Possible modulatory effect of endogenous islet catecholamines on insulin secretion

Borelli, María Inés; Gagliardino, Juan José

doi:10.1016/s0168-8227(00)81956-7

Cited by 2 publications

(2 citation statements)

References 2 publications

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“…In control islets, consistent with prior reports (Rodriguez-Diaz et al, 2011a;Teitelman et al, 1988), a small subset of β cells expressed TH. TH expression in β cells has several proposed, yet unconfirmed, roles: (1) a marker of endocrine precursor cells during early pancreas development Teitelman and Lee, 1987;Teitelman et al, 1993); (2) a marker of post-proliferative β cells on the path to senescence ; or (3) an indicator of synthesis of endogenous islet catecholamines (Borelli and Gagliardino, 2001;Borelli et al, 2003). The number of TH + β cells in VEGF-deficient islets begins to increase postnatally, when islet innervation should be reaching its mature state.…”

Section: Intra-islet Vessels Are Essential For Islet Nerve Pathfindingmentioning

confidence: 99%

Vascular endothelial growth factor coordinates islet innervation via vascular scaffolding

et al. 2014

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Neurovascular alignment is a common anatomical feature of organs, but the mechanisms leading to this arrangement are incompletely understood. Here, we show that vascular endothelial growth factor (VEGF) signaling profoundly affects both vascularization and innervation of the pancreatic islet. In mature islets, nerves are closely associated with capillaries, but the islet vascularization process during embryonic organogenesis significantly precedes islet innervation. Although a simple neuronal meshwork interconnects the developing islet clusters as they begin to form at E14.5, the substantial ingrowth of nerve fibers into islets occurs postnatally, when islet vascularization is already complete. Using genetic mouse models, we demonstrate that VEGF regulates islet innervation indirectly through its effects on intra-islet endothelial cells. Our data indicate that formation of a VEGF-directed, intra-islet vascular plexus is required for development of islet innervation, and that VEGFinduced islet hypervascularization leads to increased nerve fiber ingrowth. Transcriptome analysis of hypervascularized islets revealed an increased expression of extracellular matrix components and axon guidance molecules, with these transcripts being enriched in the isletderived endothelial cell population. We propose a mechanism for coordinated neurovascular development within pancreatic islets, in which endocrine cell-derived VEGF directs the patterning of intra-islet capillaries during embryogenesis, forming a scaffold for the postnatal ingrowth of essential autonomic nerve fibers.

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Section: Intra-islet Vessels Are Essential For Islet Nerve Pathfindingmentioning

confidence: 99%

Vascular endothelial growth factor coordinates islet innervation via vascular scaffolding

et al. 2014

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“…Moreover, dopaminergic agonists also activate the sympathoadrenal system through a primary action on dopamine receptors in the central nervous system [24]. Finally, catecholamines present in islet innervation [26][27][28] might also directly modulate insulin release [21]. Regardless of their origin, catecholamines inhibit insulin secretion through specific α2-adrenergic receptors present on β-cells [29].…”

Section: Discussionmentioning

confidence: 99%

Bromocriptine-Induced Hyperglycemia in Nonobese Diabetic Mice: Kinetics and Mechanisms of Action

Durant¹,

Coulaud²,

Homo‐Delarche³

2007

Rev Diabet Stud

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■ AbstractThe effects of bromocriptine (10 mg/kg), known to inhibit prolactin secretion and lower autoimmune processes, were studied on glucose homeostasis in non-fasted non-obese diabetic mice, a spontaneous model of type 1 diabetes. Hyperglycemia was observed 120 and 240 min after i.p. but not s.c. injection. Bromocriptine administration i.p. led to rapid and marked hyperglycemia characterized by sexual dimorphism with males having higher glycemia than females. Bromocriptine induced a rapid but transient decrease in insulinemia in males only and biphasic increases in glucagon levels and a sustained stimulatory effect on circulating corticosterone in both sexes. Bromocriptine-induced hyperglycemia involved D2-dopaminergic receptors, as demonstrated by the inhibitory effect of the D2-dopamine antagonist, metoclopramide (10 mg/kg). Simultaneous injection of bromocriptine and metoclopramide also blocked the rise in blood corticosterone. In conclusion, by inducing hyperglycemia, i.p. bromocriptine administration to prediabetic autoimmune mice may counteract its beneficial antiimmunostimulatory effects.

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Possible modulatory effect of endogenous islet catecholamines on insulin secretion

Abstract: Background: The possible participation of endogenous islet catecholamines (CAs) in the control of insulin secretion was tested.

Cited by 2 publications

References 2 publications

Vascular endothelial growth factor coordinates islet innervation via vascular scaffolding

Vascular endothelial growth factor coordinates islet innervation via vascular scaffolding

Bromocriptine-Induced Hyperglycemia in Nonobese Diabetic Mice: Kinetics and Mechanisms of Action

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