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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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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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Oral Hypoglycemic Agents: Glinides01:06

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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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Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

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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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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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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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Does glucose lowering restore GIP effects on insulin secretion?

Eleonora Grespan1, Andrea Mari1

  • 1Institute of Neuroscience, National Research Council, Padua, Italy.

Nutrition, Metabolism, and Cardiovascular Diseases : NMCD
|January 29, 2023
PubMed
Summary

In type 2 diabetes, glucose-dependent insulinotropic polypeptide (GIP) action is impaired but can recover with glucose lowering. This effect is significant only when glucose levels are near normal, potentially explaining the success of dual GIP-GLP-1 receptor agonists.

Keywords:
GIP receptorGIP receptor AgonistsGlucose-dependent insulinotropic polypeptideInsulin secretionType 2 diabetes

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Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Pharmacology

Background:

  • Impaired insulin secretion to glucose-dependent insulinotropic polypeptide (GIP) is observed in type 2 diabetes.
  • Dual GIP-GLP-1 receptor agonists show enhanced efficacy over single GLP-1 agonists, prompting renewed interest in GIP action.
  • Contrasting evidence exists regarding the restoration of GIP action with glucose lowering in type 2 diabetes.

Purpose of the Study:

  • To re-evaluate existing literature on GIP action potentiation in type 2 diabetes.
  • To analyze the impact of glucose lowering on GIP efficacy using a uniform methodology.
  • To reconcile conflicting findings on GIP action recovery.

Main Methods:

  • Systematic review and meta-analysis of relevant publications.
  • Application of a standardized analytical approach to diverse datasets.
  • Comparative analysis of GIP efficacy under varying glucose concentrations.

Main Results:

  • Heterogeneous analysis methods contributed to some contradictions in previous studies.
  • A coherent interpretation of available data indicates GIP action recovery is significant only at near-normal glucose concentrations.
  • Glucose lowering is crucial for restoring GIP efficacy, but only under specific glycemic conditions.

Conclusions:

  • Traditional diabetes treatments may not substantially restore GIP action.
  • Restoration of GIP action becomes relevant when glucose levels are virtually normalized.
  • The improved GIP action at normalized glucose may partially explain the clinical success of dual GIP-GLP-1 receptor agonists.