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Academic phase 1 study which investigates the effects of the two incretin hormones glucose-insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1) on gastric emptying, appetite, insulin release and glucose disposal in the body. The hypothesis is that incretin hormones not only stimulate insulin release but also inhibits gastric emptying. This effect can be utilized for further drug development.
Effects of GIP and GLP-1 on gastric emptying, appetite control and insulin release in relation to glucose levels in the bloodstream. Infusions of GIP and GLP-1 are given under simultaneous gastric emptying study and appetite questionnaires and blood sampling for analysis of insulin, glucose, and other gut hormones such as glucagon, ghrelin, and PYY, as well as those administered, GIP and GLP-1.
Allocation: Randomized, Control: Placebo Control, Endpoint Classification: Pharmacodynamics Study, Intervention Model: Crossover Assignment, Masking: Double Blind (Subject, Outcomes Assessor), Primary Purpose: Basic Science
Glucose-insulinotropic peptide, Glucagon-like peptide-1
Karolinska University Hospital
Published on BioPortfolio: 2014-08-27T03:15:30-0400
The incretin effect is attenuated in patients with type 2 diabetes mellitus partly due to impaired potentiation of beta-cell responsiveness to glucose by glucose dependent insulinotropic p...
The purpose of this study is to test the safety of glucose-dependent insulinotropic peptide (GIP)/GIP Analog on people with Type 2 Diabetes.
study hypothesis: treatment with GLP-1 and/or GIP is able to potentiate the maximal stimulated insulin secretion even in c-peptide negative type-1 diabetic patients classified as having no...
The purpose of this study is to determine whether Glucose-dependent Insulinotropic Polypeptide (GIP) or Glucagon Like Peptide 2 (GLP-2) has an affect on the secretion of Glucagon from the ...
The ability of glucagon-like peptide 1 to enhance beta-cell responsiveness to I.v. glucose is impaired in patients with type 2 diabetes mellitus compared with healthy individuals. We inves...
To establish whether incretin hormones affect insulin clearance, the aim of this study was to assess insulin clearance in mice with genetic deletion of receptors for both glucagon-like peptide-1 (GLP-...
Postprandial glucose is reduced in malnourished patients with anorexia nervosa (AN), but the mechanisms and duration for this remain unclear. We examined blood glucose, gastric emptying and glucoregul...
We previously demonstrated that infusion of an intestinal peptide called xenin-25 (Xen) amplifies the effects of glucose-dependent insulinotropic polypeptide (GIP) on insulin secretion rates (ISRs) an...
Equine insulin dysregulation (ID) is a common and poorly understood disorder that increases the risk of laminitis. Recent data show that the condition may be associated with alteration of the enteroin...
Insulin secretion declines with age and this contributes to the increased risk of developing impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM) in older subjects. Insulin secretion i...
A peptide of 36 or 37 amino acids that is derived from PROGLUCAGON and mainly produced by the INTESTINAL L CELLS. GLP-1(1-37 or 1-36) is further N-terminally truncated resulting in GLP-1(7-37) or GLP-1-(7-36) which can be amidated. These GLP-1 peptides are known to enhance glucose-dependent INSULIN release, suppress GLUCAGON release and gastric emptying, lower BLOOD GLUCOSE, and reduce food intake.
A pyrazine-derived DIPEPTIDYL-PEPTIDASE IV INHIBITOR and HYPOGLYCEMIC AGENT that increases the levels of the INCRETIN hormones GLUCAGON-LIKE PEPTIDE-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). It is used in the treatment of TYPE 2 DIABETES.
A receptor for GLUCAGON-LIKE PEPTIDE 2 (GLP-2) that is expressed on the surface of intestinal cells as well as neural cells. GLP-2 and other peptides act through GLP-2R to regulate cellular responses to BLOOD GLUCOSE, INFLAMMATION, and FOOD INTAKE.
A receptor for GLUCAGON-LIKE PEPTIDE 1 (GLP-1) expressed primarily on the surface of beta and ductal exocrine cells of the pancreas, as well as cells of other tissues. GLP-1 acts through GLP-1R to potentiate signaling in pancreatic cells in response to glucose-stimulated insulin secretion (GSIS).
Peptides derived from proglucagon which is also the precursor of pancreatic GLUCAGON. Despite expression of proglucagon in multiple tissues, the major production site of glucagon-like peptides (GLPs) is the INTESTINAL L CELLS. GLPs include glucagon-like peptide 1, glucagon-like peptide 2, and the various truncated forms.
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