[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.

PHYSIOLOGICAL ACTIONS OF HUMAN FOLLICLE-STIMULATING HORMONE AND ITS β-SUBUNIT IN REPTILES

1977 ◽  
Vol 74 (3) ◽  
pp. 441-447 ◽  
Author(s):  
PAUL LICHT ◽  
ANTONELLA BONA GALLO ◽  
ANNE STOCKELL HARTREE ◽  
RATNA C. SHOWNKEEN
Keyword(s):  
Biological Activity ◽  
Follicle Stimulating Hormone ◽  
Β Subunit ◽  
Binding Assays ◽  
Mammalian Tissues ◽  
Stimulation Of ◽  
Stimulating Hormone

SUMMARY The actions of human follicle-stimulating hormone (hFSH) and its β-subunit were examined in several assays in reptiles, including effects on lizard testicular activity (growth and androgen production) in vivo, and stimulation of androgen production by snake testes and competition for binding of 125I-labelled hFSH in lizards and snakes in vitro. Binding was also examined with mammalian tissues. The hFSH was highly steroidogenic in the snake and lizard; otherwise results were similar to those observed in mammals. In all cases, the potency of the β-subunit was only a few per cent of the intact hormone. The potency of hFSH in vivo compared with NIH-FSH ovine standards was several 100 times greater than in vitro. Results for stimulation of androgen production in vivo closely paralleled those for binding assays in both reptiles and mammals. In contrast to previous results for ovine FSH β-subunit, human FSH β-subunit has little if any FSH biological activity in reptiles.

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.

EFFECTS OF GASTRIN ON THE RELEASE OF INSULIN IN VITRO

1969 ◽  
Vol 43 (3) ◽  
pp. 371-375 ◽  
Author(s):  
A. LERNMARK ◽  
B. HELLMAN ◽  
H. G. COORE
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Glucose Concentration ◽  
Gastrointestinal Hormones ◽  
Mouse Pancreas ◽  
Low Glucose ◽  
Isolated Pancreas ◽  
Stimulation Of

SUMMARY Several investigations in vivo and in vitro have shown that gastrointestinal hormones stimulate insulin secretion. Whether gastrin also has such an effect was tested both with the isolated mouse pancreas and with micro-dissected pancreatic islets from obese-hyperglycaemic mice. A fairly low concentration of human synthetic gastrin I (0·15 μg./ml.) was found to inhibit the stimulation of insulin release normally obtained with increasing glucose concentrations. However, when a higher concentration of gastrin was tested on the isolated pancreas in the presence of a low glucose concentration there was a stimulation of insulin secretion.

scholarly journals Increase of gap junctions between pancreatic B-cells during stimulation of insulin secretion.

1979 ◽  
Vol 82 (2) ◽  
pp. 441-448 ◽  
Author(s):  
P Meda ◽  
A Perrelet ◽  
L Orci
Keyword(s):  
Insulin Secretion ◽  
B Cells ◽  
Gap Junctions ◽  
Freeze Fracture ◽  
Secretory Activity ◽  
Isolated Rat Islets ◽  
Pancreatic B Cells ◽  
Stimulation Of

The development of gap junctions between pancreatic B-cells was quantitatively assessed in freeze-fracture replicas of isolated rat islets under different conditions of insulin secretion. The results show that in resting B-cells, gap junctions are small and scarce but that these junctions increase when insulin secretion is stimulated. Both a short (90 min) stimulation by glucose in vitro and a prolonged (2.5 d) stimulation by glibenclamide in vivo raise the number of gap junctions; in addition, the glibenclamide stimulation causes an increase in the size of individual gap junctions. As a consequence, the total area occupied by gap junctions on the B-cell membrane and the ratio of this area to the cell volume were found significantly increased in the latter condition. The slight increase of these values observed after the glucose stimulation did not reach significance. These data indicate a change of gap junctions during the secretory activity of the pancreatic B-cells. The possibility that the coupling of the cells is affected by the treatment is discussed.

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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