scholarly journals Salivary Peptide P-C Potentiates Insulin Release and Inhibits Glucagon Release from Isolated Perfused Pancreas of the Diabetic GK Rat

1995 ◽  
Vol 67 (1) ◽  
pp. 15-20 ◽  
Author(s):  
Noboru Nakashima ◽  
Ikuko Kimura ◽  
Masayasu Kimura
Keyword(s):  
Insulin Release ◽  
Glucagon Release ◽  
Perfused Pancreas ◽  
Gk Rat ◽  
Isolated Perfused Pancreas ◽  
Salivary Peptide

Effect of galanin on glucose-, arginine-, or potassium-stimulated insulin release

1989 ◽  
Vol 256 (5) ◽  
pp. E619-E623
Author(s):  
T. Yoshimura ◽  
J. Ishizuka ◽  
G. H. Greeley ◽  
J. C. Thompson
Keyword(s):  
Insulin Release ◽  
High Glucose ◽  
Second Phase ◽  
Dependent Manner ◽  
Perfused Pancreas ◽  
Isolated Perfused Pancreas ◽  
Second Phases ◽  
High Concentrations ◽  
Dose Dependent ◽  
Stimulation Of

We have examined the effect of galanin infusion on glucose-stimulated release of insulin from the isolated perfused pancreas of the rat to better characterize the effect of galanin on the first and second phases of insulin release. The effects of galanin on insulin release stimulated by L-arginine or high concentrations of potassium were also examined. When perfusion of galanin was started 4 min before the start of perfusion of high glucose (16.7 mM), galanin (10(-8)-10(-11) M) inhibited both the first and second phases of insulin release in a dose-dependent manner. When perfusion of galanin (10(-8) or 10(-9) M) was started simultaneously with high glucose (16.7 mM), only the second phase of insulin release was suppressed (P less than 0.05). Galanin (10(-9) M) failed to inhibit insulin release stimulated by L-arginine (10 and 5 mM) or potassium (25 and 20 mM). These findings suggest that the inhibitory action of galanin on glucose-stimulated insulin release is exerted on early intracellular events that occur during the stimulation of insulin release and that are common to both phases. Because galanin does not inhibit insulin release stimulated by L-arginine or potassium, galanin may inhibit glucose-stimulated closure of potassium channels.

Interleukin-1 potentiates glucose stimulated insulin release in the isolated perfused pancreas

1988 ◽  
Vol 117 (3) ◽  
pp. 302-306 ◽  
Author(s):  
Lise D. Wogensen ◽  
Thomas Mandrup-Poulsen ◽  
Helle Markholst ◽  
Jens Mølvig ◽  
Åke Lernmark ◽  
...  
Keyword(s):  
Insulin Release ◽  
Cell Function ◽  
Interleukin 1 ◽  
Systemic Circulation ◽  
Second Phase ◽  
Interleukin 1 Beta ◽  
Perfused Pancreas ◽  
Porcine Pancreas ◽  
Isolated Perfused Pancreas

Abstract. The acute effects of recombinant human interleukin-1 beta (rIL-1) on basal and glucose-stimulated insulin release were investigated in the isolated perfused pancreas. At a concentration of 20 μg/l rIL-1 had no effect on basal insulin release, but increased the total amount of insulin released during first and second phase insulin release in response to 20 mmol/l D-glucose in the rat pancreas (P < 0.05). In addition, 26 μg/l of rIL-1 potentiated insulin release in response to square wave infusions of stimulatory concentrations of glucose (11 mmol/l) in the porcine pancreas. We hypothesize that IL-1 in the systemic circulation may affect B cell function in vivo.

