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Related Concept Videos

Glucagon-like Receptor Agonists01:24

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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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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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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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α-glucosidase inhibitors, including acarbose (Precose), miglitol (Glyset), and voglibose (Voglib) (primarily available in Asia), are drugs that control blood sugar levels by delaying the digestion of starch and disaccharides. They achieve this by inhibiting α-glucosidase enzymes in the intestine, which slow the absorption of carbohydrates in the intestine, which in turn leads to a prolonged release of the glucoregulatory hormone GLP-1 from intestinal L-cells.
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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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Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
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Related Experiment Video

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A Model of Chronic Nutrient Infusion in the Rat
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Glucolipotoxicity and GLP-1 secretion.

Jung-Hee Hong1, Dae-Hee Kim2, Moon-Kyu Lee3

  • 1Division of Endocrinology & Metabolism, Samsung Biomedical Research Institute, Seoul, South Korea.

BMJ Open Diabetes Research & Care
|February 25, 2021
PubMed
Summary
This summary is machine-generated.

Chronic glucolipotoxicity impairs glucagon-like peptide-1 (GLP-1) secretion by affecting L-cells and beta-cells. This study reveals the molecular mechanisms and suggests an early interrelationship between L-cell and beta-cell dysfunction.

Keywords:
blood glucoseglucagon-like peptide 1insulinlipids

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Related Experiment Videos

Last Updated: Nov 16, 2025

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Area of Science:

  • Endocrinology
  • Metabolic Research
  • Cell Biology

Background:

  • Glucolipotoxicity, resulting from elevated glucose and fatty acids, detrimentally impacts cellular function.
  • Glucagon-like peptide-1 (GLP-1) plays a crucial role in glucose homeostasis and insulin secretion.
  • Understanding the effects of glucolipotoxicity on GLP-1 secretion is vital for metabolic disease research.

Purpose of the Study:

  • To investigate the impact of chronic glucolipotoxicity on GLP-1 secretion in enteroendocrine L-cells.
  • To elucidate the underlying molecular mechanisms and signaling pathways affected by glucolipotoxicity.
  • To examine the in vivo effects of nutrient infusion on GLP-1 secretion and glucose metabolism in rats.

Main Methods:

  • Human NCI-H716 cells were exposed to high glucose and palmitate to induce glucolipotoxicity.
  • Gene expression, protein levels, glucose uptake, and cellular metabolites were analyzed.
  • A rat model of chronic nutrient infusion was used to assess in vivo effects on GLP-1 secretion and glucose tolerance.

Main Results:

  • Chronic glucolipotoxicity reduced GLP-1 secretion, glucose transporter expression, and NADPH levels in L-cells.
  • Key signaling molecules (pCREB, pGSK3β, β-catenin, TCF7L2) and ATP levels were decreased, while oxidative stress markers increased.
  • In vivo, nutrient infusion impaired GLP-1 secretion, glucose tolerance, and insulin secretion in rats.

Conclusions:

  • Glucolipotoxicity adversely affects GLP-1 secretion via alterations in glucose/lipid metabolism and gene expression.
  • The study highlights an early interrelationship between L-cell and beta-cell glucolipotoxicity.
  • These findings offer insights into the pathogenesis of metabolic disorders associated with dysregulated glucose and lipid metabolism.