Insulinotropic effects of cholecystokinin, gastric inhibitory polypeptide and glucagon-like peptide-1 during perifusion of short-term cultured canine isolated islets

1995 ◽  
Vol 60 (1) ◽  
pp. 61-67 ◽  
Author(s):  
Michael P.M. van der Burg ◽  
Onno R. Guicherit ◽  
Marijke Frölich ◽  
Hein G. Gooszen
Keyword(s):  
Gastric Inhibitory Polypeptide ◽  
Isolated Islets ◽  
Short Term ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Molecular docking studies and 2D analyses of DPP-4 inhibitors as candidates in the treatment of diabetes

2015 ◽  
Vol 11 (11) ◽  
pp. 3188-3193 ◽  
Author(s):  
Simone Queiroz Pantaleão ◽  
Vinicius Gonçalves Maltarollo ◽  
Sheila Cruz Araujo ◽  
Jadson Castro Gertrudes ◽  
Kathia Maria Honorio
Keyword(s):  
Molecular Docking ◽  
Glycemic Control ◽  
Gastric Inhibitory Polypeptide ◽  
Docking Studies ◽  
Molecular Docking Studies ◽  
Insulin Levels ◽  
Biological Target ◽  
Treatment Of Diabetes ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

DPP-4 is an important biological target related to the treatment of diabetes since some inhibitors can lead to an increase in the insulin levels and the prolonged activity of glucagon-like peptide-1 and gastric inhibitory polypeptide, being effective in glycemic control.

Hypersecretion of Truncated Glucagon-like Peptide-1 and Gastric Inhibitory Polypeptide in Obese Patients

1993 ◽  
Vol 10 (1) ◽  
pp. 44-49 ◽  
Author(s):  
N. Fukase ◽  
M. Igarashi ◽  
H. Takahashi ◽  
H. Manaka ◽  
K. Yamatani ◽  
...  
Keyword(s):  
Gastric Inhibitory Polypeptide ◽  
Obese Patients ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals Circulating glucagon-like peptide-1 increases in response to short-term overfeeding in men

2013 ◽  
Vol 10 (1) ◽  
pp. 33 ◽  
Author(s):  
Danny Wadden ◽  
Farrell Cahill ◽  
Peyvand Amini ◽  
Edward Randell ◽  
Sudesh Vasdev ◽  
...  
Keyword(s):  
Short Term ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Pharmacophore modeling and molecular docking studies of acridines as potential DPP-IV inhibitors

2015 ◽  
Vol 93 (7) ◽  
pp. 721-729
Author(s):  
R. Abu Khalaf ◽  
Z. Jarekji ◽  
T. Al-Qirim ◽  
D. Sabbah ◽  
G. Shattat
Keyword(s):  
Type 2 Diabetes ◽  
Gastric Inhibitory Polypeptide ◽  
Pharmacophore Modeling ◽  
Docking Studies ◽  
Glucose Levels ◽  
Dpp Iv ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Circulating Levels

Inhibition of dipeptidyl peptidase-IV (DPP-IV) prevents the inactivation of gastric inhibitory polypeptide (GIP) and glucagon-like peptide–1 (GLP-1). This increases circulating levels of active GLP-1 and GIP and stimulates insulin secretion, which results in lowering of glucose levels and improvement of the glycemic control in patients with type 2 diabetes. In this study, pharmacophore modeling and docking experiments were carried out and a series of eight novel 2-ethoxy-6,9-disubstituted acridines (13, 15, and 17a–17f) have been designed and synthesized. Then, these compounds were evaluated for their ability to inhibit DPP-IV. Most of the synthesized compounds were proven to have anti-DPP-IV activity where compound 17b displayed the best activity of 43.8% inhibition at 30 μmol/L concentration. Results of this work might be helpful for further optimization to develop more potent DPP-IV inhibitors.

