Related Experiment Video

Updated: May 8, 2026

Isolated Pancreatic Islet Treatment and Apoptosis Measurement
09:36

Isolated Pancreatic Islet Treatment and Apoptosis Measurement

Published on: May 2, 2025

Small-molecule inhibition of inflammatory β-cell death

M Lundh1, S S Scully, T Mandrup-Poulsen

  • 1Chemical Biology Program, Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA.

Diabetes, Obesity & Metabolism
|September 6, 2013
PubMed

Insights

Novel small molecules are being developed to protect pancreatic beta cells from apoptosis, addressing a key need in diabetes treatment. These therapies offer potential for new diabetes drugs by preserving beta cell function and mass.

Area of Science:

  • Endocrinology and Metabolism
  • Pharmacology
  • Cell Biology

Background:

  • Rising global diabetes prevalence necessitates innovative treatments.
  • Diabetes pathogenesis involves impaired pancreatic beta-cell function, reduced mass, and apoptosis.
  • Current diabetes therapies do not address progressive beta-cell loss.

Purpose of the Study:

  • To review the development of small-molecule inhibitors targeting beta-cell apoptosis.
  • To explore therapeutic strategies for rescuing beta-cells from cell death.

Main Methods:

  • Review of current research on small-molecule inhibitors.
  • Identification of distinct classes of beta-cell protective agents.
  • Analysis of mechanisms protecting beta-cells from apoptosis.

Main Results:

  • Several classes of small molecules demonstrate protection against inflammatory, oxidative, and metabolic stress-induced apoptosis in beta-cells.
  • These compounds target key pathways involved in beta-cell death.

Conclusions:

  • Small molecules offer a promising avenue for novel diabetes treatments by protecting beta-cells.
  • Beta-cell protective agents, used alone or in combination therapies, represent a significant opportunity for managing diabetes.
Keywords:
apoptosisglucolipotoxicityglucotoxicityinflammationlipotoxicityproinflammatory cytokinessmall-moleculesβ-cell

More Related Videos

Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes12:12

Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes

Published on: June 16, 2011

High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds12:32

High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds

Published on: January 23, 2018

Related Concept Videos

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...
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...
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...
Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

Oral Hypoglycemic Agents: α-Glucosidase Inhibitors

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...
Insulin: Biosynthesis, Chemistry, and Preparation01:25

Insulin: Biosynthesis, Chemistry, and Preparation

The endoplasmic reticulum (ER) of pancreatic β-cells synthesizes preproinsulin, which consists of a signal peptide, A and B chains, and a C-peptide. Preproinsulin is then cleaved and folded into proinsulin, which translocates to the Golgi apparatus for sorting and packaging into secretory granules. In these granules, enzymatic clipping generates insulin and C-peptide.
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment primarily uses...
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab (Humira),...