Both V1A and V1B vasopressin receptors deficiency result in impaired glucose tolerance

Nakamura, Kazuaki; Aoyagi, Toshinori; Hiroyama, Masami; Kusakawa, Shinji; Mizutani, Reiko; Sanbe, Atsushi; Yamauchi, Junji; Kamohara, Masazumi; Momose, Kazuhiro; Tanoue, Akito

doi:10.1016/j.ejphar.2009.04.008

Cited by 32 publications

(38 citation statements)

References 23 publications

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“…Therefore, we attempted to examine the insulin sensitivity in mice lacking both V1a and V1b receptors (V1abR-KO). V1abR-KO mice had a decreased insulin sensitivity and greater adiposity in total WAT (360). Similar to the finding for V1aR-KO mice, the phosphorylation of Akt in V1abR-KO was decreased compared with that in WT mice (360), indicating that the insulin signal is suppressed in the adipocytes of V1abR-KO mice.…”

Section: Lipid Metabolismsupporting

confidence: 74%

“…V1abR-KO mice had a decreased insulin sensitivity and greater adiposity in total WAT (360). Similar to the finding for V1aR-KO mice, the phosphorylation of Akt in V1abR-KO was decreased compared with that in WT mice (360), indicating that the insulin signal is suppressed in the adipocytes of V1abR-KO mice. These results suggest that the impaired insulin signal caused by V1a receptor deficiency cannot be overcome by the effects of enhanced insulin sensitivity due to V1b receptor deficiency.…”

Section: Lipid Metabolismsupporting

confidence: 74%

“…To investigate the effect of both V1a and V1b receptor deficiency, V1a and V1b receptor doubledeficient V1abR-KO mice were generated and evaluated for glucose tolerance in vivo (360). The GTT revealed that glucose and insulin levels were higher in V1abR-KO mice, which is similar to the phenotype of V1aR-KO, but not to V1bR-KO mice, indicating that deficiency of both receptors resulted in the impaired glucose tolerance.…”

Section: Glucose Homeostasis Of V1a and V1b Receptor Double-ko Mice Amentioning

confidence: 86%

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Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems

Koshimizu

Nakamura

Egashira

et al. 2012

Physiological Reviews

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314

297

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The neurohypophysial hormone arginine vasopressin (AVP) is essential for a wide range of physiological functions, including water reabsorption, cardiovascular homeostasis, hormone secretion, and social behavior. These and other actions of AVP are mediated by at least three distinct receptor subtypes: V1a, V1b, and V2. Although the antidiuretic action of AVP and V2 receptor in renal distal tubules and collecting ducts is relatively well understood, recent years have seen an increasing understanding of the physiological roles of V1a and V1b receptors. The V1a receptor is originally found in the vascular smooth muscle and the V1b receptor in the anterior pituitary. Deletion of V1a or V1b receptor genes in mice revealed that the contributions of these receptors extend far beyond cardiovascular or hormone-secreting functions. Together with extensively developed pharmacological tools, genetically altered rodent models have advanced the understanding of a variety of AVP systems. Our report reviews the findings in this important field by covering a wide range of research, from the molecular physiology of V1a and V1b receptors to studies on whole animals, including gene knockout/knockdown studies.

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Section: Lipid Metabolismsupporting

confidence: 74%

Section: Lipid Metabolismsupporting

confidence: 74%

Section: Glucose Homeostasis Of V1a and V1b Receptor Double-ko Mice Amentioning

confidence: 86%

See 1 more Smart Citation

Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems

Koshimizu

Nakamura

Egashira

et al. 2012

Physiological Reviews

Self Cite

314

297

View full text Add to dashboard Cite

show abstract

“…Furthermore, AVP, via the same receptor (V1b), exerts stimulatory effects in maintaining basal secretion of ACTH and corticosterone, and in modulating hypothalamic-pituitary-adrenal axis (HPA) activity under stress conditions [9]. In another study, insulin sensitivity signalling was oppositely modulated by AVP effects via both V1a and V1b receptors in adipose tissue of mice [35].…”

