Information om | Engelska ordet GLP-1

Exempel på hur man kan använda GLP-1 i en mening

• With the exception of insulin, most GLP-1 receptor agonists (liraglutide, exenatide, and others), and pramlintide, all diabetes medications are administered orally and are thus called oral hypoglycemic agents or oral antihyperglycemic agents.
• Although many earlier drugs were stimulants such as amphetamines, in the early 2020s, GLP-1 receptor agonists became popular for weight loss.
• Some incretins (GLP-1) also inhibit glucagon release from the alpha cells of the islets of Langerhans.
• GIP, along with glucagon-like peptide-1 (GLP-1), belongs to a class of molecules referred to as incretins, which stimulate insulin release on oral food intake.
• GLP-2 is created by specific post-translational proteolytic cleavage of proglucagon in a process that also liberates the related glucagon-like peptide-1 (GLP-1).
• In synergy with endogenous amylin, pramlintide aids in the regulation of blood glucose by slowing gastric emptying, promoting satiety via hypothalamic receptors (different receptors than for GLP-1), and inhibiting inappropriate secretion of glucagon, a catabolic hormone that opposes the effects of insulin and amylin.
• Exenatide is a glucagon-like peptide-1 receptor agonist (GLP-1 receptor agonist) also known as incretin mimetics.
• Vildagliptin inhibits the inactivation of GLP-1 by DPP-4, allowing GLP-1 and GIP to potentiate the secretion of insulin in the beta cells and suppress glucagon release by the alpha cells of the islets of Langerhans in the pancreas.
• Glucagon-like peptide-1 (GLP-1) is a 30- or 31-amino-acid-long peptide hormone deriving from the tissue-specific posttranslational processing of the proglucagon peptide.
• Different GLP-1 receptor agonists go through inactivation by dipeptidyl peptidase-4 (DPP-4) enzymes (The clinical use of GLP-1 is hampered by its short-half life in the circulation (1-2 min), because of its proteolytic degradation by the enzymes dipeptidyl peptidase-4 (DPP-4) and neutral endopeptidase).
• Studies of Epac2 knockout mice indicate that Epac-mediated signaling is required for potentiation of insulin secretion by incretins (gut hormones released from enteroendocrine cells following meal ingestion) such as glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide, In heart, chronic stimulation of β-adrenergic receptor is known to progress to arrhythmia through an Epac2-dependent mechanism.
• Liraglutide is a glucagon-like peptide-1 receptor agonist (GLP-1 receptor agonist) also known as incretin mimetics.
• GLP-1 - Functions as an "Ileal Brake" to inhibit upper GI tract motility when the distal gut is exposed to unabsorbed nutrients.
• Glucagon-like peptide-1 (GLP-1) receptor agonists, also known as GLP-1 analogs, GLP-1DAs or incretin mimetics, are a class of anorectic drugs that reduce blood sugar and energy intake by activating the GLP-1 receptor.
• Taspoglutide is a former experimental drug, a glucagon-like peptide-1 agonist (GLP-1 agonist), that was under investigation for treatment of type 2 diabetes and being codeveloped by Ipsen and Roche.
• Resistant starch dilutes energy density of food intake, maintains a bulking effect similar to non-fermentable fiber, and increases the expression of gut hormones PYY and GLP-1.
• demonstrated that the GLP-1 receptor agonists liraglutide and lixisenatide which are on the market as treatments for type 2 diabetes show promise as potential drug treatments of Alzheimer disease AD.
• Glucose lowering effects of DPP-4 inhibitors are mainly mediated by GLP-1 and gastric inhibitory polypeptide (GIP) incretin hormones which are inactivated by DPP-4.
• In early dumping syndrome, pancreatic glucagon is augmented in the early postprandial period, probably through stimulation the catecholamines involved in the generalized autonomic surge induced by the osmotic load, but at 120 min, when most of the hypoglycemias are encountered, pancreatic glucagon is no longer detectable, likely through inhibition by GLP-1.
• A 2017 meta-analysis did not support the suggestion that treatment with GLP-1 agonists or DPP-4 inhibitors increased all-cause mortality in type 2 diabetics.

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