Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
M I López-Delgado, M Morales, M L Villanueva-Peñacarrillo, W J Malaisse, I Valverd. Effects of glucagon-like peptide 1 on the kinetics of glycogen synthase a in hepatocytes from normal and diabetic rats. Endocrinology. vol 139. issue 6. 1998-06-24. PMID:9607788. |
the activation of glycogen synthase a by either insulin or glp-1 resulted not solely in an increase in maximal velocity but also in a decrease in affinity of the enzyme for uridine diphosphate-glucose; in diabetic animals, the capacity of insulin or glp-1 to increase the maximal velocity and michaelis-menten constant were less marked than in normal rats. |
1998-06-24 |
2023-08-12 |
rat |
C F Deacon, T E Hughes, J J Hols. Dipeptidyl peptidase IV inhibition potentiates the insulinotropic effect of glucagon-like peptide 1 in the anesthetized pig. Diabetes. vol 47. issue 5. 1998-05-27. PMID:9588448. |
glucagon-like peptide 1 (glp-1) has been proposed as a new therapeutic agent in the management of diabetes because of its glucose-dependent stimulation of insulin secretion, but this is limited by its rapid degradation in vivo by dipeptidyl peptidase iv (dpp iv). |
1998-05-27 |
2023-08-12 |
Not clear |
C F Deacon, T E Hughes, J J Hols. Dipeptidyl peptidase IV inhibition potentiates the insulinotropic effect of glucagon-like peptide 1 in the anesthetized pig. Diabetes. vol 47. issue 5. 1998-05-27. PMID:9588448. |
in the basal (nonfasted) state, valine-pyrrolidide potentiated the effect of intravenous glp-1 on the incremental area under the curve (auc) for glucose (-0.50 +/- 0.91 to -2.83 +/- 0.59 20 min x mmol x l(-1); p < 0.05) and insulin (23.8 +/- 30.5 to 332.5 +/- 99.6 20 min x pmol x l(-1); p < 0.05). |
1998-05-27 |
2023-08-12 |
Not clear |
C F Deacon, T E Hughes, J J Hols. Dipeptidyl peptidase IV inhibition potentiates the insulinotropic effect of glucagon-like peptide 1 in the anesthetized pig. Diabetes. vol 47. issue 5. 1998-05-27. PMID:9588448. |
when an intravenous glucose load was given during the glp-1 infusion, valine-pyrrolidide augmented the insulin response (auc, 2,086.2 +/- 600.9 to 6,247.0 +/- 1443.9 40 min x pmol x l(-1); p < 0.05). |
1998-05-27 |
2023-08-12 |
Not clear |
C F Deacon, L B Knudsen, K Madsen, F C Wiberg, O Jacobsen, J J Hols. Dipeptidyl peptidase IV resistant analogues of glucagon-like peptide-1 which have extended metabolic stability and improved biological activity. Diabetologia. vol 41. issue 3. 1998-05-26. PMID:9541166. |
glucagon-like peptide 1 (glp-1) has great potential in diabetes therapy due to its glucose-dependent stimulation of insulin secretion, but this is limited by its rapid degradation, primarily by dipeptidyl peptidase iv. |
1998-05-26 |
2023-08-12 |
Not clear |
L A Scrocchi, B A Marshall, S M Cook, P L Brubaker, D J Drucke. Identification of glucagon-like peptide 1 (GLP-1) actions essential for glucose homeostasis in mice with disruption of GLP-1 receptor signaling. Diabetes. vol 47. issue 4. 1998-05-07. PMID:9568697. |
glucagon-like peptide-1 (glp-1) acts to control blood glucose via multiple mechanisms, including regulation of insulin and glucagon secretion, gastric emptying, satiety, and peripheral insulin sensitivity. |
1998-05-07 |
2023-08-12 |
mouse |
L A Scrocchi, B A Marshall, S M Cook, P L Brubaker, D J Drucke. Identification of glucagon-like peptide 1 (GLP-1) actions essential for glucose homeostasis in mice with disruption of GLP-1 receptor signaling. Diabetes. vol 47. issue 4. 1998-05-07. PMID:9568697. |
