Potentiation of glucose-induced insulin release by glucose in the isolated pancreas of fed and fasted rats

Diabetes ◽  
1976 ◽  
Vol 25 (10) ◽  
pp. 949-954 ◽  
Author(s):  
S. Efendic ◽  
E. Cerasi ◽  
R. Luft ◽  
G. Gladnikoff
Keyword(s):  
Insulin Release ◽  
Isolated Pancreas ◽  
Fasted Rats

Potentiation of Glucose-induced Insulin Release by Glucose in the Isolated Pancreas of Fed and Fasted Rats

Diabetes ◽  
1976 ◽  
Vol 25 (10) ◽  
pp. 949-954 ◽  
Author(s):  
S. Efendic ◽  
E. Cerasi ◽  
R. Luft ◽  
G. Gladnikoff
Keyword(s):  
Insulin Release ◽  
Isolated Pancreas ◽  
Fasted Rats

Interaction of gastric inhibitory polypeptide and arginine with glucose in the perfused pancreas of rats treated with triiodothyronine

1982 ◽  
Vol 60 (3) ◽  
pp. 297-301 ◽  
Author(s):  
Michael K. Mueller ◽  
Raymond A. Pederson ◽  
John C. Brown
Keyword(s):  
Insulin Secretion ◽  
Insulin Release ◽  
Chronic Treatment ◽  
Gastric Inhibitory Polypeptide ◽  
Second Phase ◽  
Perfused Pancreas ◽  
Isolated Pancreas ◽  
Insulinotropic Effect

Chronic treatment of rats with triiodothyronine (T3) resulted in suppression of insulin release from the isolated pancreas when perfused with 8.6 mM glucose. This inhibition could be partially overcome by 16 mM glucose but the insulin release was still significantly reduced. Arginine and gastric inhibitory polypeptide (GIP) induced an insulinotropic action in both control and T3-treated preparations. This was achieved in the latter, in the absence of a second phase of insulin secretion to glucose. The insulinotropic effect of both arginine and GIP was abolished by mannoheptulose in both control and T3-treated animals.

scholarly journals Glucose-induced insulin secretion from islets of fasted rats: modulation by alternate fuel and neurohumoral agonists

2000 ◽  
Vol 166 (1) ◽  
pp. 111-120 ◽  
Author(s):  
WS Zawalich ◽  
KC Zawalich
Keyword(s):  
Protein Kinase C ◽  
Insulin Secretion ◽  
Protein Kinase ◽  
Phospholipase C ◽  
Insulin Release ◽  
Cholinergic Stimulation ◽  
Glucose Stimulation ◽  
Kinase C ◽  
Alternate Fuel ◽  
Fasted Rats

Islets from fed and 24-h-fasted rats were studied immediately after collagenase isolation. (1) After a 24-h fast, the insulin secretory responses to 8 mM glucose measured during perifusion were reduced by more than 90% from islets of fasted donors. (2) Increasing glucose to 11 or 27.5 mM resulted in enhanced insulin secretion from islets of fasted animals. (3) Fasting did not reduce islet insulin content. (4) Responses to 8 or 27.5 mM glucose were not affected if fatty acid-free albumin was used during the perifusion. (5) Inclusion of alpha-ketoisocaproate (5 mM), monomethyl succinate (10 mM) or carbachol (10 microM) significantly amplified insulin release from fasted islets in the simultaneous presence of 8 mM glucose. (6) Phospholipase C activation by glucose, carbachol or their combination was not adversely affected by fasting. (7) The response to the protein kinase C activator, phorbol 12-myristate 13-acetate (500 nM), was reduced by about 60% after fasting. (8) Extending the fast to 48 h resulted in a severe decline in response to 11 mM glucose; however, the further addition of 10 microM carbachol still enhanced release from these islets. The results confirm that caloric restriction impairs islet sensitivity to glucose stimulation and that protein kinase C may be involved in the reduction of glucose-induced insulin release from these islets. The activation of phospholipase C by cholinergic stimulation may contribute to the maintenance of insulin secretion from calorically restricted animals. These results also demonstrate that free fatty acids are not essential for glucose to evoke secretion from isolated islets of fasted donors.

EFFECT OF FASTING ON 32P TRANSLOCATIONS IN PRE-LABELLED PANCREATIC ISLETS

1978 ◽  
Vol 88 (3) ◽  
pp. 545-555 ◽  
Author(s):  
Kjell Asplund ◽  
Norbert Freinkel
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Β Cell ◽  
Early Step ◽  
Phosphate Release ◽  
Insulin Secretagogues ◽  
Stimulus Secretion Coupling ◽  
The Right ◽  
Fasted Rats

ABSTRACT The rapid, short-lived efflux of inorganic 32P-orthophosphate that occurs when pre-labelled pancreatic islets are exposed to nutrient insulin secretagogues (the "phosphate flush") has been proposed to reflect some early step in β-cell secretory activation. In the present study, glucose-initiated phosphate efflux was studied during fasting. Pancreatic islets were isolated from fed and 48-h fasted rats by collagenase digestion. After pre-labelling with 32P-orthophosphate and basal perifusion with 0.5 mg/ml glucose, tissue analyses disclosed similar stores of radioactivity in the two groups of islets. Stimulatory perifusion with glucose at this time failed to promote insulin release from islets which had been secured from fasted donors although the "phosphate flush" was preserved. However, the characteristics of phosphate efflux were altered. Maximal glucose-induced phosphate release was greater with islets from fasted animals whereas phosphate release in response to low level stimulation with glucose was diminished. Accordingly, the dose-response curve for glucose-initiated phosphate efflux in islets from fasted rats was displaced to the right and compatible with a decreased sensitivity to glucose at the activation site for the "phosphate flush." Thus, while glucose is unable to enhance insulin release in vitro after fasting, glucose still elicits increased phosphate efflux. However, the phenomenon appears to be attended by an impaired responsiveness to activation by glucose, supporting the contention that some early step in the sequence of stimulus secretion coupling in the β-cell may be obtunded after food deprivation.

