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.

PAF increases hepatic vascular resistance and glycogenolysis in vivo

1991 ◽  
Vol 260 (3) ◽  
pp. G471-G480 ◽  
Author(s):  
K. L. Hines ◽  
A. Braillon ◽  
R. A. Fisher
Keyword(s):  
Blood Flow ◽  
Blood Glucose ◽  
Glucose Concentration ◽  
Glycogen Phosphorylase ◽  
Blood Glucose Concentration ◽  
Portal Pressure ◽  
Hepatic Glycogen ◽  
Hepatic Portal ◽  
Adrenalectomized Rats

Administration of platelet-activating factor (PAF) to portal venous circulation of anesthetized fed rats produced decreases in mean arterial pressure and increases in hepatic portal pressure and blood glucose concentration. These responses to PAF were dose dependent with ED50 values of 0.02-0.05 micrograms/kg and specific as lyso- and enantio-PAF did not reproduce effects of PAF. Specific PAF receptor antagonist SRI 63-675 (75 micrograms/kg) inhibited significantly these PAF (0.1 micrograms/kg)-induced responses in rats. Administration of prazosin (500 micrograms/kg) and propranolol (400 micrograms/kg) to rats abolished phenylephrine (50 micrograms/kg)-induced increases in mean arterial pressure, hepatic portal pressure, and blood glucose concentration but did not prevent PAF (1 microgram/kg)-induced alterations in these parameters. Glycogen phosphorylase alpha levels were increased significantly in livers of rats after administration of PAF (1 microgram/kg) or phenylephrine (50 micrograms/kg). Administration of prazosin and propranolol to rats inhibited phenylephrine- but not PAF-induced activation of hepatic glycogen phosphorylase. Hepatic adenosine 3',5'-cyclic monophosphate (cAMP) concentration was increased slightly by PAF, but these increases were eliminated by adrenergic blockade, suggesting that activation of hepatic glycogen phosphorylase by PAF is not dependent on increases in cAMP. Increases in hepatic portal pressure and blood glucose concentration in response to PAF (0.1 micrograms/kg) were not attenuated in adrenalectomized rats. Moreover, PAF (0.1 micrograms/kg) stimulated increases in hepatic portal pressure after administration of the ganglionic blocking agent chlorisondamine (2.5 mg/kg) to adrenalectomized rats. Administration of PAF (0.05 micrograms/kg) to rats instrumented with pulse Doppler flow probes produced decreases in hepatic arterial and portal vein blood flow and increases in hepatic arterial and portal vascular resistance. These observations provide direct evidence that PAF regulates hepatic hemodynamics and glycogenolysis in vivo. It is suggested that PAF plays an important role in regulating hepatic blood flow and supplying extrahepatic tissues with energy substrates by sympathetic-independent mechanism(s) after its release in acute pathophysiological situations.

scholarly journals Glucose Tolerance and Insulin Release in Malnourished Rats

1976 ◽  
Vol 50 (3) ◽  
pp. 153-163 ◽  
Author(s):  
C. Weinkove ◽  
E. A. Weinkove ◽  
B. L. Pimstone
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Blood Glucose Concentration ◽  
Protein Energy Malnutrition ◽  
Insulin Response ◽  
Intravenous Glucose ◽  
Protein Energy

1. Young Wistar rats were used as an experimental model to determine the effects of protein-energy malnutrition on glucose tolerance and insulin release. 2. Malnourished rats presented some of the features commonly found in human protein-energy malnutrition, such as failure to gain weight, hypoalbuminaemia, fatty infiltration of the liver and intolerance of oral and intravenous glucose loads. 3. The rate of disappearance of glucose from the gut lumen was greater in the malnourished rats but there was no significant difference in portal blood glucose concentration between normal and malnourished rats 5 and 10 min after an oral glucose load. 4. Insulin resistance was not thought to be the cause of the glucose intolerance in the malnourished animals since these rats had a low fasting plasma insulin concentration with a normal fasting blood glucose concentration and no impairment in their hypoglycaemic response to exogenous insulin administration. Furthermore, fasting malnourished rats were unable to correct the insulin-induced hypoglycaemia despite high concentrations of hepatic glycogen. 5. Malnourished rats had lower peak plasma insulin concentrations than normal control animals after provocation with oral and intravenous glucose, intravenous tolbutamide and intravenous glucose plus aminophyllin. This was not due to a reduction in the insulin content of the pancreas or potassium deficiency. Healthy weanling rats, like the older malnourished rats, had a diminished insulin response to intravenous glucose and intravenous tolbutamide. However, their insulin response to stimulation with intravenous glucose plus aminophyllin far exceeded that of the malnourished rats. Thus the impairment of insulin release demonstrated in the malnourished rats cannot be ascribed to a ‘functional immaturity’ of the pancreas.

