Insulin and Glucagon Secretion in vivo and its Neural Control

2011 ◽  
Author(s):  
Gerald J. Taborsky
Keyword(s):  
Neural Control ◽  
Glucagon Secretion ◽  
Insulin And Glucagon Secretion

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.

Adaptive changes in insulin and glucagon secretion during cold acclimation in the rat

1986 ◽  
Vol 250 (6) ◽  
pp. E669-E676 ◽  
Author(s):  
C. I. Edwards ◽  
R. J. Howland
Keyword(s):  
Cold Acclimation ◽  
Cold Exposure ◽  
Hormone Secretion ◽  
Glucagon Secretion ◽  
Molar Ratio ◽  
Adaptive Process ◽  
Insulin And Glucagon Secretion ◽  
Pancreatic Hormone

Arginine-stimulated insulin and glucagon outputs from isolated perfused pancreata of warm-acclimated and 2-, 4-, and 6-wk cold-acclimated rats (4 degrees C) were determined to assess whether observed changes in these parameters were a result of cold exposure per se or a part of the adaptive process of cold acclimation. Progressive and sequential changes were seen in both insulin and glucagon outputs. At 2 wk cold acclimation, glucagon rose and insulin output tended to fall, at 4 wk, glucagon output remained elevated and insulin output was further reduced, and at 6 wk, glucagon output had returned to control levels, whereas insulin output was substantially further reduced. These changes resulted in reduction of the insulin-to-glucagon molar ratio of the total arginine-induced output from 7.27 +/- 1.76 (SE) in the warm acclimate to 2.31 +/- 0.79 (SE) at 2 wk, 1.42 +/- 0.29 (SE) at 4 wk, and 1.26 +/- 0.21 (SE) at 6 wk cold acclimation. The data do not provide in vitro support for the hypothesis that changes in pancreatic hormone secretion in vivo are a consequence of cold exposure and not cold acclimation.

Adrenergic regulation of glucagon and insulin secretion during immobilization stress in normal and spontaneously diabetic BB rats

1981 ◽  
Vol 240 (4) ◽  
pp. E373-E378 ◽  
Author(s):  
A. F. Nakhooda ◽  
M. J. Sole ◽  
E. B. Marliss
Keyword(s):  
Neural Control ◽  
Immobilization Stress ◽  
Glucagon Secretion ◽  
Diabetic Rats ◽  
Cardiovascular Fitness ◽  
In Vivo Model ◽  
Bb Rat ◽  
Adrenergic Stimulation ◽  
Glucagon And Insulin

To test for a possible role of adrenergic mechanisms in the altered glucagon secretion in the spontaneously diabetic "BB" rat, the responses of glucose, insulin, and glucagon to adrenergic blocking agents in diabetic and normal rats were compared at rest and during 2 h of immobilization stress. In unstressed normal rats, phentolamine alone caused a 20 mg/dl fall in glycemia, 1.2 ng/ml rise in insulin (IRI), and no change in glucagon (IRG), whereas the only effect of propranolol was a minor rise in glycemia. Stress caused increments in glycemia of 72 mg/dl and in IRG of 94 pg/ml, and no change in IRI. Phentolamine significantly attenuated the stress-related increments, and IRI increased by the same amount as in the unstressed state. Propranolol exhibited no statistically significant effects on the response to stress. These findings are consistent with alpha-adrenergic stimulation of IRG and suppression of IRI secretion. In unstressed diabetic rats (mean time 0 glycemia, 431 mg/dl), propranolol caused only a small rise in glycemia, whereas phentolamine induced marked increments of glycemia (131 mg/dl) and IRG (116 pg/ml). Stress alone did likewise (189 mg/dl, 122 pg/ml) as did stress with the phentolamine (271 mg/dl, 144 pg/ml). However propranolol significantly attenuated the stress-induced increments in glycemia (88 mg/dl) and IRG (82 pg/ml). Thus both alpha- and beta-adrenergic receptors influence IRG secretion in the diabetic rats. An in vivo model for elucidating neural control of glucoregulation has been developed that is independent of cardiovascular fitness.

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.

