Intraportal glucose infusion and pancreatic islet blood flow in anesthetized rats

Citation
Po. Carlsson et al., Intraportal glucose infusion and pancreatic islet blood flow in anesthetized rats, AM J P-REG, 279(4), 2000, pp. R1224-R1229
Citations number
31
Categorie Soggetti
Physiology
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
ISSN journal
03636119 → ACNP
Volume
279
Issue
4
Year of publication
2000
Pages
R1224 - R1229
Database
ISI
SICI code
0363-6119(200010)279:4<R1224:IGIAPI>2.0.ZU;2-M
Abstract
The aim of the study was to evaluate whether a selective increase in portal vein blood glucose concentration can affect pancreatic islet blood flow. A nesthetized rats were infused (0.1 ml/min for 3 min) directly into the port al vein with saline, glucose, or 3-O-methylglucose. The infused dose of glu cose (1 mg.kg body wt(-1).min(-1)) was chosen so that the systemic blood gl ucose concentration was unaffected. Intraportal infusion of D-glucose incre ased insulin release and islet blood flow; the osmotic control substance 3- O-methylglucose had no such effect. A bilateral vagotomy performed 20 min b efore the infusions potentiated the islet blood flow response and also indu ced an increase in whole pancreatic blood flow, whereas the insulin respons e was abolished. Administration of atropine to vagotomized animals did not change the blood flow responses to intraportal glucose infusions. When the vagotomy was combined with a denervation of the hepatic artery, there was n o stimulation of islet blood flow or insulin release after intraportal gluc ose infusion. We conclude that a selective increase in portal vein blood gl ucose concentration may participate in the islet blood flow increase in res ponse to hyperglycemia. This effect is probably mediated via periarterial n erves and not through the vagus nerve. Furthermore, this blood flow increas e can be dissociated from changes in insulin release.