Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

294
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...
294
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

6.1K
Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
6.1K
Oral Hypoglycemic Agents: Glinides01:06

Oral Hypoglycemic Agents: Glinides

136
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...
136
Hormones Regulating Blood Glucose01:16

Hormones Regulating Blood Glucose

3.0K
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...
3.0K
Protein Kinases and Phosphatases02:54

Protein Kinases and Phosphatases

13.0K
Proteins undergo chemical modifications that trigger changes in the charge, structure, and conformation of the proteins. Phosphorylation, acetylation, glycosylation, nitrosylation, ubiquitination, lipidation, methylation, and proteolysis are various protein modifications that regulate protein activity. Such modifications are usually enzyme-driven.
Protein kinases
Many proteins in the cell are regulated by phosphorylation, the addition of a phosphate group. A family of enzymes called kinases...
13.0K
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

1.1K
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...
1.1K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Schisandrin a Alleviates Ulcerative Colitis by Modulating Gut Microbiota and ALOX15-Mediated Ferroptosis.

Journal of agricultural and food chemistry·2026
Same author

Risk factors for surgical site infection following posterior internal fixation of thoracolumbar fractures.

Frontiers in surgery·2026
Same author

Absence of osteoclastogenic response to pooled polyclonal anti-citrullinated peptide/protein antibodies from patients with rheumatoid arthritis in vitro.

Clinical and experimental medicine·2026
Same author

Effect of Nutrient Enrichment on Alpha and Beta Diversity of Macroinvertebrate Community in a Boreal River of Northern China.

Biology·2026
Same author

Mechanism of Chitosan Oligosaccharides in Inhibiting <i>Phytophthora infestans</i> and Synergistic Enhancement with Conventional Fungicides: A Strategy for the Management of Potato Late Blight.

Journal of agricultural and food chemistry·2026
Same author

Neurotransmitters in memory destabilization: An integrative perspective framed by prediction error and novelty.

Cognitive, affective & behavioral neuroscience·2026

Related Experiment Video

Updated: May 30, 2025

Modeling an Enzyme Active Site using Molecular Visualization Freeware
14:37

Modeling an Enzyme Active Site using Molecular Visualization Freeware

Published on: December 25, 2021

9.6K

Glucokinase and glucokinase activator.

Changhong Li1, Yi Zhang2, Li Chen2

  • 1Nanjing AscendRare and Hua Medicine, Nanjing, Jiangsu 210000, China.

Life Metabolism
|January 28, 2025
PubMed
Summary

Glucokinase (GK) dysfunction contributes to Type 2 diabetes. New GK activators, like dorzagliatin, show promise in repairing pancreatic and liver defects, offering hope for T2D treatment.

Keywords:
Type 2 diabetesglucokinase activatorglucokinasesglucose homeostasisliverpancreatic β cells

More Related Videos

Measuring Relative Insulin Secretion using a Co-Secreted Luciferase Surrogate
05:58

Measuring Relative Insulin Secretion using a Co-Secreted Luciferase Surrogate

Published on: June 25, 2019

7.4K
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

14.0K

Related Experiment Videos

Last Updated: May 30, 2025

Modeling an Enzyme Active Site using Molecular Visualization Freeware
14:37

Modeling an Enzyme Active Site using Molecular Visualization Freeware

Published on: December 25, 2021

9.6K
Measuring Relative Insulin Secretion using a Co-Secreted Luciferase Surrogate
05:58

Measuring Relative Insulin Secretion using a Co-Secreted Luciferase Surrogate

Published on: June 25, 2019

7.4K
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

14.0K

Area of Science:

  • Biochemistry
  • Endocrinology
  • Metabolic Diseases

Background:

  • Glucokinase (GK) is essential for glucose homeostasis, acting as a glucose sensor in pancreatic islets and the liver.
  • Dysfunctional GK, either loss-of-function (hyperglycemia) or gain-of-function (hypoglycemia), significantly impacts glucose metabolism.
  • Progressive loss of GK at mRNA and protein levels in islets and liver is hypothesized as a key mechanism in Type 2 diabetes (T2D) pathogenesis.

Purpose of the Study:

  • To explore the role of Glucokinase (GK) in Type 2 diabetes (T2D) pathogenesis.
  • To review the development of Glucokinase activators (GKAs) as a therapeutic strategy for T2D.
  • To highlight the potential of novel GKAs, exemplified by dorzagliatin, in addressing underlying defects in T2D.

Main Methods:

  • Review of existing literature on Glucokinase function and its role in diabetes.
  • Analysis of the mechanisms behind early Glucokinase activator (GKA) development failures.
  • Evaluation of the therapeutic potential and success of dorzagliatin in T2D treatment.

Main Results:

  • Glucokinase (GK) dysfunction is implicated in hyperglycemia and hypoglycemia.
  • Early Glucokinase activator (GKA) development was hindered by incomplete understanding of their mechanism of action.
  • Dorzagliatin demonstrates success in T2D treatment, suggesting a viable model for GK-based therapies.

Conclusions:

  • Glucokinase (GK) plays a critical role in glucose regulation, and its progressive loss is linked to Type 2 diabetes (T2D).
  • The development of effective Glucokinase activators (GKAs) offers a promising therapeutic avenue for T2D.
  • Dorzagliatin's success validates the strategy of targeting GK to repair pancreatic and liver defects in T2D patients.