Section: Discussionmentioning

confidence: 97%

Sex differences in the association between plasma copeptin and incident type 2 diabetes: the Prevention of Renal and Vascular Endstage Disease (PREVEND) study

et al. 2012

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Aims/hypothesis Vasopressin plays a role in osmoregulation, glucose homeostasis and inflammation. Therefore, plasma copeptin, the stable C-terminal portion of the precursor of vasopressin, has strong potential as a biomarker for the cardiometabolic syndrome and diabetes. Previous results were contradictory, which may be explained by differences between men and women in responsiveness of the vasopressin system. The aim of this study was to evaluate the usefulness of copeptin for prediction of future type 2 diabetes in men and women separately. Methods From the Prevention of Renal and Vascular Endstage Disease (PREVEND) study, 4,063 women and 3,909 men without diabetes at baseline were included. A total of 208 women and 288 men developed diabetes during a median follow-up of 7.7 years. Results In multivariable-adjusted models, we observed a stronger association of copeptin with risk of future diabetes in women (OR 1.49 [95% CI 1.24, 1.79]) than in men (OR 1.01 [95% CI 0.85, 1.19]) (p interaction <0.01). The addition of copeptin to the Data from the Epidemiological Study on the Insulin Resistance Syndrome (DESIR) clinical model improved the discriminative value (C-statistic,+0.007, p00.02) and reclassification (integrated discrimination improvement [IDI] 0 0.004, p<0.01) in women. However, we observed no improvement in men. The additive value of copeptin in women was maintained when other independent predictors, such as glucose, high sensitivity C-reactive protein (hs-CRP) and 24 h urinary albumin excretion (UAE), were included in the model. Conclusions/interpretation The association of plasma copeptin with the risk of developing diabetes was stronger in women than in men. Plasma copeptin alone, and along with existing biomarkers (glucose, hs-CRP and UAE), significantly improved the risk prediction for diabetes in women.

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“…Previous studies have demonstrated that a 60% fat diet induces insulin resistance as well as obesity and creates a reasonable model for studying pathophysiological features of the cardiovascular system in diet-induced obesity (8,25,41). To evaluate HFD-induced glucose intolerance and insulin resistance, we performed glucose tolerance tests (GTTs) and insulin tolerance tests (ITTs) after 12 wk of NCD or HFD feeding as previously demonstrated (4,36). Mice were fasted for 16 h before receiving an intraperitoneal administration of 1.5 g glucose/kg body wt in saline.…”

Section: Methodsmentioning

confidence: 99%

Cardiac mTOR rescues the detrimental effects of diet-induced obesity in the heart after ischemia-reperfusion

Aoyagi

Higa

Aoyagi

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Diet-induced obesity deteriorates the recovery of cardiac function after ischemia-reperfusion (I/R) injury. While mechanistic target of rapamycin (mTOR) is a key mediator of energy metabolism, the effects of cardiac mTOR in ischemic injury under metabolic syndrome remains undefined. Using cardiac-specific transgenic mice overexpressing mTOR (mTOR-Tg mice), we studied the effect of mTOR on cardiac function in both ex vivo and in vivo models of I/R injury in high-fat diet (HFD)-induced obese mice. mTOR-Tg and wild-type (WT) mice were fed a HFD (60% fat by calories) for 12 wk. Glucose intolerance and insulin resistance induced by the HFD were comparable between WT HFD-fed and mTOR-Tg HFD-fed mice. Functional recovery after I/R in the ex vivo Langendorff perfusion model was significantly lower in HFD-fed mice than normal chow diet-fed mice. mTOR-Tg mice demonstrated better cardiac function recovery and had less of the necrotic markers creatine kinase and lactate dehydrogenase in both feeding conditions. Additionally, mTOR overexpression suppressed expression of proinflammatory cytokines, including IL-6 and TNF-α, in both feeding conditions after I/R injury. In vivo I/R models showed that at 1 wk after I/R, HFD-fed mice exhibited worse cardiac function and larger myocardial scarring along myofibers compared with normal chow diet-fed mice. In both feeding conditions, mTOR overexpression preserved cardiac function and prevented myocardial scarring. These findings suggest that cardiac mTOR overexpression is sufficient to prevent the detrimental effects of diet-induced obesity on the heart after I/R, by reducing cardiac dysfunction and myocardial scarring.

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Both V1A and V1B vasopressin receptors deficiency result in impaired glucose tolerance

Cited by 32 publications

References 23 publications

Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems

Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems

Sex differences in the association between plasma copeptin and incident type 2 diabetes: the Prevention of Renal and Vascular Endstage Disease (PREVEND) study

Cardiac mTOR rescues the detrimental effects of diet-induced obesity in the heart after ischemia-reperfusion

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