Related Experiment Video

Updated: Aug 24, 2026

Assessing Replication and Beta Cell Function in Adenovirally-transduced Isolated Rodent Islets
09:31

Assessing Replication and Beta Cell Function in Adenovirally-transduced Isolated Rodent Islets

Published on: June 25, 2012

Long-term beneficial effects of vanadate, tungstate, and molybdate on insulin secretion and function of cultured beta

Hui-Kang Liu1, Brian D Green, Neville H McClenaghan

  • 1School of Biomedical Sciences, University of Ulster, Coleraine, Northern Ireland, UK.

Pancreas
|April 21, 2004
PubMed

Insights

Ultratrace elements like vanadate, tungstate, and molybdate show promise for managing diabetes. Studies on pancreatic beta cells reveal these elements can improve insulin secretion and glucose response, potentially aiding antihyperglycemic action.

Area of Science:

  • Biochemistry
  • Endocrinology
  • Cell Biology

Background:

  • Ultratrace elements (vanadate, tungstate, molybdate) demonstrate antihyperglycemic properties in diabetic animal models.
  • The specific impact of these elements on pancreatic beta cell function remains incompletely understood.

Purpose of the Study:

  • To investigate the effects of vanadate, tungstate, and molybdate on pancreatic beta cell function.
  • To determine if these ultratrace elements influence insulin content and secretion in beta cells.

Main Methods:

  • Clonal BRIN BD11 cells were cultured with varying doses of vanadate, tungstate, and molybdate.
  • Cellular insulin content and glucose-induced insulin secretion were measured.
  • Effects on insulin secretion mediated by protein kinase A (PKA) and protein kinase C (PKC) were assessed.

Main Results:

  • Vanadate (4 µmol/L) enhanced glucose-stimulated insulin secretion without altering insulin content but desensitized PKA/PKC-mediated secretion.
  • Tungstate (300 µmol/L) and molybdate (1 mmol/L) increased cellular insulin content and improved basal and stimulated insulin release.
  • These elements enhanced beta cell responsiveness to glucose and other secretagogues.

Conclusions:

  • Ultratrace elements significantly impact pancreatic beta cell function.
  • These effects on insulin secretion and responsiveness may underlie the observed antihyperglycemic actions of vanadate, tungstate, and molybdate.

More Related Videos

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

Sustained Administration of β-cell Mitogens to Intact Mouse Islets Ex Vivo Using Biodegradable Poly(lactic-co-glycolic acid) Microspheres09:31

Sustained Administration of β-cell Mitogens to Intact Mouse Islets Ex Vivo Using Biodegradable Poly(lactic-co-glycolic acid) Microspheres

Published on: November 5, 2016

Related Concept Videos

Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
Oral Hypoglycemic Agents: Biguanides and Glitazones01:26

Oral Hypoglycemic Agents: Biguanides and Glitazones

Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood glucose levels...
Hormones Regulating Blood Glucose01:16

Hormones Regulating Blood Glucose

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.
In addition to accelerating glucose uptake and utilization, insulin has...
Oral Hypoglycemic Agents: Glinides01:06

Oral Hypoglycemic Agents: Glinides

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...
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

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 co-secreted in...
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...