Animal models of Central Diabetes Insipidus: Human relevance of acquired beyond hereditary syndromes and the role of oxytocin

Bernal, Antonio; Mahía, Javier; Puerto, Amadeo

doi:10.1016/j.neubiorev.2016.02.023

Cited by 17 publications

(25 citation statements)

References 221 publications

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“…The greater consumption of food/sodium along with the intake of hypertonic saline solution by ME/OT animals during the night‐time period of maximum activity (30‐48 hours post‐surgery) and the consequent increase in osmolality/plasma sodium concentration may be responsible for the magnitude of their polydipsic response. These results support the close relationship observed in various studies between sodium intake and the polydipsic response of animals with mediobasal hypothalamic lesions …”

Section: Discussionsupporting

confidence: 92%

“…The findings of the present study confirm previous reports on the high food consumption of ME‐lesioned animals between 30 and 48 hours post‐surgery . This may result from the impact of the lesion on mediobasal‐periventricular hypothalamic centres that participate in food intake, including the ME.…”

Section: Discussionsupporting

confidence: 91%

“…Lesions in the ME of rats produce a well‐documented neurological model of polydipsia and polyuria. ME lesions may interrupt some of the brain systems (eg, posterior hypothalamus‐hypophyseal axis) involved in hydromineral regulation, causing major derangements in the neuroendocrine control and regulation of water and sodium metabolism …”

Section: Discussionmentioning

confidence: 99%

“…OT participates in sodium excretion either alone, in synergy with ADH, and/or indirectly through the cardiac secretion of atrial natriuretic peptide (ANP) . It has also been related to CDI symptoms induced by electrolytic lesion of the ME …”

Section: Introductionmentioning

confidence: 99%

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Effects of oxytocin administration on the hydromineral balance of median eminence‐lesioned rats

Mahía

Bernal

Puerto

2019

J Neuroendocrinology

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In the clinical setting, acute injuries in hypothalamic mediobasal regions, along with polydipsia and polyuria, have been observed in patients with cerebral salt wasting (CSW). CSW is also characterised by hypovolaemia and hyponatraemia as a result of an early increase in natriuretic peptide activity. Salt and additional amounts of fluid are the main treatment for this disorder. Similarly, experimental lesions to these brain regions, which include the median eminence (ME), produce a well‐documented neurological model of polydipsia and polyuria in rats, which is preceded by an early sodium excretion of unknown cause. In the present study, oxytocin (OT) was used to increase the renal sodium loss and prolong the hydroelectrolyte abnormalities of ME‐lesioned animals during the first few hours post‐surgery. The objective was to determine whether OT‐treated ME‐lesioned animals increase their sodium appetite and water intake to restore the volume and composition of extracellular body fluid. Electrolytic lesion of the ME increased water intake, urinary volume and sodium excretion of food‐deprived rats and also decreased urine osmolality and estimated plasma sodium concentration. OT administration at 8 hours post‐surgery reduced water intake, urine output and plasma sodium concentration and also increased urine osmolality and urine sodium excretion between 8 and 24 hours post‐lesion. From 24 to 30 hours, more water and hypertonic NaCl was consumed by OT‐treated ME‐lesioned rats than by physiological saline‐treated‐ME‐lesioned animals. Food availability from 30 to 48 hours reduced the intake of hypertonic saline solution by ME/OT animals, which increased their water and food intake during this period. OT administration therefore appears to enhance the natriuretic effect of ME lesion, producing hydroelectrolyte changes that reduce the water intake of food‐deprived animals. Conversely, the presence of hypertonic NaCl increases the fluid intake of these animals, possibly as a result of the plasma sodium depletion and hypovolaemic states previously generated. Finally, the subsequent increase in food intake by ME/OT animals reduces their need for hypertonic NaCl but not water, possibly in response to osmotic thirst. These results are discussed in relation to a possible transient activation of the ME with the consequent secretion of natriuretic peptides stored in terminal swellings, which would be augmented by OT administration. Electrolytic lesion of the ME may therefore represent a useful neurobiological model of CSW.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Effects of oxytocin administration on the hydromineral balance of median eminence‐lesioned rats