Regulation of glucagon-like peptide-1 secretion from rat ileum by neurotransmitters and peptides

1995 ◽  
Vol 147 (1) ◽  
pp. 25-31 ◽  
Author(s):  
C Herrmann-Rinke ◽  
A Vöge ◽  
M Hess ◽  
B Göke
Keyword(s):  
Gastric Inhibitory Polypeptide ◽  
Aminobutyric Acid ◽  
Arterial Infusion ◽  
Incretin Hormone ◽  
Rat Ileum ◽  
Calcitonin Gene ◽  
Glucagon Like Peptide ◽  
Complex Regulation ◽  
Glucagon Like Peptide 1 ◽  
Stimulation Of

Abstract Food ingestion induces a rapid increase in the insulinotropic glucagon-like peptide-1 (GLP-1) in plasma. Paradoxically, GLP-1 originates from the lower intestines and therefore a complex regulation of postprandial GLP-1 secretion must exist. This was addressed in the present study by utilizing an isolated vascularly perfused rat ileum preparation. Peptides and neurotransmitters thought to be candidate mediators triggering GLP-1 secretion were arterially infused and GLP-1 was measured in the venous effluent. Arterial infusion of cholinergic agonists strongly enhanced GLP-1 secretion which was counteracted by the addition of atropine. Histamine, dopamine, 5-hydoxytryptamine, γ-aminobutyric acid, and norepinephrine had no effect. Peptides of the bombesin family were strong stimulants whereas tachykinins, enkephalins, dynorphin, TRH, calcitonin-gene-related peptide and members of the secretin family, vasoactive intestinal peptide, peptide histidine isoleucine and neuropeptide Y, were less effective. The second incretin hormone, gastric inhibitory polypeptide (GIP), was the most potent stimulant of GLP-1 secretion in our study. It enhanced GLP-1 release up to sixfold above basal during the early phase followed by a sustained secretion at 400% above basal. This stimulation remained unaffected by atropine. In conclusion, in addition to luminal stimulation of nutrients, a cholinergic impulse as well as peptidergic mediators (among them possibly GIP and GRP) may have an impact on postprandial GLP-1 secretion from the rat ileum. Journal of Endocrinology (1995) 147, 25–31

Reduced gastric inhibitory polypeptide but normal glucagon-like peptide 1 response to oral glucose in postmenopausal women with impaired glucose tolerance

1997 ◽  
pp. 127-131 ◽  
Author(s):  
B Ahren ◽  
H Larsson ◽  
JJ Holst
Keyword(s):  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Postmenopausal Women ◽  
Plasma Levels ◽  
Insulin Response ◽  
Gastric Inhibitory Polypeptide ◽  
Oral Glucose ◽  
Glucose Ingestion ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

OBJECTIVE: The gastrointestinal hormones, gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1), are both released from the gut after oral glucose ingestion and stimulate insulin secretion. This study examined the release of these hormones in subjects with impaired glucose tolerance (IGT), which precedes the development of non-insulin-dependent diabetes. DESIGN AND METHODS: Six postmenopausal women with IGT, aged 59 years, underwent a 75 g oral glucose tolerance test and plasma levels of GIP and GLP-1 were determined regularly during the following 2 h. The results were compared with those in seven age- and weight-matched women with normal glucose tolerance (NGT). RESULTS: Basal plasma levels of GIP and GLP-1 were not different between the groups. In response to the oral glucose ingestion, plasma levels of both GIP and GLP-1 increased in both groups. The plasma GIP increase after glucose ingestion was, however, reduced in women with IGT. Thus, the GIP response as determined as the area under the curve for the 60 min after oral glucose was 34.8 +/- 3.2 pmol/l per min in women with IGT versus 56.4 +/- 7.8 pmol/l per min in those with NGT (P = 0.021). In contrast, the GLP-1 response to oral glucose was not different between the groups. By definition, the glucose response to oral glucose was markedly increased in women with IGT, and the insulin response during the second hour after glucose ingestion was exaggerated. CONCLUSIONS: The GIP response to oral glucose is impaired in postmenopausal women with IGT, whereas the plasma GLP-1 response is not affected.

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