ON THE ACTION OF TOLBUTAMIDE IN NORMAL MAN

1973 ◽  
Vol 72 (3) ◽  
pp. 506-518 ◽  
Author(s):  
A. Widström ◽  
E. Cerasi
Keyword(s):  
Blood Glucose ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Insulin Response ◽  
Blocking Agent ◽  
Significant Inhibition ◽  
Normal Man ◽  
Adrenergic Blocking ◽  
Plasma Insulin Response

ABSTRACT The plasma insulin response to intravenously administered tolbutamide was measured in healthy subjects under experimentally induced variations in the blood glucose concentration. Decreasing blood glucose concentration down to 51 and 25% of the basal level by the iv administration of 0.05 and 0.10 IU of insulin/kg body weight, respectively, resulted in significant inhibition of the insulin response to tolbutamide. The degree of inhibition was correlated to the extent of the hypoglycaemia. This inhibition seems to be only partially mediated by catecholamines, since blocking the α-adrenergic receptors with phentolamine could not restore the action of tolbutamide. Furthermore, whereas the prevention of the hypoglycaemia that normally follows tolbutamide administration resulted in an enhancement of the insulin response to the drug, phentolamine had no such effect. These results indicate that the decrease in blood glucose concentration as such, rather than activation of the adrenergic mechanisms, is responsible for the inhibition of tolbutamide-induced insulin release. Hence, the blood glucose level at the time of tolbutamide administration seems to determine the insulin response to the drug. The administration of the β-adrenergic blocking agent propranolol, in doses known to suppress glucose-induced insulin release in man, had no effect on the insulin response to tolbutamide. Our studies thus do not confirm the reports of other investigators that sulphonylureas may act on the islet cell as β-adrenergic agonists.

scholarly journals Pre- and postnatal low protein diet affect pancreatic islet blood flow and insulin release in adult rats.

Endocrinology ◽  
1996 ◽  
Vol 137 (9) ◽  
pp. 3797-3801 ◽  
Author(s):  
V Iglésias-Barreira ◽  
M T Ahn ◽  
B Reusens ◽  
S Dahri ◽  
J J Hoet ◽  
...  
Keyword(s):  
Blood Flow ◽  
Insulin Release ◽  
Pancreatic Islet ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Adult Rats ◽  
Low Protein ◽  
Islet Blood Flow

EFFECT OF SYNTHETIC HUMAN 1,39-CORTICOTROPHIN ON BLOOD GLUCOSE LEVEL IN MICE

1970 ◽  
Vol 65 (3) ◽  
pp. 481-489
Author(s):  
F. A. László ◽  
I. Szijj ◽  
F. Durszt ◽  
K. Kovács
Keyword(s):  
Blood Glucose ◽  
Blood Glucose Level ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
The Other ◽  
Glucose Content ◽  
High Blood Glucose ◽  
Adrenocortical Activity ◽  
Initial Blood

ABSTRACT The hypoglycaemic action of synthetic human 1,39-corticotrophin was determined in mice and its effectiveness compared with highly purified porcine corticotrophin. Synthetic human 1,39-corticotrophin (0.01 mg = 1.0 IU) and porcine corticotrophin (1.0 IU) induced a transient hypoglycaemia. After the administration of the porcine corticotrophin the decrease in the blood glucose concentration was somewhat more marked and prolonged. Adrenocortical activity was not necessary for the development of hypoglycaemia. In adrenalectomized mice, dexamethasone substitution by increasing the initial blood glucose content, made the effect more pronounced. Pretreatment with corticotrophin reduced the extent of the alloxan-induced transitory hyperglycaemia. On the other hand, it did not influence the high blood glucose values in manifest alloxan diabetic animals. It is possible that corticotrophin induces hypoglycaemia through insulin release. This is an extra-adrenal effect of corticotrophin as it is also observed in adrenalectomized mice.

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.

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