[Ala6]gastrin-releasing peptide-10: an analogue with dissociated biological activities

1989 ◽  
Vol 257 (2) ◽  
pp. E235-E240
Author(s):  
H. Mukai ◽  
K. Kawai ◽  
S. Suzuki ◽  
H. Ohmori ◽  
K. Yamashita ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Biological Activities ◽  
Glucagon Secretion ◽  
Gastrin Releasing Peptide ◽  
Gastrin Secretion ◽  
Insulin And Glucagon Secretion ◽  
Mammalian Tissues ◽  
Stimulation Of

COOH-terminal decapeptide of gastrin-releasing peptide (GRP-10) is a bombesin-like peptide, which has bioactivities to stimulate gastrin, insulin, and glucagon secretion. We have synthesized an analogue of GRP-10 that inhibits GRP-10's stimulation of insulin secretion both in vivo and in vitro and glucagon secretion in vivo, while potentiating the stimulation of gastrin secretion. The amino acid sequence of this peptide is H-Gly-Asn-Trp-Ala-Ala-Gly-His-Leu-Met-NH2 ([Ala6]GRP-10). Because the stimulation of insulin and gastrin secretion by GRP-10 has been ascribed to a direct effect on B- and G-cells, these findings suggest that there are two subtypes of receptors for bombesin-like peptides in mammalian tissues.

ATP-sensitive potassium channels participate in glucose uptake in skeletal muscle and adipose tissue

2002 ◽  
Vol 283 (6) ◽  
pp. E1178-E1184 ◽  
Author(s):  
Takashi Miki ◽  
Kohtaro Minami ◽  
Li Zhang ◽  
Mizuo Morita ◽  
Tohru Gonoi ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glucose Uptake ◽  
Skeletal Muscles ◽  
Glucagon Secretion ◽  
Channel Activity ◽  
Wild Type ◽  
Insulin And Glucagon Secretion ◽  
Uptake Experiment

ATP-sensitive potassium (KATP) channels are known to be critical in the control of both insulin and glucagon secretion, the major hormones in the maintenance of glucose homeostasis. The involvement of KATPchannels in glucose uptake in the target tissues of insulin, however, is not known. We show here that Kir6.2(−/−) mice lacking Kir6.2, the pore-forming subunit of these channels, have no KATPchannel activity in their skeletal muscles. A 2-deoxy-[3H]glucose uptake experiment in vivo showed that the basal and insulin-stimulated glucose uptake in skeletal muscles and adipose tissues of Kir6.2(−/−) mice is enhanced compared with that in wild-type (WT) mice. In addition, in vitro measurement of glucose uptake indicates that disruption of the channel increases the basal glucose uptake in Kir6.2(−/−) extensor digitorum longus and the insulin-stimulated glucose uptake in Kir6.2(−/−) soleus muscle. In contrast, glucose uptake in adipose tissue, measured in vitro, was similar in Kir6.2(−/−) and WT mice, suggesting that the increase in glucose uptake in Kir6.2(−/−) adipocytes is mediated by altered extracellular hormonal or neuronal signals altered by disruption of the KATP channels.

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)

Stimulation of insulin and glucagon secretion by vasoactive intestinal peptide.

1977 ◽  
Vol 232 (2) ◽  
pp. E197 ◽  
Author(s):  
M Schebalin ◽  
S I Said ◽  
G M Makhlouf
Keyword(s):  
Insulin Secretion ◽  
Vasoactive Intestinal Peptide ◽  
Insulin Response ◽  
Glucagon Secretion ◽  
Endocrine Function ◽  
Insulin And Glucagon Secretion ◽  
Pancreatic Endocrine Function ◽  
Insulin Response To Glucose ◽  
Made In

In vivo, vasoactive intestinal peptide (VIP) produces simultaneous increases in blood glucose and insulin levels. In order to determine whether VIP, like its homologues, also stimulates insulin secretion directly, studies were made in controlled glucose media employing the vascularly perfused cat pancreas. VIP stimulated insulin secretion significantly in the presence of constant physiological concentrations of glucose. The highest insulin response to VIP (100.3+/-8.1 muU/min) approached the highest insulin response to glucose (119.9 +/- 12.0 muU/min). In the absence of glucose, the insulin response to VIP was insignificant. Unexpectedly, VIP was found to be a more effective stimulant of glucagon than of insulin secretion. The highest glucagon response to VIP (327+/-51% of control levels) was attained in the presence of physiological concentrations of glucose and equalled the glucagon response obtained upon withdrawal of glucose from the perfusate. The glucagon response to VIP was blocked by increasing the glucose in the perfusate. These studies indicate the VIP present in pancreatic islets might play a role in the local control of pancreatic endocrine function.

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