scholarly journals Effects of glucose and glucagon on the fructose 2,6-bisphosphate content of pancreatic islets and purified pancreatic B-cells. A comparison with isolated hepatocytes

1984 ◽  
Vol 221 (3) ◽  
pp. 759-764 ◽  
Author(s):  
A Sener ◽  
E Van Schaftingen ◽  
M Van de Winkel ◽  
D G Pipeleers ◽  
F Malaisse-Lagae ◽  
...  
Keyword(s):  
B Cells ◽  
Pancreatic Islets ◽  
Isolated Hepatocytes ◽  
Saturation Curve ◽  
Isolated Pancreatic Islets ◽  
Early Increase ◽  
Glucose Phosphorylation ◽  
Pancreatic B Cells ◽  
Glucose Stimulated Insulin Secretion ◽  
Related Increase

Glucose caused a sustained and dose-related increase in the fructose 2,6-bisphosphate content of isolated pancreatic islets, as well as of purified pancreatic B-cells. With isolated B-cells, the glucose saturation curve was sigmoidal and superimposable on that obtained with hepatocytes isolated from unfed rats. However, the response to glucose was notably faster in purified B-cells than in isolated hepatocytes. In contrast again with the situation prevailing in the liver, glucagon failed to decrease significantly the concentration of fructose 2,6-bisphosphate in either islets or purified B-cells. It is proposed that, in the process of glucose-stimulated insulin secretion, an early increase in fructose 2,6-bisphosphate formation may, by causing activation of 6-phosphofructo-1-kinase, allow glycolysis to keep pace with the rate of glucose phosphorylation.

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.

Defective regulation of glucokinase in rat pancreatic islet cell tumours

1987 ◽  
Vol 115 (4) ◽  
pp. 514-520 ◽  
Author(s):  
Sigurd Lenzen ◽  
Markus Tiedge ◽  
Peter R. Flatt ◽  
Clifford J. Bailey ◽  
Uwe Panten
Keyword(s):  
B Cells ◽  
Pancreatic Islets ◽  
Islet Cell ◽  
Pancreatic Islet Cell ◽  
Hexokinase Activity ◽  
Radiation Induced ◽  
Glucose Phosphorylation ◽  
Islet Cell Tumours ◽  
Total Glucose ◽  
Rat Pancreatic Islet

Abstract. The role of glucokinase in the regulation of insulin secretion was examined in normal rat pancreatic islets and in chemically- and radiation-induced rat pancreatic B-cell tumours which show an impaired insulin secretory response to glucose. In normal rats glucokinase activity in cytoplasmic fractions of pancreatic islets was decreased with the duration of fasting and increased by refeeding or insulin administration. This observation is consistent with the induction of glucokinase by insulin. Hexokinase activity was only slightly reduced during fasting. Glucokinase activity decreased in cytoplasmic fractions of streptozotocin-nicotinamideinduced rat pancreatic islet cell tumours. Glucokinase activity contributed about 75% to the total glucose phosphorylation capacity in cytoplasmic fractions of normal pancreatic islets and of small (< 1 mg) streptozotocin-nicotinamide-tumours. This proportion decreased to about 20% in the large streptozotocin-nicotinamide tumours. Glucokinase activity in cytoplasmic fractions of transplantable radiation-induced NEDH (New England Deaconess Hospital) rat B-cell tumours was seven times lower than in normal pancreatic islets and contributed only 15% to the total glucose phosphorylation capacity. In contrast, hexokinase activity of the NEDH tumour B-cells was 2.5 times higher than normal. Decreased glucokinase activity in the chemically- and radiation-induced tumour B-cells appears to result from a loss of the ability of insulin to induce this enzyme and may explain the lack of insulin secretory responsiveness of these tumour B-cells.

scholarly journals Glucose stimulates and insulin inhibits release of pancreatic TRH in vitro

2000 ◽  
pp. 60-65 ◽  
Author(s):  
J Benicky ◽  
V Strbak
Keyword(s):  
B Cells ◽  
Pancreatic Islets ◽  
High Glucose ◽  
Adenosine Monophosphate ◽  
Isolated Pancreatic Islets ◽  
Glucose Addition ◽  
Adult Rat ◽  
Camp Stimulation ◽  
Stimulation Of

