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

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...
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...
Glucose Absorption Into the Small Intestine01:26

Glucose Absorption Into the Small Intestine

Complex carbohydrates consumed cannot be absorbed into the small intestine in their original form. First, they must be hydrolyzed to a monosaccharide form such as glucose or galactose. These monosaccharides are then transported across the intestinal membrane and into the blood via transcellular transport. The intestinal epithelial cells allow the movement of these monosaccharides with a defined 'entry' through membrane transporter proteins present on their apical membrane and 'exit' via the...
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...
Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but this inhibition is released...
Hyperglycemia01:29

Hyperglycemia

Hyperglycemia is an abnormally high blood glucose level. It is diagnosed by fasting glucose ≥126 mg/dL, 2-hour oral glucose tolerance test (or OGTT) ≥200 mg/dL, random glucose ≥200 mg/dL with symptoms, or HbA1c ≥6.5%. However, HbA1c results may be unreliable in certain conditions, such as anemia or hemoglobinopathies, and the diagnosis should be confirmed unless classic symptoms are present. Postprandial hyperglycemia is typically considered significant when glucose levels exceed 180 mg/dL two...

You might also read

Related Articles

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

Sort by
Same author

Corrigendum to 'Biosynthesis, characterisation and biocompatibility of a unique and elastomeric medium chain-length polyhydroxyalkanoate for kidney glomerular tissue engineering' [Mater. Today Bio 33 (2025), 101932].

Materials today. Bio·2026
Same author

Heparanase inhibition prevents glycocalyx damage and albuminuria in experimental minimal change disease.

Clinical and translational medicine·2026
Same author

PLCε regulates podocyte differentiation and TGF-β1 responses via alteration of SMAD2/SMAD3 ratio.

Cell communication and signaling : CCS·2026
Same author

Endothelial-erythrocyte glycocalyx exchange enables liquid biopsies of endothelial function.

Nature communications·2026
Same author

Physical activity among children and young people with chronic kidney diseases: a scoping review.

Pediatric nephrology (Berlin, Germany)·2026
Same author

Molecular mechanisms in podocytopathies: finding suitable targets for a new era of glomerular gene therapy.

Clinical kidney journal·2026

Related Experiment Video

Updated: Jun 12, 2026

Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes
08:03

Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes

Published on: June 25, 2017

Podocytes, glucose and insulin.

Gavin I Welsh1, Richard J M Coward

  • 1Academic and Children's Renal Unit, Bristol University, Southmead Hospital, Bristol, UK.

Current Opinion in Nephrology and Hypertension
|June 12, 2010
PubMed
Summary
This summary is machine-generated.

Diabetic nephropathy, a leading cause of kidney failure, involves podocyte dysfunction due to hyperglycemia and insulin resistance. Understanding these cellular changes offers hope for new treatments targeting podocyte health.

More Related Videos

Glucose-Stimulated Insulin Secretion via Perfusion through the Mice Vasculature with an Intact Pancreas
04:41

Glucose-Stimulated Insulin Secretion via Perfusion through the Mice Vasculature with an Intact Pancreas

Published on: July 25, 2025

Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy
08:47

Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy

Published on: December 7, 2017

Related Experiment Videos

Last Updated: Jun 12, 2026

Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes
08:03

Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes

Published on: June 25, 2017

Glucose-Stimulated Insulin Secretion via Perfusion through the Mice Vasculature with an Intact Pancreas
04:41

Glucose-Stimulated Insulin Secretion via Perfusion through the Mice Vasculature with an Intact Pancreas

Published on: July 25, 2025

Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy
08:47

Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy

Published on: December 7, 2017

Area of Science:

  • Nephrology
  • Diabetology
  • Cell Biology

Background:

  • Podocytes are crucial for glomerular filtration barrier integrity and preventing albuminuria.
  • Diabetic nephropathy is the primary cause of end-stage renal disease globally.
  • Key cellular changes in diabetes include insulin signaling failure and hyperglycemia.

Purpose of the Study:

  • To review the impact of hyperglycemia and insulin resistance on podocyte function.
  • To explore the emerging role of these factors in podocyte biology.
  • To highlight advancements in understanding podocyte cellular processes in diabetes.

Main Methods:

  • Literature review of recent research on podocyte biology in diabetic nephropathy.
  • Analysis of cellular pathways affected by hyperglycemia in podocytes.
  • Examination of insulin sensitivity modulation in podocytes.

Main Results:

  • Hyperglycemia triggers both harmful and protective cellular pathways within podocytes.
  • Podocytes communicate with other glomerular cells via these pathways.
  • Podocytes are insulin-sensitive, directly influenced by factors affecting insulin sensitivity.

Conclusions:

  • Recent progress has significantly advanced our understanding of podocyte cellular processes in diabetes and insulin resistance.
  • This enhanced knowledge is expected to drive the development of novel therapeutic strategies.
  • New treatments aim to combat diabetic nephropathy, the leading cause of kidney failure.