Glutamate stimulates insulin secretion and improves glucose tolerance in rats

1995 ◽  
Vol 269 (3) ◽  
pp. E551-E556 ◽  
Author(s):  
G. Bertrand ◽  
R. Puech ◽  
M. M. Loubatieres-Mariani ◽  
J. Bockaert
Keyword(s):  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Insulin Release ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Dependent Manner ◽  
Intravenous Glucose ◽  
Acid Receptor ◽  
Fasted Rats

We previously showed in vitro that glutamate stimulates insulin release via an alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor. Here we address a more physiological question concerning the in vivo effect of intravenously or orally administered glutamate on insulinemia and glycemia in fed and fasted rats. In anesthetized fed rats, the intravenous administration of glutamate at 9 and 30 mg/kg transiently increased insulinemia in a dose-dependent manner. The insulin-secretory effect of glutamate (9 mg/kg) was blocked by an antagonist of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. In anesthetized fasted rats, glutamate at 9 mg/kg was ineffective, but during an intravenous glucose tolerance test (0.5 g/kg), glutamate markedly potentiated insulin release and increased the glucose disappearance rate. In conscious rats, the intragastric administration of glutamate at 200 mg/kg elicited a transient insulin response in fed animals and had no effect in fasted animals but, during an oral glucose tolerance test (1 g/kg), enhanced insulin secretion and reduced the hyperglycemia. Glutamate was effective at plasma concentrations of 200-300 microM. In conclusion, intravenously and orally administered glutamate stimulates insulin secretion in vivo via an excitatory amino acid receptor and improves glucose tolerance.

Differential metabolic requirement for initiation and augmentation of insulin release by glucose: a study with rat pancreatic islets

1994 ◽  
Vol 143 (3) ◽  
pp. 497-503 ◽  
Author(s):  
F Ishihara ◽  
T Aizawa ◽  
N Taguchi ◽  
Y Sato ◽  
K Hashizume
Keyword(s):  
Low Temperature ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
High Glucose ◽  
Glucose Oxidation ◽  
Glucose Utilization ◽  
Incubation Temperature ◽  
Islet Cells ◽  
Metabolic Requirement ◽  
Fasted Rats

Abstract Insulin release, glucose utilization (3H2O formation from [5-3H]glucose), and glucose oxidation (14CO2 formation from [4C(U)] glucose) were determined in pancreatic islets from 96-h fasted rats at 37 ° C and those from fed rats at 22 ° C, using the islets from fed rats incubated at 37 ° C as controls. In the islets from 96-h fasted rats and those from fed rats incubated at 22 ° C, we could not demonstrate significant insulin release in response to high glucose concentrations of up to 16·7 mmol/l. However, 16·7 mmol/l glucose clearly augmented insulin release caused by a depolarizing concentration (50 mmol/l) of K+ in these islets: i.e. 16·7 mmol/l glucose plus 50 mmol/l K+ produced significantly greater insulin release than 50 mmol/l K alone. Glucose utilization and oxidation by the islet cells were suppressed by 96-h fasting of the rats or by lowering the incubation temperature to 22 ° C, and depolarization with K at 50 mmol/l did not at all augment glucose utilization and oxidation by the islets. Thus we conclude that reduction of glucose metabohsm in islets from fasted rats and in those incubated at low temperature eliminated initiation, but not augmentation, of insulin release by 16·7 mmol/l glucose. The data indicate that the metabolic threshold for the initiation of insulin release is significantly higher than it is for the augmentation of release by glucose. Journal of Endocrinology (1994) 143, 497–503

THE EFFECT OF FASTING AND SELECTIVE RE-FEEDING ON INSULIN RELEASE IN THE RAT

1973 ◽  
Vol 72 (1) ◽  
pp. 46-53 ◽  
Author(s):  
D. S. Turner ◽  
D. A. B. Young
Keyword(s):  
Insulin Release ◽  
Acute Effect ◽  
Secretory Response ◽  
Release Mechanism ◽  
Β Cell ◽  
Intestinal Hormones ◽  
Intravenous Glucose ◽  
Glucose Ingestion ◽  
Glucose Test ◽  
Insulin Secretory Response

ABSTRACT The insulin secretory response in the rat to intravenous glucose was found to be greatly impaired by fasting for three days, whereas that to orally administered glucose was not significantly affected. Rats fasted for two days were given either protein or starch pellets for six hours, and then fasted for a further eighteen hours before the intravenous glucose test. The protein pre-feeding failed to affect significantly the subsequent insulin secretory response to intravenous glucose, whereas starch prefeeding greatly enhanced it. It is suggested that intestinal hormones released by glucose ingestion may exert not only an acute effect on insulin release, but also a 'priming' effect on the insulin release mechanism of the β cell, which enables it to respond to the subsequent stimulus of glucose alone.

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