scholarly journals Influence of Insulin in the Ventromedial Hypothalamus on Pancreatic Glucagon Secretion In Vivo

Diabetes ◽  
2010 ◽  
Vol 59 (6) ◽  
pp. 1521-1527 ◽  
Author(s):  
S. A. Paranjape ◽  
O. Chan ◽  
W. Zhu ◽  
A. M. Horblitt ◽  
E. C. McNay ◽  
...  
Keyword(s):  
Glucagon Secretion ◽  
Ventromedial Hypothalamus ◽  
Pancreatic Glucagon

Somatostatin, insulin, and glucagon secretion from isolated perfused pancreas of obese rats

1981 ◽  
Vol 241 (2) ◽  
pp. E146-E150
Author(s):  
S. Seino ◽  
Y. Seino ◽  
J. Takemura ◽  
K. Tsuda ◽  
H. Kuzuya ◽  
...  
Keyword(s):  
Hormone Secretion ◽  
Glucagon Secretion ◽  
Ventromedial Hypothalamus ◽  
Perfused Pancreas ◽  
Isolated Perfused Pancreas ◽  
Insulin And Glucagon Secretion ◽  
Perfusion Experiment ◽  
Pancreatic Hormone ◽  
And Control

A comparison of the somatostatin with the insulin and glucagon secretions in hypothalamic obesity and genetic obesity was made using the isolated perfused pancreas of rats. In our perfusion experiment, the somatostatin response to 19 mM arginine in the presence of 4.4 mM glucose was significantly greater in both ventromedial hypothalamus (VMH)-lesioned and Zucker fa/fa rats than in their controls, as was the perfusate insulin. The perfusate arginine-stimulated glucagon secretion appeared no different in obese and control rats. Because hyperinsulinemia in vivo and hyperresponses to arginine of perfusate insulin and somatostatin were observed in both VMH-lesioned and Zucker fa/fa rats, whereas the perfusate glucagon secretion in the presence of 4.4 mM glucose was unchanged by obesity, the secretory behavior of some pancreatic hormones seems similar in VMH-lesioned and Zucker fa/fa rats in certain conditions. These results suggest that some abnormalities of pancreatic hormone secretion may be caused by a mechanism common to obesity, whether caused experimentally or genetically.

Role of pancreatic somatostatin in determining glucagon response to arginine and morphine

1987 ◽  
Vol 252 (6) ◽  
pp. E751-E755
Author(s):  
L. J. Klaff ◽  
G. J. Taborsky
Keyword(s):  
Insulin Secretion ◽  
Beta Cells ◽  
Glucagon Secretion ◽  
Direct Stimulation ◽  
Pancreatic Glucagon ◽  
Insulin And Glucagon Secretion ◽  
Important Regulator ◽  
Dog Pancreas ◽  
High Doses

It has been proposed that pancreatic somatostatin (SS) tonically inhibits pancreatic glucagon secretion. In keeping with this hypothesis, we have previously shown that infusion of a nonimmunoreactive analogue of SS, [D-Ala5,D-Trp8]somatostatin (SSa), which in low doses inhibits SS secretion without inhibiting glucagon or insulin secretion, is associated with a large increase in glucagon and small increase in insulin secretion. Although direct stimulation of the alpha- and beta-cells by the analogue could not be excluded, high doses of the analogue appeared to inhibit insulin and glucagon secretion. These data therefore suggested that the effect of the analogue on insulin and glucagon secretion was indirect and due to reduction of tonic inhibition on the alpha- and beta-cells by SS. If pancreatic SS is an important regulator of glucagon secretion, then alterations in pancreatic SS should influence the glucagon response to secretagogues. Therefore, in the present study, we have examined the glucagon response to two different stimuli, arginine and morphine, either before or during suppression of pancreatic SS secretion. Intravenous injection of arginine produced a rapid increase of pancreatic glucagon output from the in vivo dog pancreas. When basal pancreatic SS output was suppressed by infusion of SSa, arginine injection produced a twofold larger glucagon response. Infusion of morphine directly into the pancreatic artery of the dog decreased pancreatic SS output and increased pancreatic glucagon output. When SS was suppressed by SSa infusion, morphine did not further suppress pancreatic SS secretion and the glucagon response to morphine was abolished.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Failure of chronic hyperinsulinemia to suppress pancreatic glucagon in vivo in the rat

