Arginine vasopressin: Direct and indirect action on metabolism

Yoshimura, Mitsuhiro; Conway-Campbell, Becky; Ueta, Yoichi

doi:10.1016/j.peptides.2021.170555

Cited by 34 publications

(33 citation statements)

References 199 publications

(235 reference statements)

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“…The V1bR agonist stimulated glucagon secretion at an early time point (10 minutes) but not at later postinjection times ( Figure 7A ), probably due to the limited metabolic stability of this peptide agonist (note that the parent compound arginine vasopressin, AVP, has a plasma half-life of only 15–20 minutes). However, the V1bR agonist had little or no effect on blood glucose and plasma insulin levels ( Supplemental Figure 8 , A and B), perhaps due to enhanced V1bR activity in other peripheral tissues ( 34 ).…”

Section: Resultsmentioning

confidence: 99%

“…The V1bR is part of a family of receptors that is activated by AVP, a nonapeptide synthesized by distinct neuronal subpopulations of the hypothalamus ( 49 ). Other members of this family are the V1a and V2 receptor subtypes ( 34 ). Under physiological conditions, an increase in plasma osmolality represents the major trigger of AVP release, leading to antidiuresis via activation of V2 receptors expressed by kidney collecting duct cells ( 50 ).…”

Section: Discussionmentioning

confidence: 99%

“…The V1bR is expressed in various regions of the brain and in several peripheral tissues ( 34 ). The best known function of the V1bR is to stimulate the release of ACTH from the pituitary gland ( 53 ).…”

Section: Discussionmentioning

confidence: 99%

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Gq signaling in α cells is critical for maintaining euglycemia

Liu¹,

Dattaroy²,

Simpson³

et al. 2021

JCI Insight

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Glucagon, a hormone released from pancreatic α cells, plays a key role in maintaining euglycemia. New insights into the signaling pathways that control glucagon secretion may stimulate the development of novel therapeutic agents. In this study, we investigated the potential regulation of α cell function by G proteins of the G q family. The use of a chemogenetic strategy allowed us to selectively activate G q signaling in mouse α cells in vitro and in vivo. Acute stimulation of α cell G q signaling led to elevated plasma glucagon levels, accompanied by increased insulin release and improved glucose tolerance. Moreover, chronic activation of this pathway greatly improved glucose tolerance in obese mice. We also identified an endogenous G q -coupled receptor (vasopressin 1b receptor; V1bR) that was enriched in mouse and human α cells. Agonist-induced activation of the V1bR strongly stimulated glucagon release in a G q -dependent fashion. In vivo studies indicated that V1bR-mediated glucagon release played a key role in the counterregulatory hyperglucagonemia under hypoglycemic and glucopenic conditions. These data indicate that α cell G q signaling represents an important regulator of glucagon secretion, resulting in multiple beneficial metabolic effects. Thus, drugs that target α cell–enriched G q -coupled receptors may prove useful to restore euglycemia in various pathophysiological conditions.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Gq signaling in α cells is critical for maintaining euglycemia

Liu¹,

Dattaroy²,

Simpson³

et al. 2021

JCI Insight

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“…We found that Six3 kiss males had comparable body weight to control ( Six3 flfl ) males from 3 to 12 weeks of age ( Figure 6 I), indicating the significant change in body weight developing after 4 weeks of age in Six3 syn males is unlikely to be driven by Six3 in kisspeptin neurons. We therefore shifted our focus to AVP and SS expressing neurons of the PVN and PeVN which are known to regulate metabolic status and the growth axis [ 52 , 53 ]. Using immunohistochemistry, we found that Six3 syn males and Six3 fl/fl controls had a comparable number of SS-expressing neurons in the PVN ( Figure 6 J, M), but Six3 syn males had a greater number of SS-expressing neurons in the PeVN compared to control mice ( Figure 6 K, N).…”

Section: Resultsmentioning

confidence: 99%

Deletion of Six3 in post-proliferative neurons produces weakened SCN circadian output, improved metabolic function, and dwarfism in male mice

Meadows

Breuer

Lavalle

et al. 2022

Molecular Metabolism

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Objective The increasing prevalence of obesity makes it important to increase the understanding of the maturation and function of the neuronal integrators and regulators of metabolic function. Methods Behavioral, molecular, and physiological analyses of transgenic mice with Sine oculis 3 ( Six3 ) deleted in mature neurons using the Synapsin cre allele. Results Conditional deletion of the homeodomain transcription factor Six3 in mature neurons causes dwarfism and weakens circadian wheel-running activity rhythms but increases general activity at night, and improves metabolic function, without impacting pubertal onset or fertility in males. The reduced growth in 6-week-old Six3 fl/fl :Synapsin cre ( Six3 syn ) males correlates with increased somatostatin (SS) expression in the hypothalamus and reduced growth hormone (GH) in the pituitary. In contrast, 12-week-old Six3 syn males have increased GH release, despite an increased number of the inhibitory SS neurons in the periventricular nucleus. GH is important in glucose metabolism, muscle function, and bone health. Interestingly, Six3 syn males have improved glucose tolerance at 7, 12, and 18 weeks of age, which, in adulthood, is associated with increased % lean mass and increased metabolic rates. Further, 12-week-old Six3 syn males have reduced bone mineralization and a lower bone mineral density, indicating that reduced GH levels during early life cause a long-term reduction in bone mineralization. Conclusion Our study points to the novel role of Six3 in post-proliferative neurons to regulate metabolic function through SS neuron control of GH release.

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“…Similar to oxytocin, AVP also affects a broad spectrum of metabolic parameters [ 173 ]. For example, acute endogenous activation of PVN AVP neurons decreases food intake, and peripheral administration of AVP further decreases brown adipose tissue thermogenesis in healthy rodent models [ 174 , 175 , 176 ].…”

Section: Sensory Cvos and Hypothalamic Circuits In Metabolic Regulationmentioning

confidence: 99%

Sensory Circumventricular Organs, Neuroendocrine Control, and Metabolic Regulation

2021

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The central nervous system is critical in metabolic regulation, and accumulating evidence points to a distributed network of brain regions involved in energy homeostasis. This is accomplished, in part, by integrating peripheral and central metabolic information and subsequently modulating neuroendocrine outputs through the paraventricular and supraoptic nucleus of the hypothalamus. However, these hypothalamic nuclei are generally protected by a blood-brain-barrier limiting their ability to directly sense circulating metabolic signals—pointing to possible involvement of upstream brain nuclei. In this regard, sensory circumventricular organs (CVOs), brain sites traditionally recognized in thirst/fluid and cardiovascular regulation, are emerging as potential sites through which circulating metabolic substances influence neuroendocrine control. The sensory CVOs, including the subfornical organ, organum vasculosum of the lamina terminalis, and area postrema, are located outside the blood-brain-barrier, possess cellular machinery to sense the metabolic interior milieu, and establish complex neural networks to hypothalamic neuroendocrine nuclei. Here, evidence for a potential role of sensory CVO-hypothalamic neuroendocrine networks in energy homeostasis is presented.

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Arginine vasopressin: Direct and indirect action on metabolism

Cited by 34 publications

References 199 publications

Gq signaling in α cells is critical for maintaining euglycemia

Gq signaling in α cells is critical for maintaining euglycemia

Deletion of Six3 in post-proliferative neurons produces weakened SCN circadian output, improved metabolic function, and dwarfism in male mice

Sensory Circumventricular Organs, Neuroendocrine Control, and Metabolic Regulation

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