OBJECTIVE: Pancreatic TRH is present in insulin-producing B-cells of the islets of Langerhans. There is fragmentary evidence that it may be involved in glucoregulation. The aim of our present study was to analyze how glucose and insulin affect TRH secretion by the pancreatic islets. DESIGN: Isolated pancreatic islets were incubated with different concentrations of glucose, insulin and glucagon, and TRH release was measured. RESULTS: In the present study, 6 and 12mmol/l d-glucose caused significant TRH release from isolated adult rat pancreatic islets when compared with that in the presence of the same concentrations of biologically ineffective l-glucose. Thirtymmol/l d-glucose was also ineffective, but this was not due to depression of secretion by hyperosmolarity since isosmotic compensation for the high glucose addition did not restore its stimulatory effect. Five micromol/l dibutyryl cyclic 3',5'-adenosine monophosphate (db-cAMP) increased both basal and glucose-stimulated TRH release, but this effect was not seen with 50micromol/l db-cAMP. Stimulation of phosphodiesterase by imidazole resulted in decreased basal but not glucose-stimulated release of TRH. Glucagon (10(-7)mol/l) did not affect either basal or glucose-stimulated release of TRH, while insulin (10(-7) and 10(-6)mol/l) inhibited both. CONCLUSION: Our present data showing that glucose stimulates and insulin inhibits pancreatic TRH release are compatible with the possibility that this substance may play a role in glucoregulation.

scholarly journals Nutrient Responsive Nesfatin-1 Regulates Energy Balance and Induces Glucose-Stimulated Insulin Secretion in Rats

Endocrinology ◽  
2011 ◽  
Vol 152 (10) ◽  
pp. 3628-3637 ◽  
Author(s):  
R. Gonzalez ◽  
R. L. S. Perry ◽  
X. Gao ◽  
M. P. Gaidhu ◽  
R. G. Tsushima ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Insulin Secretion ◽  
Glucose Uptake ◽  
Pancreatic Islets ◽  
Whole Body ◽  
Isolated Pancreatic Islets ◽  
Brown Adipose ◽  
Glucose Stimulated Insulin Secretion ◽  
Body Energy

Nesfatin-1 is a recently discovered anorexigen, and we first reported nesfatin-like immunoreactivity in the pancreatic β-cells. The aim of this study was to characterize the effects of nesfatin-1 on whole-body energy homeostasis, insulin secretion, and glycemia. The in vivo effects of continuous peripheral delivery of nesfatin-1 using osmotic minipumps on food intake and substrate partitioning were examined in ad libitum-fed male Fischer 344 rats. The effects of nesfatin-1 on glucose-stimulated insulin secretion (GSIS) were examined in isolated pancreatic islets. L6 skeletal muscle cells and isolated rat adipocytes were used to assess the effects of nesfatin-1 on basal and insulin-mediated glucose uptake as well as on major steps of insulin signaling in these cells. Nesfatin-1 reduced cumulative food intake and increased spontaneous physical activity, whole-body fat oxidation, and carnitine palmitoyltransferase I mRNA expression in brown adipose tissue but did not affect uncoupling protein 1 mRNA in the brown adipose tissue. Nesfatin-1 significantly enhanced GSIS in vivo during an oral glucose tolerance test and improved insulin sensitivity. Although insulin-stimulated glucose uptake in L6 muscle cells was inhibited by nesfatin-1 pretreatment, basal and insulin-induced glucose uptake in adipocytes from nesfatin-1-treated rats was significantly increased. In agreement with our in vivo results, nesfatin-1 enhanced GSIS from isolated pancreatic islets at both normal (5.6 mm) and high (16.7 mm), but not at low (2 mm), glucose concentrations. Furthermore, nesfatin-1/nucleobindin 2 release from rat pancreatic islets was stimulated by glucose. Collectively, our data indicate that glucose-responsive nesfatin-1 regulates insulin secretion, glucose homeostasis, and whole-body energy balance in rats.