1991 ◽  
Vol 69 (3) ◽  
pp. 437-443 ◽  
Author(s):  
Patricia L. Brubaker ◽  
Tsutomu Kazumi ◽  
Tsutomu Hirano ◽  
Mladen Vranic ◽  
George Steiner
Keyword(s):  
Drinking Water ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Glucagon Secretion ◽  
Glucagon Release ◽  
Plasma Glucagon ◽  
Pancreatic Glucagon ◽  
Glucose Levels ◽  
Endogenous Release

To determine the effects of chronic hyperinsulinemia on glucagon release, rats were made hyperinsulinemic for 14 days by supplementation of drinking water with sucrose (10%; sucrose-fed) to increase endogenous release or by implantation of osmotic minipumps (subcutaneous, s.c; or intraperitoneal, i.p.) to deliver exogenous insulin (6 U/day). Both s.c. and i.p. rats also had sucrose in the drinking water to prevent hypoglycemia. Plasma insulin levels were significantly elevated in sucrose-fed, s.c, and i.p. rats. However, glucose levels were significantly elevated in sucrose-fed rats only. Surprisingly, plasma glucagon concentrations were elevated in i.p. and s.c. rats and were not suppressed in sucrose-fed rats. Inverse relationships were found between the plasma levels of insulin and glucose (n = 65; r = −0.42, p < 0.0001) and between glucose and glucagon (n = 73; r = −0.46, p < 0.0001). However, unexpectedly, a positive correlation between insulin and glucagon (n = 65; r = 0.47, p < 0.0001) was established. As suppression of plasma glucagon levels below basal was not observed in any of the hyperinsulinemic or hyperglycemic rats, we wished to establish further whether pancreatic glucagon release could be suppressed below basal levels in the rat by another means. Thus, high doses of somatostatin (50–100 μg∙kg−1∙min−1) were infused for 45 min into normal rats without or with a concomitant hyperinsulinemic, hyperglycemic glucose clamp. Somatostatin fully suppressed insulin, but although plasma glucagon levels were decreasd by somatostatin infusion relative to saline-infused animals, there was still no suppression below basal levels. Thus, the rat A cells are less sensitive to somatostatin than are those of other species. The results of this study demonstrate that chronic endogenous or exogenous hyperinsulinemia does not inhibit glucagon secretion, even in the presence of hyperglycemia. Factors other than insulin may therefore play an important role in the regulation of the pancreatic A cell in the chronic hyperinsulinemic rat.Key words: glycemia, insulin, glucagon, somatostatin, very low density lipoprotein.

Effects of PACAP1–27 on the canine endocrine pancreas in vivo: interaction with cholinergic mechanism

2003 ◽  
Vol 81 (7) ◽  
pp. 720-729 ◽  
Author(s):  
Nobuharu Yamaguchi ◽  
Tamar Rita Minassian ◽  
Sanae Yamaguchi
Keyword(s):  
Endocrine Pancreas ◽  
Venous Blood ◽  
Insulin Response ◽  
Glucagon Secretion ◽  
Venous Blood Flow ◽  
Dependent Manner ◽  
Cholinergic Mechanism ◽  
Insulin And Glucagon Secretion ◽  
Anesthetized Dogs

The aim of the present study was to characterize the effects of pituitary adenylate cyclase activating polypeptide (PACAP) on the endocrine pancreas in anesthetized dogs. PACAP1–27 and a PACAP receptor (PAC1) blocker, PACAP6–27, were locally administered to the pancreas. PACAP1–27 (0.005–5 μg) increased basal insulin and glucagon secretion in a dose-dependent manner. PACAP6–27 (200 μg) blocked the glucagon response to PACAP1–27 (0.5 μg) by about 80%, while the insulin response remained unchanged. With a higher dose of PACAP6–27 (500 μg), both responses to PACAP1–27 were inhibited by more than 80%. In the presence of atropine with an equivalent dose (128.2 μg) of PACAP6–27 (500 μg) on a molar basis, the insulin response to PACAP1–27 was diminished by about 20%, while the glucagon response was enhanced by about 80%. The PACAP1–27-induced increase in pancreatic venous blood flow was blocked by PACAP6–27 but not by atropine. The study suggests that the endocrine secretagogue effect of PACAP1–27 is primarily mediated by the PAC1 receptor, and that PACAP1–27 may interact with muscarinic receptor function in PACAP-induced insulin and glucagon secretion in the canine pancreas in vivo.Key words: atropine, PACAP, PAC1, muscarinic, interaction.

