Insulin Production and Glucose Metabolism in Isolated Pancreatic Islets of Rats With NIDDM

Diabetes ◽  
1988 ◽  
Vol 37 (9) ◽  
pp. 1226-1233 ◽  
Author(s):  
B. Portha ◽  
M.-H. Giroix ◽  
P. Serradas ◽  
N. Welsh ◽  
C. Hellerstrom ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Pancreatic Islets ◽  
Insulin Production ◽  
Isolated Pancreatic Islets

Insulin production and glucose metabolism in isolated pancreatic islets of rats with NIDDM

Diabetes ◽  
1988 ◽  
Vol 37 (9) ◽  
pp. 1226-1233 ◽  
Author(s):  
B. Portha ◽  
M. H. Giroix ◽  
P. Serradas ◽  
N. Welsh ◽  
C. Hellerstrom ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Pancreatic Islets ◽  
Insulin Production ◽  
Isolated Pancreatic Islets

scholarly journals Glucose homeostasis is impaired in mice deficient in the neuropeptide 26RFa (QRFP)

2020 ◽  
Vol 8 (1) ◽  
pp. e000942
Author(s):  
Mouna El-Mehdi ◽  
Saloua Takhlidjt ◽  
Fayrouz Khiar ◽  
Gaëtan Prévost ◽  
Jean-Luc do Rego ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Pancreatic Islets ◽  
Glucose Homeostasis ◽  
Gene Knockout ◽  
Hepatic Glucose Production ◽  
Biologically Active ◽  
Mutant Mice ◽  
Insulin Production ◽  
Coding Region ◽  
The Impact

Introduction26RFa (pyroglutamyl RFamide peptide (QRFP)) is a biologically active peptide that has been found to control feeding behavior by stimulating food intake, and to regulate glucose homeostasis by acting as an incretin. The aim of the present study was thus to investigate the impact of 26RFa gene knockout on the regulation of energy and glucose metabolism.Research design and methods26RFa mutant mice were generated by homologous recombination, in which the entire coding region of prepro26RFa was replaced by the iCre sequence. Energy and glucose metabolism was evaluated through measurement of complementary parameters. Morphological and physiological alterations of the pancreatic islets were also investigated.ResultsOur data do not reveal significant alteration of energy metabolism in the 26RFa-deficient mice except the occurrence of an increased basal metabolic rate. By contrast, 26RFa mutant mice exhibited an altered glycemic phenotype with an increased hyperglycemia after a glucose challenge associated with an impaired insulin production, and an elevated hepatic glucose production. Two-dimensional and three-dimensional immunohistochemical experiments indicate that the insulin content of pancreatic β cells is much lower in the 26RFa−/− mice as compared with the wild-type littermates.ConclusionDisruption of the 26RFa gene induces substantial alteration in the regulation of glucose homeostasis, with in particular a deficit in insulin production by the pancreatic islets. These findings further support the notion that 26RFa is an important regulator of glucose homeostasis.

scholarly journals Glucose homeostasis is impaired in mice deficient for the neuropeptide 26RFa (QRFP)

2019 ◽  
Author(s):  
Mouna El Mehdi ◽  
Saloua Takhlidjt ◽  
Fayrouz Khiar ◽  
Gaëtan Prévost ◽  
Jean-Luc do Rego ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Pancreatic Islets ◽  
Glucose Homeostasis ◽  
Biologically Active ◽  
Mutant Mice ◽  
Insulin Production ◽  
Active Peptide ◽  
Important Regulator ◽  
Biologically Active Peptide ◽  
The Impact

