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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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Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

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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.
Insulin and C-peptide are...
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Dipeptidyl Peptidase 4 Inhibitors01:23

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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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Regulation of Food Intake01:30

Regulation of Food Intake

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Short-term regulation of food intake primarily involves neural signals from the gastrointestinal (GI) tract, blood nutrient levels, and GI tract hormones. Communication between the gut and brain via vagal nerve fibers plays a significant role in evaluating the contents of the gut. Clinical studies have shown that protein ingestion produces a more prolonged response in these nerve fibers compared to an equivalent amount of glucose. Additionally, the activation of stretch receptors caused by GI...
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GPCRs Regulate Adenylyl Cylase Activity01:09

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Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
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Hormones Regulating Blood Glucose01:16

Hormones Regulating Blood Glucose

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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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Related Experiment Video

Updated: Apr 6, 2026

Mixed Primary Cultures of Murine Small Intestine Intended for the Study of Gut Hormone Secretion and Live Cell Imaging of Enteroendocrine Cells
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Does GLP-1 suppress its own basal secretion?

Dariush Elahi1, Dennis A Ruff1, Olga D Carlson2

  • 1a ICON Early Phase Services, LLC , San Antonio , TX , USA .

Endocrine Research
|July 18, 2015
PubMed
Summary

Exogenous glucagon-like peptide-1 (GLP-1) administration did not suppress endogenous GLP-1 secretion. This study investigated negative feedback control of incretin release, finding no evidence of such regulation for basal GLP-1 secretion.

Keywords:
GLP-1glucose clampinsulinnegative feedback

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Mechanisms Underlying Gut Hormone Secretion Using the Isolated Perfused Rat Small Intestine
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Area of Science:

  • Endocrinology
  • Metabolic Regulation
  • Hormone Secretion

Background:

  • Negative feedback mechanisms are crucial in endocrine system regulation.
  • Incretins, like glucagon-like peptide-1 (GLP-1), are vital for glucose homeostasis and are of recent research interest.
  • The existence of negative feedback control on incretin secretion itself remains unclear.

Purpose of the Study:

  • To test the hypothesis that administering exogenous glucagon-like peptide-1 (GLP-1) or its metabolite suppresses endogenous GLP-1 release.
  • To investigate the regulatory mechanisms governing incretin secretion.

Main Methods:

  • Evaluated endogenous GLP-1 release using two protocols in lean and obese subjects.
  • Protocol A: Measured GLP-1 levels during GLP-1(9-36) amide infusion.
  • Protocol B: Assessed PYY and GLP-2 as biomarkers for endogenous GLP-1 release during GLP-1(7-36) amide infusion.

Main Results:

  • Plasma levels of GLP-1(7-36) amide did not change during GLP-1(9-36) amide infusion (Protocol A).
  • PYY and GLP-2 levels remained unchanged during GLP-1(7-36) amide infusion (Protocol B).

Conclusions:

  • Negative feedback control, where exogenous hormone infusion inhibits endogenous release, was not observed for basal GLP-1 secretion.
  • The findings suggest that basal GLP-1 secretion may not be regulated by this specific negative feedback loop.