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Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

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 the...
Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

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 significant...
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.
Acarbose and miglitol are typically...
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
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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 manages...
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Isolated Pancreatic Islet Treatment and Apoptosis Measurement
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Published on: May 2, 2025

Interleukin-1 antagonists for diabetes.

Thomas Mandrup-Poulsen1,

  • 1University of Copenhagen, Panum Institute (12.2.10), Faculty of Health and Medical Sciences, Department of Biomedical Sciences, Section for Endocrinological Research, Blegdamsvej 3, DK-2200 Copenhagen N, Denmark. tmpo@sund.ku.dk

Expert Opinion on Investigational Drugs
|May 28, 2013
PubMed
Summary

Interleukin-1 (IL-1) antagonists show potential for treating diabetes by targeting inflammation, but results vary. Further research is needed to confirm their efficacy in type 1 and type 2 diabetes.

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Area of Science:

  • Endocrinology
  • Immunology
  • Metabolic Diseases

Background:

  • Diabetes mellitus is a growing global health crisis with limited curative treatments.
  • Current therapies manage symptoms and complications but do not address underlying pathogenetic mechanisms.
  • Chronic inflammation plays a key role in beta-cell dysfunction and insulin resistance.

Purpose of the Study:

  • To explore the potential of anti-inflammatory biologics, specifically Interleukin-1 (IL-1) antagonists, as novel therapeutic interventions for diabetes.
  • To evaluate the clinical proof-of-concept for targeting pro-inflammatory cytokines in diabetes management.

Main Methods:

  • Review of clinical trial data for IL-1 antagonists in type 1 and type 2 diabetes.
  • Analysis of molecular pathways linking inflammation to beta-cell failure and insulin resistance.
  • Assessment of the impact of anti-inflammatory biologics on diabetes progression and complications.

Main Results:

  • Phase IIa trials of IL-1 antagonists in recent-onset type 1 diabetes did not meet primary endpoints.
  • Promising Phase I and IIa results in type 2 diabetes require further Phase III confirmation.
  • Observed treatment responses are variable, potentially linked to diabetes sub-phenotypes.

Conclusions:

  • IL-1 antagonists represent a potential therapeutic avenue for diabetes, targeting key inflammatory pathways.
  • Further investigation and Phase III trials are essential to validate efficacy and identify patient subgroups who benefit most.
  • Understanding diabetes heterogeneity is crucial for optimizing the use of targeted anti-inflammatory therapies.