AbstractIntroduction26RFa (QRFP) is a biologically active peptide that has been found to control feeding behaviour by stimulating food intake, and to regulate glucose homeostasis by acting as an incretin. The aim of the present study was thus to investigate the impact of 26RFa gene knockout on the regulation of energy and glucose metabolism.Research design and methods26RFa mutant mice were generated by homologous recombination, in which the entire coding region of prepro-26RFa was replaced by the iCre sequence. Energy and glucose metabolism was evaluated through measurement of complementary parameters. Morphological and physiological alterations of the pancreatic islets were also investigated.ResultsOur data do not reveal significant alteration of energy metabolism in the 26RFa-deficient mice except the occurrence of an increased basal metabolic rate. By contrast, 26RFa mutant mice exhibit an altered glycemic phenotype with an increased hyperglycemia after a glucose challenge associated with an impaired insulin production, and an elevated hepatic glucose production. 2D and 3D immunohistochemical experiments indicate that the insulin content of pancreatic β cells is much lower in the 26RFa-/- mice as compared to the wild-type littermates.ConclusionDisruption of the 26RFa gene induces substantial alteration in the regulation of glucose homeostasis with, in particular, a deficit in insulin production by the pancreatic islets. These findings further support the notion that 26RFa is an important regulator of glucose homeostasis.Significance of this studyWhat is already known about this subject?26RFa is a biologically active peptide produced in abundance in the gut and the pancreas. 26RFa has been found to regulate glucose homeostasis by acting as an incretin and by increasing insulin sensitivity.What are the new findings?Disruption of the 26RFa gene induces substantial alteration in the regulation of glucose homeostasis with, in particular, a deficit in insulin production by the pancreatic islets, assessing therefore the notion that 26RFa is an important regulator of glucose homeostasis.How might these results change the focus of research or clinical practice?Identification of a novel actor in the regulation of glucose homeostasis is crucial to better understand the general control of glucose metabolism in physiological and pathophysiological conditions, and opens new fields of investigation to develop innovative drugs to treat diabetes mellitus.

scholarly journals Quinine-induced modifications of insulin release and glucose metabolism by isolated pancreatic islets

FEBS Letters ◽  
1975 ◽  
Vol 57 (3) ◽  
pp. 280-284 ◽  
Author(s):  
J.C. Henquin ◽  
B. Horemans ◽  
M. Nenquin ◽  
J. Verniers ◽  
A.E. Lambert
Keyword(s):  
Glucose Metabolism ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Isolated Pancreatic Islets

scholarly journals The effect of starvation on phosphodiesterase activity and the content of adenosine 3′:5′-cyclic monophosphate in isolated mouse pancreatic islets

1974 ◽  
Vol 142 (3) ◽  
pp. 653-658 ◽  
Author(s):  
Kirsten Capito ◽  
Carl Jørgen Hedeskov
Keyword(s):  
Glucose Metabolism ◽  
Cyclic Amp ◽  
Pancreatic Islets ◽  
Maximum Activity ◽  
Secretory Process ◽  
Phosphodiesterase Activity ◽  
Primary Defect ◽  
Isolated Pancreatic Islets ◽  
Cyclic Monophosphate ◽  
Mouse Pancreatic Islets

1. The concentration of cyclic AMP and the activity of phosphodiesterase were measured in isolated pancreatic islets from fed or 48h-starved mice. 2. Two different phosphodiesterases were detected. Neither the maximum activity nor the Km values of these enzymes were changed by starvation. 3. The concentration of cyclic AMP in non-incubated islets was the same in islets from fed and starved mice. 4. Incubation with 3.3mm-glucose for 5–30min had no effect on the concentration of cyclic AMP, irrespective of the nutritional state of the mice. Incubation with 16.7mm-glucose for 5–30min raised the concentration of cyclic AMP by about 30% in islets from fed mice. This rise was prevented by addition of mannoheptulose (3mg/ml). Incubation with 16.7mm-glucose had no effect on the cyclic AMP content in islets from starved mice. 5. In islets from fed mice 10min incubation with 5mm-caffeine had no effect on the concentration of cyclic AMP in the presence of 3.3 or 16.7mm-glucose, whereas the cyclic AMP content was increased approx. 150% in islets from starved mice. 6. After 10min incubation with 1mm-3-isobutyl-1-methylxanthine in the presence of 3.3 or 16.7mm-glucose the concentration of cyclic AMP was raised by 250% in islets from fed mice and by 400% in islets from starved mice. 7. A threefold function of glucose in the insulin-secretory process is suggested, according to which the decreased islet glucose metabolism is the primary defect in the insulin-secretory mechanism during starvation.

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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