we demonstrate here a gene dosage effect for the incretin action of glp-1, as heterozygous glp-1r +/- mice exhibit an abnormal glycemic response to oral glucose challenge in association with reduced circulating levels of glucose-stimulated insulin. |
1998-05-07 |
2023-08-12 |
mouse |
L A Scrocchi, B A Marshall, S M Cook, P L Brubaker, D J Drucke. Identification of glucagon-like peptide 1 (GLP-1) actions essential for glucose homeostasis in mice with disruption of GLP-1 receptor signaling. Diabetes. vol 47. issue 4. 1998-05-07. PMID:9568697. |
despite the demonstration that glp-1 stimulates proinsulin gene transcription, pancreatic insulin mrna transcripts were similar in wild-type and glp-1r -/- mice. |
1998-05-07 |
2023-08-12 |
mouse |
D Flamez, A Van Breusegem, L A Scrocchi, E Quartier, D Pipeleers, D J Drucker, F Schui. Mouse pancreatic beta-cells exhibit preserved glucose competence after disruption of the glucagon-like peptide-1 receptor gene. Diabetes. vol 47. issue 4. 1998-05-07. PMID:9568699. |
previous work suggested that glucagon-like peptide 1 (glp-1) can acutely regulate insulin secretion in two ways, 1) by acting as an incretin, causing amplification of glucose-induced insulin release when glucose is given orally as opposed to intravenous glucose injection; and 2) by keeping the beta-cell population in a glucose-competent state. |
1998-05-07 |
2023-08-12 |
mouse |
D Flamez, A Van Breusegem, L A Scrocchi, E Quartier, D Pipeleers, D J Drucker, F Schui. Mouse pancreatic beta-cells exhibit preserved glucose competence after disruption of the glucagon-like peptide-1 receptor gene. Diabetes. vol 47. issue 4. 1998-05-07. PMID:9568699. |
absence of pancreatic glp-1 receptor function was observed in glp-1 receptor -/- mice, as exemplified by loss of [125i]glp-1 binding to pancreatic islets in situ and by the lack of glp-1 potentiation of glucose-induced insulin secretion from perifused islets. |
1998-05-07 |
2023-08-12 |
mouse |
D Flamez, A Van Breusegem, L A Scrocchi, E Quartier, D Pipeleers, D J Drucker, F Schui. Mouse pancreatic beta-cells exhibit preserved glucose competence after disruption of the glucagon-like peptide-1 receptor gene. Diabetes. vol 47. issue 4. 1998-05-07. PMID:9568699. |
acute glucose competence of the beta-cells, assessed by perifusing islets with stepwise increases of the medium glucose concentration, was well preserved in glp-1 receptor -/- islets in terms of insulin secretion. |
1998-05-07 |
2023-08-12 |
mouse |
D Flamez, A Van Breusegem, L A Scrocchi, E Quartier, D Pipeleers, D J Drucker, F Schui. Mouse pancreatic beta-cells exhibit preserved glucose competence after disruption of the glucagon-like peptide-1 receptor gene. Diabetes. vol 47. issue 4. 1998-05-07. PMID:9568699. |
furthermore, neither islet nor total pancreatic insulin content was significantly changed in the glp-1 receptor -/- mice when compared with age-and sex-matched controls. |
1998-05-07 |
2023-08-12 |
mouse |
D Flamez, A Van Breusegem, L A Scrocchi, E Quartier, D Pipeleers, D J Drucker, F Schui. Mouse pancreatic beta-cells exhibit preserved glucose competence after disruption of the glucagon-like peptide-1 receptor gene. Diabetes. vol 47. issue 4. 1998-05-07. PMID:9568699. |
in conclusion, mouse islets exhibit preserved insulin storage capacity and glucose-dependent insulin secretion despite the loss of functional glp-1 receptors. |