Effects of Substance P and Substance P-(6–ll) on Hormone Release from Isolated Perfused Pancreas: Their Opposite Actions on Rat and Canine Islets*

Endocrinology ◽  
1985 ◽  
Vol 117 (5) ◽  
pp. 1996-2000 ◽  
Author(s):  
YUKINOBU CHIBA ◽  
KOICHI KAWAI ◽  
YUKICHI OKUDA ◽  
EISUKE MUNEKATA ◽  
KAMEJIRO YAMASHITA
Keyword(s):  
Substance P ◽  
Hormone Release ◽  
Perfused Pancreas ◽  
Isolated Perfused Pancreas

scholarly journals The possible mechanisms by which phanoside stimulates insulin secretion from rat islets

2007 ◽  
Vol 192 (2) ◽  
pp. 389-394 ◽  
Author(s):  
Nguyen Khanh Hoa ◽  
Åke Norberg ◽  
Rannar Sillard ◽  
Dao Van Phan ◽  
Nguyen Duy Thuan ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
B Cells ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Pertussis Toxin ◽  
Insulin Response ◽  
Gk Rat ◽  
Isolated Pancreatic Islets ◽  
Gk Rats ◽  
Rat Islets

We recently showed that phanoside, a gypenoside isolated from the plant Gynostemma pentaphyllum, stimulates insulin secretion from rat pancreatic islets. To study the mechanisms by which phanoside stimulates insulin secretion. Isolated pancreatic islets of normal Wistar (W) rats and spontaneously diabetic Goto-Kakizaki (GK) rats were batch incubated or perifused. At both 3.3 and 16.7 mM glucose, phanoside stimulated insulin secretion several fold in both W and diabetic GK rat islets. In perifusion of W islets, phanoside (75 and 150 μM) dose dependently increased insulin secretion that returned to basal levels when phanoside was omitted. When W rat islets were incubated at 3.3 mM glucose with 150 μM phanoside and 0.25 mM diazoxide to keep K-ATP channels open, insulin secretion was similar to that in islets incubated in 150 μM phanoside alone. At 16.7 mM glucose, phanoside-stimulated insulin secretion was reduced in the presence of 0.25 mM diazoxide (P<0.01). In W islets depolarized by 50 mM KCl and with diazoxide, phanoside stimulated insulin release twofold at 3.3 mM glucose but did not further increase the release at 16.7 mM glucose. When using nimodipine to block L-type Ca2+ channels in B-cells, phanoside-induced insulin secretion was unaffected at 3.3 mM glucose but decreased at 16.7 mM glucose (P<0.01). Pretreatment of islets with pertussis toxin to inhibit exocytotic Ge-protein did not affect insulin response to 150 μM phanoside. Phanoside stimulated insulin secretion from Wand GK rat islets. This effect seems to be exerted distal to K-ATP channels and L-type Ca2+ channels, which is on the exocytotic machinery of the B-cells.

Endogenous hyperglycemia restores insulin release impaired by somatostatin analogue

1981 ◽  
Vol 240 (4) ◽  
pp. E407-E413
Author(s):  
G. J. Taborsky ◽  
D. Porte
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Release ◽  
Beta Cell Function ◽  
Cell Function ◽  
Dependent Diabetes Mellitus ◽  
Somatostatin Analogue ◽  
Base Line ◽  
Glucagon Release ◽  
Insulin Deficiency ◽  
Insulin Responses

These studies assessed the ability of des-Asn5-[D-Trp8-D-Ser13]-somatostatin (d-ATS-SS) to selectively inhibit insulin release and produce a hyperglycemia sufficient to compensate for the original impairment. d-ATS-SS at 0.017 micrograms/min inhibited basal insulin output (delta = -38 +/- 6%, P less than 0.005) and increased basal pancreatic glucagon output (delta - +21 +/- 6%, P less than 0.05, n = 5). d-ATS-SS at 0.17 micrograms/min markedly inhibited insulin output (delta = -84 +/- 4%, P less than 0.0005) and slightly inhibited glucagon output (delta = -14 +/- 6%, P less than 0.05, n = 5). d-ATS-SS at 0.055 micrograms/min decreased basal and stimulated insulin release but not basal nor stimulated glucagon release. By 3.5 of analogue infusion, plasma glucose had risen by 116 +/- 13 mg/dl, and base-line insulin levels and the insulin responses to both isoproterenol and arginine, but not glucose, increased toward control values. We conclude that d-ATS-SS produces selective insulinopenia resulting in hyperglycemia which in turn compensates for the original impairment. Thus, the hyperglycemia observed in other states of selective insulin deficiency (e.g., noninsulin-dependent diabetes mellitus) may compensate for defects in beta-cell function.

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