QUANTITATIVE STUDIES ON ISOLATED PANCREATIC ISLETS OF MAMMALS

1964 ◽  
Vol 45 (3) ◽  
pp. 476-486 ◽  
Author(s):  
Claes Hellerström ◽  
Inge-Bert Täljedal ◽  
Bo Hellman
Keyword(s):  
Acid Phosphatase ◽  
B Cells ◽  
Pancreatic Islets ◽  
Phosphatase Activity ◽  
Acid Phosphatase Activity ◽  
List Type ◽  
Acid Phosphatases ◽  
Isolated Pancreatic Islets ◽  
Quantitative Studies ◽  
Tissue Homogenates

ABSTRACT Quantitative studies of non-specific acid phosphatases were performed on isolated pancreatic islets from obese-hyperglycaemic mice. The islets of these animals are composed of a rather pure population of B cells. The following observations were made: Acid phosphatases originating in the islet tissue, showed maximal enzyme activities at about pH 3.5 and 5.3 using p-nitrophenyl phosphate as substrate. The acid phosphatase activity of the exocrine tissue showed a single distinct maximum at about pH 5.3. The islet acid phosphatases were inhibited by sodium fluoride, sodium tartrate and formaldehyde. They were stable against storage in crude tissue homogenates at + 4° C and + 20° C for 48 hours. The pancreatic islets exhibited a significantly higher acid phosphatase activity than the exocrine parenchyma. Starvation for 7 days did not alter the enzyme levels in the islets or acini when measured at pH 5.3, while a probably increased enzyme activity was obtained in both these regions at pH 3.5. There was no evidence for a relationship between the insulin secretion and the acid phosphatase activity of the B cells.

Effect of streptozotocin injection on expression of immunoreactive foilistatin and βA and βB subunits of inhibin/activin in rat pancreatic islets

1995 ◽  
Vol 132 (3) ◽  
pp. 363-369 ◽  
Author(s):  
Kenji Ogawa ◽  
Kenichiro Ono ◽  
Masamichi Kurohmaru ◽  
Yoshihiro Hayashi
Keyword(s):  
B Cells ◽  
Pancreatic Islets ◽  
Islet Cells ◽  
Short Form ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
Rat Pancreatic Islets ◽  
Long Form ◽  
Pancreatic B Cells ◽  
The University

Ogawa K, Ono K, Kurohmaru M, Hayashi Y. Effect of streptozotocin injection on expression of immunoreactive follistatin and βA and βB subunits of inhibin/activin in rat pancreatic islets. Eur J Endocrinol 1995;132:363–9. ISSN 0804–4643 The effect of streptozotocin (STZ) on expression of immunoreactive follistatin and β-subunits of inhibin/activin in pancreatic islets was studied by immunohistochemistry. To localize immunoreactive follistatin in pancreatic islets, two different anti-follistatin sera were used. Anti-follistatin(300–315) serum detects only long-form follistatin, while anti-follistatin(123–134) serum detects both long- and C-terminal truncated short-form follistatin in sodium dodecyl sulfate polyacrylamide gel electrophoresis and immunoblotting. Although an intense reaction with anti-follistatin(123–134) was found in pancreatic B cells, a reaction with anti-follistatin(300–315) was not present in any type of cells. This result suggests that only short-form follistatin is expressed in pancreatic islets. It was confirmed that immunoreaction with anti-βA(1–10)-Tyr serum was found in pancreatic B cells. The anti-βB(1–10)-Tyr reaction was intense in A cells but weak in B cells. These findings suggest that the expression pattern of each β-subunit differs in each type of islet cells. At 2 weeks after STZ injection (65 mg/kg), insulin immunoreaction still remained in B cells, although most pancreatic B cells were destroyed. In contrast, immunoreactions of follistatin and β-subunits in B cells disappeared 24 h after STZ treatment. These results indicate that STZ affects the production of follistatin or β-subunits of inhibin/activin in pancreatic B cells rather than insulin secretion. Kenji Ogawa, Department of Veterinary Anatomy, Faculty of Agriculture, The University of Tokyo, Bunkyo-ku, Tokyo 113, Japan

scholarly journals Enhanced insulin secretion responsiveness and islet adrenergic desensitization after chronic norepinephrine suppression is discontinued in fetal sheep