1998-05-07 |
2023-08-12 |
mouse |
J Schirra, K Sturm, P Leicht, R Arnold, B Göke, M Katschinsk. Exendin(9-39)amide is an antagonist of glucagon-like peptide-1(7-36)amide in humans. The Journal of clinical investigation. vol 101. issue 7. 1998-04-23. PMID:9525985. |
the potency of synthetic glp-1 in stimulating insulin secretion and in inhibiting glucagon secretion indicates the putative physiological function of glp-1. |
1998-04-23 |
2023-08-12 |
human |
L Márquez, M A Trapote, M A Luque, I Valverde, M L Villanueva-Peñacarrill. Inositolphosphoglycans possibly mediate the effects of glucagon-like peptide-1(7-36)amide on rat liver and adipose tissue. Cell biochemistry and function. vol 16. issue 1. 1998-04-23. PMID:9580153. |
in skeletal muscle and liver, the action of glp-1 is not associated with an activation of adenylate cyclase, and in cultured murine myocytes and hepatoma cell lines, it was found that glp-1 provokes the generation of inositolphosphoglycan molecules (ipgs), which are considered second messengers of insulin action. |
1998-04-23 |
2023-08-12 |
rat |
L Márquez, M A Trapote, M A Luque, I Valverde, M L Villanueva-Peñacarrill. Inositolphosphoglycans possibly mediate the effects of glucagon-like peptide-1(7-36)amide on rat liver and adipose tissue. Cell biochemistry and function. vol 16. issue 1. 1998-04-23. PMID:9580153. |
in the present work, we document in isolated normal rat adipocytes and hepatocytes that glp-1 exerts a rapid decrease of the radiolabelled glycosylphosphatidylinositols (gpis)--precursors of ipgs--in the same manner as insulin, indicating their hydrolysis and the immediate short-lived generation of ipgs. |
1998-04-23 |
2023-08-12 |
rat |
J Gromada, J J Holst, P Rorsma. Cellular regulation of islet hormone secretion by the incretin hormone glucagon-like peptide 1. Pflugers Archiv : European journal of physiology. vol 435. issue 5. 1998-04-07. PMID:9479010. |
glp-1 modulates insulin, glucagon and somatostatin secretion by binding to guanine nucleotide binding protein-coupled receptors resulting in the activation of adenylate cyclase and generation of cyclic adenosine monophosphate (camp). |
1998-04-07 |
2023-08-12 |
human |
J Gromada, J J Holst, P Rorsma. Cellular regulation of islet hormone secretion by the incretin hormone glucagon-like peptide 1. Pflugers Archiv : European journal of physiology. vol 435. issue 5. 1998-04-07. PMID:9479010. |
the stimulatory action of glp-1 on insulin secretion, contrary to that of the currently used hypoglycaemic sulphonylureas, is glucose dependent and requires the presence of normal or elevated concentrations of the sugar. |
1998-04-07 |
2023-08-12 |
human |
D J Drucke. Glucagon-like peptides. Diabetes. vol 47. issue 2. 1998-04-03. PMID:9519708. |
glp-1 regulates blood glucose via stimulation of glucose-dependent insulin secretion, inhibition of gastric emptying, and inhibition of glucagon secretion. |
1998-04-03 |
2023-08-12 |
Not clear |
Y Wang, H K Kole, C Montrose-Rafizadeh, R Perfetti, M Bernier, J M Ega. Regulation of glucose transporters and hexose uptake in 3T3-L1 adipocytes: glucagon-like peptide-1 and insulin interactions. Journal of molecular endocrinology. vol 19. issue 3. 1998-03-26. PMID:9460645. |
glucagon-like peptide-1 (7-36 amide) (glp-1) is known to increase insulin release when given as a bolus in the fasted and fed state. |
1998-03-26 |
2023-08-12 |
Not clear |