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

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

1.2K
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...
1.2K
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

6.2K
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,...
6.2K

You might also read

Related Articles

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

Sort by
Same author

Pancreatic α-cells are functionally heterogeneous and sex-dependently regulated by neighboring endocrine cells.

Communications biology·2026
Same author

AI-guided analysis of human pancreatic islet sociology reveals distinct cell compositional changes in type 1 diabetes.

bioRxiv : the preprint server for biology·2026
Same author

Pancreatic α-cells integrate immune and neuronal stimuli for insulin secretion.

Cell reports·2026
Same author

p21-senescent cells drive pancreatic islet dysfunction through targetable paracrine signaling in type 2 diabetes.

JCI insight·2026
Same author

Distinct senescent β-cell senotypes differentially drive islet aging and dysfunction.

bioRxiv : the preprint server for biology·2026
Same author

A loss of function variant in <i>SLC30A8/ZnT8</i> drives proteomic changes associated with lowered apoptosis in human stem cell-derived islets.

medRxiv : the preprint server for health sciences·2026

Related Experiment Video

Updated: Jun 12, 2025

Measurement of Insulin- and Contraction-Stimulated Glucose Uptake in Isolated and Incubated Mature Skeletal Muscle from Mice
08:01

Measurement of Insulin- and Contraction-Stimulated Glucose Uptake in Isolated and Incubated Mature Skeletal Muscle from Mice

Published on: May 16, 2021

5.7K

Exercise activates AMPK in mouse and human pancreatic islets to decrease senescence.

Priscila Carapeto1,2, Kanako Iwasaki1, Francesko Hela1

  • 1Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.

Nature Metabolism
|September 24, 2024
PubMed
Summary
This summary is machine-generated.

Endurance exercise reduces beta-cell senescence, a factor in type 2 diabetes. This effect is linked to increased glucagon and AMPK activation, offering potential new therapies for diabetes management.

More Related Videos

A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination
12:33

A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination

Published on: June 25, 2014

65.2K
Author Spotlight: Advancing Diabetes Research with Static Exercise Training in Mice
03:17

Author Spotlight: Advancing Diabetes Research with Static Exercise Training in Mice

Published on: March 29, 2024

440

Related Experiment Videos

Last Updated: Jun 12, 2025

Measurement of Insulin- and Contraction-Stimulated Glucose Uptake in Isolated and Incubated Mature Skeletal Muscle from Mice
08:01

Measurement of Insulin- and Contraction-Stimulated Glucose Uptake in Isolated and Incubated Mature Skeletal Muscle from Mice

Published on: May 16, 2021

5.7K
A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination
12:33

A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination

Published on: June 25, 2014

65.2K
Author Spotlight: Advancing Diabetes Research with Static Exercise Training in Mice
03:17

Author Spotlight: Advancing Diabetes Research with Static Exercise Training in Mice

Published on: March 29, 2024

440

Area of Science:

  • Cellular biology
  • Endocrinology
  • Metabolic diseases

Background:

  • Beta-cell senescence is implicated in type 2 diabetes mellitus (T2DM).
  • Exercise impacts aging markers, but its effect on beta-cell senescence is unknown.

Purpose of the Study:

  • To investigate the impact of endurance exercise training on beta-cell senescence in insulin-resistant models.
  • To elucidate the molecular mechanisms underlying exercise-induced changes in beta-cell senescence.

Main Methods:

  • Short-term endurance exercise (treadmill running) in mouse models of insulin resistance.
  • In vivo and in vitro experiments assessing beta-cell senescence markers.
  • Analysis of serum glucagon, AMPK signaling, and NRF2 nuclear translocation.
  • Treatment of human T2DM islets with serum from exercised donors.

Main Results:

  • Exercise training decreased beta-cell senescence in mouse models.
  • This effect was mediated by increased serum glucagon, activating AMPK signaling in beta-cells.
  • AMPK activation led to NRF2 nuclear translocation and reduced senescence markers.
  • Human T2DM islets treated with exercised serum showed decreased senescence markers.

Conclusions:

  • Exercise training reduces pancreatic beta-cell senescence.
  • The mechanism involves glucagon-AMPK-NRF2 signaling.
  • Exercise demonstrates therapeutic potential for T2DM by targeting beta-cell aging.