Stimulation of intestinal glucoreceptors in rats increases pancreatic islet blood flow through vagal mechanisms

1999 ◽  
Vol 276 (1) ◽  
pp. R233-R236 ◽  
Author(s):  
Per-Ola Carlsson ◽  
Masanori Iwase ◽  
Leif Jansson
Keyword(s):  
Blood Flow ◽  
Pancreatic Islet ◽  
Serum Insulin ◽  
Glucose Infusion ◽  
Vagus Nerves ◽  
Intraduodenal Infusion ◽  
Flow Response ◽  
Islet Blood Flow ◽  
Blood Flow Increase ◽  
Blood Glucose Concentrations

The aim of the study was to evaluate whether intestinal glucoreceptors participate in the regulation of pancreatic islet blood flow. For this purpose, anesthetized rats were infused (0.1 ml/min for 3 min) with saline, glucose, or 3- O-methylglucose directly into the duodenum. The glucose (1 mg/kg body wt) infusion rate was chosen to prevent any effects on systemic or intraportal blood glucose concentrations. Intraduodenal infusion ofd-glucose increased both serum insulin concentration and islet blood flow, whereas the osmotic control substance 3- O-methylglucose had no such effects. A bilateral abdominal vagotomy performed before the infusions totally abolished both the insulin and blood flow response to glucose infusion. The absence of an increased islet blood flow in response to glucose infusion in the denervated, transplanted pancreas was a further indication of the crucial importance of the regulation of islet blood flow by the vagus nerves. It is concluded that intestinal glucoreceptors participate in the mediation of glucose-induced islet blood flow increase.

scholarly journals Duct ligation and pancreatic islet blood flow in rats: physiological growth of islets does not affect islet blood perfusion

2005 ◽  
Vol 153 (2) ◽  
pp. 345-351 ◽  
Author(s):  
Leif Jansson ◽  
Birgitta Bodin ◽  
Örjan Källskog ◽  
Arne Andersson
Keyword(s):  
Blood Flow ◽  
Pancreatic Islet ◽  
Serum Insulin ◽  
Blood Perfusion ◽  
Islet Function ◽  
Sprague Dawley ◽  
Islet Mass ◽  
Islet Blood Flow ◽  
Sprague Dawley Rats ◽  
Duct Ligation

Objectives: The aim of this study was to evaluate islet blood-flow changes during stimulated growth of the islet organ without any associated functional impairment of islet function. Design: A duct ligation encompassing the distal two-thirds of the pancreas was performed in adult, male Sprague–Dawley rats. Methods: Pancreatic islet blood flow was measured in duct-ligated and sham-operated rats 1, 2 or 4 weeks after surgery. In some animals studied 4 weeks after surgery, islet blood flow was also measured also during hyperglycaemic conditions. Results: A marked atrophy of the exocrine pancreas was seen in all duct-ligated rats. Blood glucose and serum insulin concentrations were normal. An increased islet mass was only seen 4 weeks after surgery. No differences in islet blood perfusion were noted at any time point after duct ligation. In both sham-operated and duct-ligated rats islet blood flow was increased during hyperglycaemia; the response was, however, slightly more pronounced in the duct-ligated part of the gland. Conclusions: Normal, physiological islet growth does not cause any major changes in the islet blood perfusion or its regulation. This is in contrast to findings during increased functional demands on the islets or during deteriorated islet function, when increased islet blood flow is consistently seen.

Intraportal glucose infusion and pancreatic islet blood flow in anesthetized rats

2000 ◽  
Vol 279 (4) ◽  
pp. R1224-R1229 ◽  
Author(s):  
Per-Ola Carlsson ◽  
Masanori Iwase ◽  
Leif Jansson
Keyword(s):  
Blood Flow ◽  
Blood Glucose ◽  
Portal Vein ◽  
Insulin Release ◽  
Pancreatic Islet ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Islet Blood Flow ◽  
Blood Flow Increase ◽  
Selective Increase

