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

Feedback Regulation of Calcium Concentration01:27

Feedback Regulation of Calcium Concentration

3.4K
Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...
3.4K
Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

5.1K
Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
5.1K
Synthesis and Functions of Calcitonin00:51

Synthesis and Functions of Calcitonin

1.8K
Calcitonin, a vital polypeptide hormone, regulates calcium levels within body fluids. It is released by the parafollicular cells, also known as C cells, situated in the follicular epithelium of the thyroid gland. Calcitonin responds to fluctuations in blood calcium levels and the influence of gastrointestinal hormones like gastrin and cholecystokinin.
The exact mechanisms by which calcitonin operates in calcium homeostasis remain elusive, but its significance is evident in several vital...
1.8K
Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

4.9K
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...
4.9K
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

2.2K
Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
2.2K
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

5.5K
Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
5.5K

You might also read

Related Articles

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

Sort by
Same author

Towards the construction of a virtual yeast.

Nature·2026
Same author

Author Correction: Long-term, in toto live imaging of cardiomyocyte behaviour during mouse ventricle chamber formation at single-cell resolution.

Nature cell biology·2026
Same author

Construction of an actin cytoskeleton-related gene signature for predicting prognosis and therapeutic response in glioblastoma: based on machine learning.

Translational cancer research·2026
Same author

ANXA11 suppression restores muscular function in the mdx mouse model of Duchenne muscular dystrophy (DMD).

Nature communications·2026
Same author

Identification of hsa-miR-144-3p as a novel immunotherapeutic target for glioblastoma based on disulfidptosis-related analysis.

Discover oncology·2026
Same author

Non-invasive CT-based Deep Learning for Human Papillomavirus Status Prediction in Oropharyngeal Cancer.

Academic radiology·2026

Related Experiment Video

Updated: Jun 27, 2025

Analysis of Beta-cell Function Using Single-cell Resolution Calcium Imaging in Zebrafish Islets
08:50

Analysis of Beta-cell Function Using Single-cell Resolution Calcium Imaging in Zebrafish Islets

Published on: July 3, 2018

14.8K

Galectin-3 impairs calcium transients and β-cell function.

Qian Jiang1,2,3, Qijin Zhao1,2,3, Yibing Chen1,2,3

  • 1State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100050, China.

Nature Communications
|May 1, 2024
PubMed
Summary
This summary is machine-generated.

Galectin-3 (Gal3), elevated in diabetes, impairs insulin secretion by affecting calcium channels in pancreatic beta cells. Inhibiting Gal3 improves glucose control, suggesting it as a therapeutic target for type 2 diabetes.

More Related Videos

Imaging Calcium Dynamics in Subpopulations of Mouse Pancreatic Islet Cells
08:03

Imaging Calcium Dynamics in Subpopulations of Mouse Pancreatic Islet Cells

Published on: November 26, 2019

8.2K
Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
11:00

Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes

Published on: September 18, 2017

10.1K

Related Experiment Videos

Last Updated: Jun 27, 2025

Analysis of Beta-cell Function Using Single-cell Resolution Calcium Imaging in Zebrafish Islets
08:50

Analysis of Beta-cell Function Using Single-cell Resolution Calcium Imaging in Zebrafish Islets

Published on: July 3, 2018

14.8K
Imaging Calcium Dynamics in Subpopulations of Mouse Pancreatic Islet Cells
08:03

Imaging Calcium Dynamics in Subpopulations of Mouse Pancreatic Islet Cells

Published on: November 26, 2019

8.2K
Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
11:00

Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes

Published on: September 18, 2017

10.1K

Area of Science:

  • Endocrinology
  • Immunology
  • Metabolic disease research

Background:

  • Macrophages and inflammation are increased in pancreatic islets during diabetes, correlating with beta-cell dysfunction.
  • Galectin-3 (Gal3), primarily from macrophages, is elevated in islets of high-fat diet (HFD)-fed and diabetic db/db mice.

Purpose of the Study:

  • To investigate the role of galectin-3 (Gal3) in pancreatic beta-cell dysfunction and its potential as a therapeutic target for type 2 diabetes.

Main Methods:

  • Assessed Gal3 levels in islets from HFD-fed and db/db mice.
  • Examined the effect of Gal3 on glucose-stimulated insulin secretion (GSIS) in vitro and in vivo.
  • Investigated the interaction between Gal3 and calcium voltage-gated channel auxiliary subunit gamma 1 (CACNG1).
  • Evaluated the impact of Gal3 inhibition on glucose homeostasis in mouse models.

Main Results:

  • Gal3 acutely reduces GSIS in mouse and human beta-cell lines and primary islets.
  • Gal3 binds to CACNG1, inhibiting calcium influx and subsequent GSIS.
  • Beta-cell-specific CACNG1 deficiency mimics Gal3 treatment effects.
  • Genetic or pharmacologic inhibition of Gal3 significantly improves GSIS and glucose homeostasis in HFD-fed and db/db mice.

Conclusions:

  • Galectin-3 plays a critical role in pancreatic beta-cell dysfunction associated with type 2 diabetes.
  • Gal3's mechanism involves inhibiting calcium influx via CACNG1.
  • Inhibition of Gal3 presents a promising therapeutic strategy for improving glucose homeostasis in type 2 diabetes.