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 Transporters01:27

Glucose Transporters

Glucose transporters facilitate the transport of glucose across the cell membrane. In addition to glucose, some glucose transporters can also aid the movement of other hexoses such as fructose, mannose, and galactose.
Facilitated diffusion-glucose transporters (GLUTs) are encoded by the solute-linked carrier (SLC) family 2, subfamily A gene family, or SLC2A. The 14 GLUT protein members are distributed into three classes:
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...
Secondary Active Transport01:32

Secondary Active Transport

One example of how cells use the energy contained in electrochemical gradients is demonstrated by glucose transport into cells. The ion vital to this process is sodium (Na+), which is typically present in higher concentrations extracellularly than in the cytosol. Such a concentration difference is due, in part, to the action of an enzyme "pump" embedded in the cellular membrane that actively expels Na+ from a cell. Importantly, as this pump contributes to the high concentration of...
Secondary Active Transport01:55

Secondary Active Transport

One example of how cells use the energy contained in electrochemical gradients is demonstrated by glucose transport into cells. The ion vital to this process is sodium (Na+), which is typically present in higher concentrations extracellularly than in the cytosol. Such a concentration difference is due, in part, to the action of an enzyme “pump” embedded in the cellular membrane that actively expels Na+ from a cell. Importantly, as this pump contributes to the high concentration of...
Membrane Proteins01:30

Membrane Proteins

Plasma membranes have integral transmembrane proteins involved in facilitated transport. These proteins are collectively referred to as transport proteins, and they function as either channels for the material or as carriers themselves. Channel proteins have hydrophilic domains exposed to the intracellular and extracellular fluids and a hydrophilic channel through their core that provides a hydrated opening for solutes to pass through the membrane layers. Passage through the channel allows...
Inborn Errors of Metabolism01:20

Inborn Errors of Metabolism

Phenylketonuria (PKU) is a protein metabolism disorder characterized by high blood levels of the amino acid phenylalanine. This results from a mutation in the gene responsible for phenylalanine hydroxylase, an enzyme that converts phenylalanine into tyrosine. When this enzyme is deficient, phenylalanine builds up in the blood, leading to symptoms such as vomiting, rashes, seizures, growth deficiency, and severe mental retardation. An early diagnosis and a diet restricting phenylalanine intake...

You might also read

Related Articles

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

Sort by
Same author

Shaped by Mountains, Driven by Climate: The Rise of the Neotropical Carex sect. Fecundae.

Annals of botany·2026
Same author

Chemical composition and radionuclide activity concentration data in cements, SCMs, aggregates, ceramics and other materials that could be valorised in construction materials.

Data in brief·2026
Same author

Erratum: Addendum: A novel estimate of biological aging by multiple fitness tests is associated with risk scores for age-related diseases.

Frontiers in physiology·2026
Same author

Deletion of <i>C2orf34</i>, <i>PREPL</i> and <i>SLC3A1</i> causes atypical hypotonia-cystinuria syndrome.

BMJ case reports·2025
Same author

Capping Effects on Spin and Charge Excitations in Parent and Superconducting Nd_{1-x}Sr_{x}NiO_{2}.

Physical review letters·2024
Same author

Allelic variants of the estrogen receptor genes and frailty phenotype in postmenopausal women.

Climacteric : the journal of the International Menopause Society·2024

Related Experiment Video

Updated: Jun 30, 2026

Quantitative Measurement of GLUT4 Translocation to the Plasma Membrane by Flow Cytometry
05:39

Quantitative Measurement of GLUT4 Translocation to the Plasma Membrane by Flow Cytometry

Published on: November 7, 2010

[Glucose transporter type 1 (GLUT-1) deficiency].

A Cano1, I Ticus, B Chabrol

  • 1Centre de référence des maladies héréditaires du métabolisme, hôpital La-Timone-Enfants, 264, rue Saint-Pierre, 13005 Marseille, France.

Revue Neurologique
|September 24, 2008
PubMed
Summary

Glucose transporter type 1 (GLUT-1) deficiency syndrome impairs brain glucose transport, causing severe neurological issues in infants. Early diagnosis and ketogenic diets help manage seizures, but cognitive deficits persist, requiring further research.

More Related Videos

Measuring Uptake of the Glucose Analog, 6-(N-(7-Nitrobenz-2-Oxa-1,3-Diazol-4-yl)Amino)-6-Deoxyglucose, in Intact Murine Neural Retina
07:04

Measuring Uptake of the Glucose Analog, 6-(N-(7-Nitrobenz-2-Oxa-1,3-Diazol-4-yl)Amino)-6-Deoxyglucose, in Intact Murine Neural Retina

Published on: March 14, 2025

Measuring Glucose Uptake in Drosophila Models of TDP-43 Proteinopathy
07:07

Measuring Glucose Uptake in Drosophila Models of TDP-43 Proteinopathy

Published on: August 3, 2021

Related Experiment Videos

Last Updated: Jun 30, 2026

Quantitative Measurement of GLUT4 Translocation to the Plasma Membrane by Flow Cytometry
05:39

Quantitative Measurement of GLUT4 Translocation to the Plasma Membrane by Flow Cytometry

Published on: November 7, 2010

Measuring Uptake of the Glucose Analog, 6-(N-(7-Nitrobenz-2-Oxa-1,3-Diazol-4-yl)Amino)-6-Deoxyglucose, in Intact Murine Neural Retina
07:04

Measuring Uptake of the Glucose Analog, 6-(N-(7-Nitrobenz-2-Oxa-1,3-Diazol-4-yl)Amino)-6-Deoxyglucose, in Intact Murine Neural Retina

Published on: March 14, 2025

Measuring Glucose Uptake in Drosophila Models of TDP-43 Proteinopathy
07:07

Measuring Glucose Uptake in Drosophila Models of TDP-43 Proteinopathy

Published on: August 3, 2021

Area of Science:

  • Neurology
  • Genetics
  • Metabolic Disorders

Context:

  • Glucose transporter type 1 (GLUT-1) deficiency syndrome (GDD) is a rare neurological disorder.
  • It results from impaired glucose transport across the blood-brain barrier.
  • GDD presents with severe infantile-onset epilepsy, microcephaly, and developmental delays.

Purpose:

  • To summarize the clinical characteristics, diagnosis, and current treatment of GLUT-1 deficiency syndrome.
  • To highlight the diagnostic hallmarks, including low cerebrospinal fluid glucose levels.
  • To discuss the genetic basis and ongoing research into novel therapeutic strategies.

Summary:

  • GDD is characterized by refractory infantile seizures, developmental delays, and neurological abnormalities due to insufficient glucose supply to the brain.
  • Diagnosis relies on low cerebrospinal fluid/blood glucose ratio, confirmed by molecular analysis of the SCL2A1 gene.
  • Ketogenic diet is effective for seizures but not cognitive impairment, necessitating further treatment research.

Impact:

  • This research underscores the importance of suspecting GDD in children with unexplained neurological disorders.
  • Accurate diagnosis through lumbar puncture and genetic testing is crucial for timely intervention.
  • Understanding GDD's pathophysiology may unlock new treatments for cognitive deficits and improve patient outcomes.