The aim of the study was to evaluate whether a selective increase in portal vein blood glucose concentration can affect pancreatic islet blood flow. Anesthetized rats were infused (0.1 ml/min for 3 min) directly into the portal vein with saline, glucose, or 3- O-methylglucose. The infused dose of glucose (1 mg · kg body wt−1 · min−1) was chosen so that the systemic blood glucose concentration was unaffected. Intraportal infusion of d-glucose increased insulin release and islet blood flow; the osmotic control substance 3- O-methylglucose had no such effect. A bilateral vagotomy performed 20 min before the infusions potentiated the islet blood flow response and also induced an increase in whole pancreatic blood flow, whereas the insulin response 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 no stimulation of islet blood flow or insulin release after intraportal glucose infusion. We conclude that a selective increase in portal vein blood glucose concentration may participate in the islet blood flow increase in response to hyperglycemia. This effect is probably mediated via periarterial nerves and not through the vagus nerve. Furthermore, this blood flow increase can be dissociated from changes in insulin release.

Blood lipids affect rat islet blood flow regulation through β3-adrenoceptors

2014 ◽  
Vol 307 (8) ◽  
pp. E653-E663 ◽  
Author(s):  
Enyin Lai ◽  
Ulrika Pettersson ◽  
Alberto Delgado Verdugo ◽  
Per-Ola Carlsson ◽  
Birgitta Bodin ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pancreatic Islet ◽  
Blood Lipids ◽  
Parasympathetic Nervous System ◽  
Serum Insulin ◽  
Insulin Response ◽  
Simultaneous Increase ◽  
Acute Administration ◽  
Islet Blood Flow ◽  
Anesthetized Rats

Pancreatic islet blood perfusion varies according to the needs for insulin secretion. We examined the effects of blood lipids on pancreatic islet blood flow in anesthetized rats. Acute administration of Intralipid to anesthetized rats increased both triglycerides and free fatty acids, associated with a simultaneous increase in total pancreatic and islet blood flow. A preceding abdominal vagotomy markedly potentiated this and led acutely to a 10-fold increase in islet blood flow associated with a similar increase in serum insulin concentrations. The islet blood flow and serum insulin response could be largely prevented by pretreatment with propranolol and the selective β3-adrenergic inhibitor SR-59230A. The nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester prevented the blood flow increase but was less effective in reducing serum insulin. Increased islet blood flow after Intralipid administration was also seen in islet and whole pancreas transplanted rats, i.e., models with different degrees of chronic islet denervation, but the effect was not as pronounced. In isolated vascularly perfused single islets Intralipid dilated islet arterioles, but this was not affected by SR-59230A. Both the sympathetic and parasympathetic nervous system are important for the coordination of islet blood flow and insulin release during hyperlipidemia, with a previously unknown role for β3-adrenoceptors.

Glucose-induced changes in pancreatic islet blood flow mediated by central nervous system

1986 ◽  
Vol 251 (6) ◽  
pp. E644-E647 ◽  
Author(s):  
L. Jansson ◽  
C. Hellerstrom
Keyword(s):  
Central Nervous System ◽  
Blood Flow ◽  
Nervous System ◽  
Glucose Concentration ◽  
Serum Insulin ◽  
Serum Glucose ◽  
Insulin Concentration ◽  
Similar Amount ◽  
Serum Insulin Concentration ◽  
Islet Blood Flow

Earlier experiments with the microsphere technique suggested that a heightened serum glucose concentration consistently leads to an increase in islet blood flow (IBF). Several lines of evidence suggest that this glucose-sensitive control mechanism is located at an extrapancreatic site. The purpose of this study was to define the possible role of the central nervous system in such a mechanism. D-glucose, L-glucose, 3-O-methylglucose, or saline were therefore infused into the carotid artery, each at a dose of 1 mg X kg body wt-1 X min-1 for 3 min, and the pancreatic and islet blood flows were measured. None of these substances affected the systemic serum glucose level. The intracarotid infusion of D-glucose, however, caused a rapid increase in both the serum insulin concentration and IBF. The blood flow to the whole pancreas nevertheless remained unchanged, indicating a redistribution of flow within the gland. Carotid infusion of the other test substances or a similar amount of D-glucose given in a femoral vein did not affect these parameters. Both the increase in serum insulin concentration and the increase in IBF caused by D-glucose could be abolished by vagotomy or administration of atropine. When the systemic blood glucose concentration was increased by intraperitoneal glucose administration (2 g/kg body wt), vagotomy blocked the increase in islet blood flow but not the concomitant insulin release. These observations suggest that the glucose-induced increase in IBF is mediated by vagal cholinergic influences.

