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

Pathophysiology of Diabetes01:20

Pathophysiology of Diabetes

2.3K
Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility,...
2.3K
Hypoglycemia and Glucagon01:15

Hypoglycemia and Glucagon

513
Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
513
Inborn Errors of Metabolism01:20

Inborn Errors of Metabolism

497
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...
497

You might also read

Related Articles

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

Sort by
Same author

Safeguarding nanovesicles and their payload: A framework for stable storage.

Colloids and surfaces. B, Biointerfaces·2026
Same author

Beyond arrhythmias: Exploring heart failure in arrhythmogenic cardiomyopathy.

International journal of cardiology·2026
Same author

Bispecific CAR T and CAR NK cells in dual-threat immunotherapy: opportunities and challenges.

Molecular biology reports·2026
Same author

Cathepsin Z/X: Breaking Down the Known and Unknown.

International journal of molecular sciences·2026
Same author

Left Ventricular Hypertrabeculation: Historical Evolution, Diagnostic Pitfalls, and a Pragmatic Clinical Approach.

Reviews in cardiovascular medicine·2026
Same author

Decoy Nanoparticles and Protein Corona Modulation: A Novel Frontier in Sepsis Treatment.

International journal of nanomedicine·2026

Related Experiment Video

Updated: Nov 10, 2025

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
07:36

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Published on: November 20, 2015

11.6K

Neonatal Hypoglycemia and Brain Vulnerability.

Laura Costanza De Angelis1,2, Giorgia Brigati1, Giulia Polleri1

  • 1Neonatal Intensive Care Unit, Department Mother and Child, IRCCS Istituto Giannina Gaslini, Genoa, Italy.

Frontiers in Endocrinology
|April 2, 2021
PubMed
Summary

Neonatal hypoglycemia, a common condition, can cause severe brain damage if prolonged. Understanding cerebral glucose homeostasis and injury mechanisms is key to developing effective treatments for affected newborns.

Keywords:
brain damagebrain energeticsglucose homeostasisglucose sensing neuronsneonatal hypoglycemia

More Related Videos

A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy
10:30

A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy

Published on: May 16, 2015

19.9K
The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia
08:47

The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia

Published on: November 19, 2008

36.0K

Related Experiment Videos

Last Updated: Nov 10, 2025

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
07:36

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Published on: November 20, 2015

11.6K
A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy
10:30

A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy

Published on: May 16, 2015

19.9K
The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia
08:47

The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia

Published on: November 19, 2008

36.0K

Area of Science:

  • Neonatal medicine
  • Neuroscience
  • Biochemistry

Background:

  • Neonatal hypoglycemia is a frequent condition, often a transient metabolic adaptation after birth.
  • Factors like limited metabolic stores or increased energy expenditure can disrupt glucose homeostasis.
  • While mild hypoglycemia's effects are unclear, severe, prolonged cases are linked to cerebral damage.

Purpose of the Study:

  • To review cerebral glucose homeostasis in neonates.
  • To elucidate mechanisms of brain injury resulting from neonatal hypoglycemia.
  • To discuss potential therapeutic strategies for neonatal hypoglycemia.

Main Methods:

  • Literature review of neonatal hypoglycemia.
  • Analysis of mechanisms underlying hypoglycemia-induced neurotoxicity.
  • Synthesis of current and potential treatment approaches.

Main Results:

  • Specific brain regions show vulnerability to hypoglycemia, including the cerebral cortex, hippocampus, and caudate-putamen.
  • Hypoglycemia-induced neuronal depolarization elevates glutamate and aspartate, leading to excitotoxicity.
  • Extracellular zinc release activates poly ADP-ribose polymerase-1, contributing to neuronal death.

Conclusions:

  • Neonatal hypoglycemia poses a risk for brain injury through excitotoxicity and other mechanisms.
  • Further research into cerebral glucose regulation and neuroprotective strategies is warranted.
  • Effective management of neonatal hypoglycemia is crucial to prevent long-term neurological deficits.