PANCREATIC GLUCAGON SECRETION

1970 ◽  
pp. 527-531
Author(s):  
R.H. UNGER ◽  
E. AGUILAR-PARADA ◽  
A. EISENTRAUT
Keyword(s):  
Glucagon Secretion ◽  
Pancreatic Glucagon

Hepatic handling of pancreatic glucagon and glucose during meals in rats

1984 ◽  
Vol 247 (5) ◽  
pp. R827-R832 ◽  
Author(s):  
W. Langhans ◽  
K. Pantel ◽  
W. Muller-Schell ◽  
E. Eggenberger ◽  
E. Scharrer
Keyword(s):  
Blood Glucose ◽  
Portal Vein ◽  
Hepatic Vein ◽  
Blood Glucose Concentration ◽  
Glucagon Secretion ◽  
Liver Glycogen ◽  
Pancreatic Glucagon ◽  
Hepatic Portal Vein ◽  
Hepatic Portal ◽  
Induced Changes

Prandial changes in plasma pancreatic glucagon, blood glucose, and liver glycogen levels were studied during the first meal after 12 h of food deprivation in rats. To determine whether pancreatic glucagon secretion is influenced by the composition of the diet, the experiments were performed in rats fed high-carbohydrate (HC), high-fat (HF), or high-protein (HP) diets. Plasma glucagon levels in the hepatic portal vein increased about 100% during meals in all feeding groups, whereas glucagon levels in the hepatic vein changed very little. Blood glucose concentration in the hepatic portal vein increased during meals in HC diet-fed rats but decreased in HF and in HP diet-fed rats. Blood glucose in the hepatic vein also increased in HC and HP diet-fed rats. In addition, liver glycogen content decreased during meals in HC and HP diet-fed rats and by 14 min after the meal in HF diet-fed rats. These results demonstrate that a considerable amount of the glucagon released during meals in HC, HF, and HP diet-fed rats remains in the liver. This is consistent with the hypothesis that the liver is important for the satiety effect of glucagon. The results also suggest that glucagon contributes to the meal-induced changes in hepatic carbohydrate metabolism observed in all groups.

Evidence of a paracrine role for pancreatic somatostatin in vivo

1983 ◽  
Vol 245 (6) ◽  
pp. E598-E603 ◽  
Author(s):  
G. J. Taborsky
Keyword(s):  
Insulin Release ◽  
Glucagon Secretion ◽  
Base Line ◽  
Anesthetized Dogs ◽  
D Cells ◽  
Glucagon And Insulin ◽  
Line P ◽  
A And B Cells

Somatostatin (SS) in the D cells of the pancreatic islets has been hypothesized to tonically inhibit the secretion of glucagon and insulin from the neighboring A and B cells. To test this hypothesis directly, a nonimmunoreactive analogue of somatostatin [( D-Ala5-D-Trp8]SS) was infused intravenously at 0.55–17 micrograms/min into anesthetized dogs to suppress the secretion of pancreatic somatostatin and observe the effects of that suppression on glucagon and insulin release. Infusions of this analogue into anesthetized dogs at both a low dose (1.7 micrograms X min-1 X 30 min iv, n = 7) and at a medium dose (5.5 micrograms X min-1 X 30 min iv, n = 7) suppressed the release of somatostatin-like immunoreactivity (SLI) from the in situ canine pancreas by 31 +/- 10% of base line (P less than 0.025) and 45 +/- 6% of base line (P less than 0.0005), respectively. These doses increased glucagon secretion markedly (by 179 +/- 39 and 250 +/- 60% of base line, both P less than 0.005) and increased insulin secretion moderately (by 35 +/- 17 and 62 +/- 27% of base line, respectively, both P less than 0.05). The highest dose of analogue (17 micrograms/min, n = 9) produced less stimulation of glucagon release (delta = +95 +/- 35% of basal, P less than 0.025) and marked inhibition of insulin release (delta = -61 +/- 9% of basal, P less than 0.0005) despite a larger inhibition of pancreatic SLI release (delta = -84 +/- 3% of basal, P less than 0.0005).(ABSTRACT TRUNCATED AT 250 WORDS)

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