2014 ◽  
Vol 306 (1) ◽  
pp. E58-E64 ◽  
Author(s):  
Xiaochuan Chen ◽  
Alice S. Green ◽  
Antoni R. Macko ◽  
Dustin T. Yates ◽  
Amy C. Kelly ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Chronic Exposure ◽  
Uncoupling Protein ◽  
Adrenergic Blockade ◽  
Protein Subunit ◽  
Β Cell ◽  
Fetal Sheep ◽  
Isolated Pancreatic Islets ◽  
Glucose Stimulated Insulin Secretion

Intrauterine growth-restricted (IUGR) fetuses experience prolonged hypoxemia, hypoglycemia, and elevated norepinephrine (NE) concentrations, resulting in hypoinsulinemia and β-cell dysfunction. Previously, we showed that acute adrenergic blockade revealed enhanced insulin secretion responsiveness in the IUGR fetus. To determine whether chronic exposure to NE alone enhances β-cell responsiveness afterward, we continuously infused NE into fetal sheep for 7 days and, after terminating the infusion, evaluated glucose-stimulated insulin secretion (GSIS) and glucose-potentiated arginine-induced insulin secretion (GPAIS). During treatment, NE-infused fetuses had greater ( P < 0.05) plasma NE concentrations and exhibited hyperglycemia ( P < 0.01) and hypoinsulinemia ( P < 0.01) compared with controls. GSIS during the NE infusion was also reduced ( P < 0.05) compared with pretreatment values. GSIS and GPAIS were approximately fourfold greater ( P < 0.01) in NE fetuses 3 h after the 7 days that NE infusion was discontinued compared with age-matched controls or pretreatment GSIS and GPAIS values of NE fetuses. In isolated pancreatic islets from NE fetuses, mRNA concentrations of adrenergic receptor isoforms (α1D, α2A, α2C, and β1), G protein subunit-αi-2, and uncoupling protein 2 were lower ( P < 0.05) compared with controls, but β-cell regulatory genes were not different. Our findings indicate that chronic exposure to elevated NE persistently suppresses insulin secretion. After removal, NE fetuses demonstrated a compensatory enhancement in insulin secretion that was associated with adrenergic desensitization and greater stimulus-secretion coupling in pancreatic islets.

scholarly journals Melatonin modifies basal and stimulated insulin secretion via NADPH oxidase

2016 ◽  
Vol 231 (3) ◽  
pp. 235-244 ◽  
Author(s):  
Daniel Simões ◽  
Patrícia Riva ◽  
Rodrigo Antonio Peliciari-Garcia ◽  
Vinicius Fernandes Cruzat ◽  
Maria Fernanda Graciano ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Nadph Oxidase ◽  
Pancreatic Islets ◽  
Membrane Receptors ◽  
Melatonin Treatment ◽  
Isolated Pancreatic Islets ◽  
Ros Homeostasis ◽  
Basal Insulin Secretion ◽  
Glucose Stimulated Insulin Secretion

Melatonin is a hormone synthesized in the pineal gland, which modulates several functions within the organism, including the synchronization of glucose metabolism and glucose-stimulated insulin secretion (GSIS). Melatonin can mediate different signaling pathways in pancreatic islets through two membrane receptors and via antioxidant or pro-oxidant enzymes modulation. NADPH oxidase (NOX) is a pro-oxidant enzyme responsible for the production of the reactive oxygen specie (ROS) superoxide, generated from molecular oxygen. In pancreatic islets, NOX-derived ROS can modulate glucose metabolism and regulate insulin secretion. Considering the roles of both melatonin and NOX in islets, the aim of this study was to evaluate the association of NOX and ROS production on glucose metabolism, basal and GSIS in pinealectomized rats (PINX) and in melatonin-treated isolated pancreatic islets. Our results showed that ROS content derived from NOX activity was increased in PINX at baseline (2.8 mM glucose), which was followed by a reduction in glucose metabolism and basal insulin secretion in this group. Under 16.7 mM glucose, an increase in both glucose metabolism and GSIS was observed in PINX islets, without changes in ROS content. In isolated pancreatic islets from control animals incubated with 2.8 mM glucose, melatonin treatment reduced ROS content, whereas in 16.7 mM glucose, melatonin reduced ROS and GSIS. In conclusion, our results demonstrate that both basal and stimulated insulin secretion can be regulated by melatonin through the maintenance of ROS homeostasis in pancreatic islets.

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