L83Q, V88M, 497CC-->GG, deltaR202, I209F, 700delC, 908insT, A294P, P322H, P322S) in COS-7 cells. Eleven of these, including P322H, were characterized by a complete loss of function, but the mutation P322S demonstrated a mild clinical and in vitro phenotype. This was characterized by a late diagnosis without

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Kim, Dong Hee, Kwang Kon Kim, Tae Hwan Lee, et al. "Transcription Factor TonEBP Stimulates Hyperosmolality-Dependent Arginine Vasopressin Gene Expression in the Mouse Hypothalamus." Frontiers in Endocrinology 12 (March 16, 2021). http://dx.doi.org/10.3389/fendo.2021.627343.

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The hypothalamic neuroendocrine system is strongly implicated in body energy homeostasis. In particular, the degree of production and release of arginine vasopressin (AVP) in the hypothalamus is affected by plasma osmolality, and that hypothalamic AVP is responsible for thirst and osmolality-dependent water and metabolic balance. However, the osmolality-responsive intracellular mechanism within AVP cells that regulates AVP synthesis is not clearly understood. Here, we report a role for tonicity-responsive enhancer binding protein (TonEBP), a transcription factor sensitive to cellular tonicity,

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Wyniger, Lorena, Nicole Beuret, Jonas Rutishauser, and Eleonora Seelig. "Diagnosis and Treatment of Hereditary Central Diabetes Insipidus in a Swiss Family with a Mutation in the AVP Gene." JCEM Case Reports, December 3, 2022. http://dx.doi.org/10.1210/jcemcr/luac023.

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Abstract Central hereditary diabetes insipidus is a genetic disorder characterized by polydipsia and polyuria. Most known mutations are located in the arginine-vasopressin (AVP) gene. Here, we describe a Swiss family with an autosomal dominant mutation in the AVP gene region encoding for the carrier protein neurophysin II (P55R). In addition, we discuss the algorithm for diagnosing and treating patients with hereditary central DI based on this Swiss family.

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Yamashita, Sumie, Astuko Hata, Takeshi Usui, et al. "Novel AVPR2 mutation causing partial nephrogenic diabetes insipidus in a Japanese family." Journal of Pediatric Endocrinology and Metabolism 29, no. 5 (2016). http://dx.doi.org/10.1515/jpem-2015-0323.

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AbstractX-linked recessive congenital nephrogenic diabetes insipidus (NDI) is caused by mutations of the arginine vasopressin type 2 receptor gene (AVPR2). More than 200 mutations of theWe herein report a Japanese kindred with partial NDI. The proband is an 8-year-old boy who was referred to our hospital for nocturnal enuresis. Water deprivation test and hypertonic saline test suggested partial renal antidiuretic hormone arginine vasopressin (AVP) resistance.Analysis of genomic DNA revealed a novel missense mutation (p.L161P) in the patient. The patient’s mother was heterozygous for the mutati

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Mechaly, I., F. Macari, C. Lautier, JJ Serrano, G. Cros, and F. Grigorescu. "Identification and sequence analysis of arginine vasopressin mRNA in normal and Brattleboro rat aortic tissue." European Journal of Endocrinology, July 1, 1998, 123–26. http://dx.doi.org/10.1530/eje.0.1390123.

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Arginine vasopressin (AVP), a hormone of the hypothalamic-pituitary axis, was also localized in peripheral tissues. To explore AVP precursor gene expression at the vascular level, we have investigated gene transcripts by reverse transcription-polymerase chain reaction (RT-PCR) and sequencing in aortic tissue of normal rat and in the particular genetic condition of the homozygous (di/di) Brattleboro rat strain suffering from diabetes insipidus. In these rats, a gene deletion induces an unprocessed AVP precursor in the hypothalamus with undetectable immunoreactive AVP, in contrast to the detecti

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