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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:
Inborn Errors of Metabolism01:20

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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...
Toxicity Testing in Animals01:23

Toxicity Testing in Animals

Toxicity tests in animals are grounded on two main assumptions: first, the effects observed in laboratory animals can be extrapolated to humans, especially when adjusted for body surface area; second, high-dose exposure in animals is essential to identify potential human hazards from lower doses. This is based on the quantal dose-response concept, which faces the challenge of extrapolating results from relatively few test animals to much larger human populations. For example, a 0.01% incidence...
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Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
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Hypoglycemia and Glucagon

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...

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Related Experiment Video

Updated: Jun 19, 2026

How to Create Conditioned Taste Aversion for Grazing Ground Covers in Woody Crops with Small Ruminants
05:55

How to Create Conditioned Taste Aversion for Grazing Ground Covers in Woody Crops with Small Ruminants

Published on: April 30, 2016

Galactose toxicity in animals.

Kent Lai1, Louis J Elsas, Klaas J Wierenga

  • 1Division of Medical Genetics, Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, UT 84132, USA. kent.lai@hsc.utah.edu

IUBMB Life
|October 28, 2009
PubMed
Summary

Galactose metabolism is vital, but pathway defects cause toxicity. This review covers galactose toxicity from metabolic disorders and hypergalactosemia, including animal models and therapies.

Area of Science:

  • Biochemistry
  • Metabolic Disorders
  • Toxicology

Background:

  • The Leloir pathway is essential for galactose metabolism in most organisms.
  • Perturbations in this pathway, due to enzyme deficiencies or excess galactose, lead to toxicity.
  • Molecular mechanisms of galactose toxicity remain poorly understood despite extensive research.

Purpose of the Study:

  • To review galactose toxicity stemming from congenital metabolic disorders and experimental hypergalactosemia.
  • To provide an updated overview of research on animal models of galactose toxicity.
  • To discuss advances in the clinical management and therapeutic strategies for galactose metabolism disorders.

Main Methods:

  • Literature review of galactose metabolism and toxicity.

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Last Updated: Jun 19, 2026

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  • Analysis of congenital galactosemia and experimental hypergalactosemia models.
  • Synthesis of research on animal models and clinical advancements.

    • Main Results:

    • Galactose toxicity arises from disruptions in the Leloir pathway, impacting human and animal health.
    • Animal models are crucial for elucidating toxicity mechanisms and testing interventions.
    • Progress has been made in understanding and managing galactosemia and related conditions.

    Conclusions:

    • Understanding galactose metabolism and toxicity is critical for treating related disorders.
    • Continued research in animal models and clinical settings is essential for improving patient outcomes.
    • Integrated approaches combining basic science and clinical management are key to addressing galactose toxicity.