Mahía

Bernal

Puerto

2019

J Neuroendocrinology

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“…By definition, patients with CDI had acquired sufficient disruption to the hypothalamic–pituitary neurones to impair AVP release; it could therefore be reasonably anticipated that they would exhibit an equivalent and significant decrease in OT release. Although these results may potentially be explained as a result of the similarity and potential interaction between AVP and OT systems [25, 26], or as a result of dendritic release of OT in other regions of the brain [27], it should be acknowledged that HC concentrations were also higher than expected. This may relate to issues of noise in the ELISA method.…”

Section: Discussionmentioning

confidence: 99%

Hypopituitarism is associated with lower oxytocin concentrations and reduced empathic ability

2017

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PurposeCentral diabetes insipidus is characterised by arginine vasopressin deficiency. Oxytocin is structurally related to vasopressin and is synthesised in the same hypothalamic nuclei, thus we hypothesised that patients with acquired central diabetes insipidus and anterior hypopituitarism would display an oxytocin deficiency. Moreover, psychological research has demonstrated that oxytocin influences social and emotional behaviours, particularly empathic behaviour. We therefore further hypothesised that central diabetes insipidus patients would perform worse on empathy-related tasks, compared to age-matched and gender-matched clinical control (clinical control-isolated anterior hypopituitarism) and healthy control groups.MethodFifty-six participants (age 46.54 ± 16.30 yrs; central diabetes insipidus: n = 20, 8 males; clinical control: n = 15, 6 males; healthy control: n = 20, 7 males) provided two saliva samples which were analysed for oxytocin and completed two empathy tasks.ResultsHypopituitary patients (both central diabetes insipidus and clinical control groups) had significantly lower oxytocin concentrations compared to healthy control participants. Hypopituitary patients also performed significantly worse on both the reading the mind in the eyes task and the facial expression recognition task compared to healthy control participants. Regression analyses further revealed that central diabetes insipidus patients’ oxytocin concentrations significantly predicted their performance on easy items of the reading the mind in the eyes task.ConclusionsHypopituitarism may therefore be associated with reduced oxytocin concentrations and impaired empathic ability. While further studies are needed to replicate these findings, our data suggest that oxytocin replacement may offer a therapeutic approach to improve psychological well-being in patients with hypopituitarism.

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Hereditary Neurohypophyseal Diabetes Insipidus

Rutishauser

Beuret

Prescianotto-Baschong

et al. 2019

Experientia Supplementum

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Neurohypophyseal diabetes insipidus (DI) is most often caused by trauma, including operations, and infiltrating processes in the hypothalamic-pituitary region. Irradiation, ischemia, infections, or autoimmunity can also underlie the disease. Since the middle of the 19 th century, familial forms of neurohypophyseal DI have been described. Most commonly, the disease is transmitted in an autosomal-dominant fashion; very rarely, autosomal-recessive inheritance has been observed. Hereditary neurohypophyseal DI is caused by mutations in the gene encoding the antidiuretic hormone vasopressin (AVP) and its carrier protein neurophysin II (NPII). Symptoms result from the lack of hormone, or from the inability of mutant AVP to activate its renal receptor, and respond to treatment with desmopressin (DDAVP). Dominant mutations cause retention of the hormone precursor in the endoplasmic reticulum (ER) of vasopressinergic neurons in the hypothalamus, resulting in cellular dysfunction and eventually neuronal death. This so-called "neurotoxicity hypothesis" was initially established on the basis of autopsy studies in affected humans and has been supported by heterologous cell-culture expression experiments and murine knock-in models. Current data show that retained mutants fail to be eliminated by the cell's quality control system and accumulate in fibrillar aggregations within the ER. Autosomal-dominant neurohypophyseal DI may thus be viewed as a neurodegenerative disease confined to vasopressinergic neurons.

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Animal models of Central Diabetes Insipidus: Human relevance of acquired beyond hereditary syndromes and the role of oxytocin

Cited by 17 publications

References 221 publications

Effects of oxytocin administration on the hydromineral balance of median eminence‐lesioned rats

Effects of oxytocin administration on the hydromineral balance of median eminence‐lesioned rats

Hypopituitarism is associated with lower oxytocin concentrations and reduced empathic ability

Hereditary Neurohypophyseal Diabetes Insipidus

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