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Related Concept Videos

Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

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Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
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The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
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Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

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Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a...
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Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

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Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but...
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Oral Hypoglycemic Agents: Glinides01:06

Oral Hypoglycemic Agents: Glinides

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Repaglinide (Prandin) and Nateglinide (Starlix), known as glinides, are oral insulin secretagogues that stimulate insulin release from pancreatic β cells by closing the ATP-sensitive potassium channels (KATP channel). Repaglinide controls insulin release from pancreatic β cells by managing potassium efflux. It shares two binding sites with sulfonylureas and also has a unique site, indicating overlapping mechanisms of action. With a rapid onset and a 4-7 hour duration, it effectively...
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Hormones Regulating Blood Glucose01:16

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Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
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Updated: May 24, 2025

Homogeneous Time-resolved Förster Resonance Energy Transfer-based Assay for Detection of Insulin Secretion
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Glucose-dependent insulinotropic polypeptide (GIP).

Timo D Müller1, Alice Adriaenssens2, Bo Ahrén3

  • 1Institute for Diabetes and Obesity, Helmholtz Munich, Germany; German Center for Diabetes Research, DZD, Germany; Walther-Straub Institute for Pharmacology and Toxicology, Ludwig-Maximilians-University Munich (LMU), Germany.

Molecular Metabolism
|March 2, 2025
PubMed
Summary
This summary is machine-generated.

Glucose-dependent insulinotropic polypeptide (GIP) is a key incretin hormone. Recent research shows GIP receptor modification offers therapeutic potential for obesity, diabetes, and other disorders.

Keywords:
DiabetesGIPGLP-1IncretinInsulinObesity

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Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Pharmacology

Background:

  • Glucose-dependent insulinotropic polypeptide (GIP) is the first identified incretin hormone, crucial for glucose tolerance.
  • GIP has been less therapeutically developed than glucagon-like peptide-1 (GLP-1) for diabetes and obesity.
  • Renewed interest in GIP stems from evidence suggesting GIP receptor agonism/antagonism benefits metabolic disorders.

Purpose of the Study:

  • To provide a comprehensive review of GIP biology.
  • To explore the therapeutic implications of modifying GIP receptor signaling.

Main Methods:

  • Literature review of GIP biology.
  • Analysis of pharmacological studies on GIP receptor modulation.

Main Results:

  • GIP exhibits pleiotropic metabolic effects beyond the endocrine pancreas.
  • GIP receptor signaling modification shows promise in preclinical and clinical studies.

Conclusions:

  • GIP is a versatile hormone with significant metabolic roles.
  • Targeting GIP receptor signaling presents therapeutic opportunities for obesity, diabetes, nausea, and neurodegenerative diseases.