A specific β3-adrenoceptor agonist induces increased pancreatic islet blood flow and insulin secretion in rats

1996 ◽  
Vol 298 (3) ◽  
pp. 287-292 ◽  
Author(s):  
Nadia Atef ◽  
Max Lafontan ◽  
Alexandre Double ◽  
Christophe Hélary ◽  
Alain Ktorza ◽  
...  
Keyword(s):  
Blood Flow ◽  
Insulin Secretion ◽  
Pancreatic Islet ◽  
Islet Blood Flow ◽  
Adrenoceptor Agonist

Endothelin-1 and pancreatic islet vasculature: studies in vivo and on isolated, vascularly perfused pancreatic islets

2007 ◽  
Vol 292 (6) ◽  
pp. E1616-E1623 ◽  
Author(s):  
En Yin Lai ◽  
A. Erik G. Persson ◽  
Birgitta Bodin ◽  
Örjan Källskog ◽  
Arne Andersson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pancreatic Islet ◽  
Vascular Reactivity ◽  
Blood Perfusion ◽  
Receptor Subtype ◽  
Endothelin 1 ◽  
Islet Blood Flow ◽  
Endothelin B

Endothelin-1 (ET-1) is a potent endothelium-derived vasoconstrictor, which also stimulates insulin release. The aim of the present study was to evaluate whether exogenously administered ET-1 affected pancreatic islet blood flow in vivo in rats and the islet arteriolar reactivity in vitro in mice. Furthermore, we aimed to determine the ET-receptor subtype that was involved in such responses. When applying a microsphere technique for measurements of islet blood perfusion in vivo, we found that ET-1 (5 nmol/kg) consistently and markedly decreased total pancreatic and especially islet blood flow, despite having only minor effects on blood pressure. Neither endothelin A (ETA) receptor (BQ-123) nor endothelin-B (ETB) receptor (BQ-788) antagonists, alone or in combination, could prevent this reduction in blood flow. To avoid confounding interactions in vivo, we also examined the arteriolar vascular reactivity in isolated, perfused mouse islets. In the latter preparation, we demonstrated a dose-dependent constriction in response to ET-1. Administration of BQ-123 prevented this, whereas BQ-788 induced a right shift in the response. In conclusion, the pancreatic islet vasculature is highly sensitive to exogenous ET-1, which mediates its effect mainly through ETA receptors.

Increased islet blood flow in obese rats: role of the autonomic nervous system

1992 ◽  
Vol 262 (5) ◽  
pp. E736-E740 ◽  
Author(s):  
N. Atef ◽  
A. Ktorza ◽  
L. Picon ◽  
L. Penicaud
Keyword(s):  
Blood Flow ◽  
Insulin Secretion ◽  
Pancreatic Islet ◽  
Ventromedial Hypothalamus ◽  
Zucker Rats ◽  
Islet Blood Flow ◽  
Obese Rats ◽  
Increased Sensitivity ◽  
Obese Zucker Rats

Hyperinsulinemia, a main feature of both human and animal obesity, has been demonstrated to be due to both an increased sensitivity to nutrient secretagogues and an impairment of the nervous regulation of insulin secretion. Recent studies have shown that pancreatic islet blood flow increases under conditions associated with an enhanced insulin secretion. The aim of this study was to determine whether or not changes in islet blood flow are present in hyperinsulinemic obese rats. Using the nonradioactive microsphere technique, we were able to show a significantly higher islet blood flow in obese rats either of the Zucker strain or Wistar rats after lesion of the ventromedial hypothalamus than in their respective lean controls. Subdiaphragmatic vagotomy had no significant effect on basal islet blood flow of lean rats, whereas it decreased significantly that of obese Zucker rats. Conversely, clonidine, an alpha 2-adrenergic agonist, induced a higher decrease of islet blood flow in obese than in lean Zucker rats. The injection of an intravenous bolus of glucose (375 mg/kg iv) increased significantly more islet blood flow in obese than in lean Zucker rats. It is concluded that obese rats present an increased pancreatic islet blood flow, which may result, at least in part, from exaggerated parasympathetic activity and lower than normal sympathetic activity. This could participate in the hyperinsulinemia observed in these rats.

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