Related Experiment Video
Updated: Jul 10, 2026
15:10
A Dual Tracer PET-MRI Protocol for the Quantitative Measure of Regional Brain Energy Substrates Uptake in the Rat
Published on: December 28, 2013
Ketone bodies, potential therapeutic uses.
R L Veech1, B Chance, Y Kashiwaya
1Unit on Metabolic Control, LMMB/NIAAA, Rockville, Maryland, USA.
IUBMB Life
|September 25, 2001
Summary
Ketosis, marked by elevated D-beta-hydroxybutyrate (betaOHB), offers survival benefits and potentially more efficient brain energy. BetaOHB may also protect neurons and benefit neurological disorders.
Area of Science:
- Biochemistry
- Neuroscience
- Metabolic Disorders
Background:
- Ketosis, defined by elevated D-beta-hydroxybutyrate (betaOHB) and acetoacetate, historically aided survival by providing alternative brain fuel during starvation.
- BetaOHB may offer a more oxygen-efficient energy source for the brain, observed in studies on rat hearts and sperm.
- BetaOHB has demonstrated neuroprotective effects, reducing cell death in neuronal cultures modeling Alzheimer's and Parkinson's diseases.
Purpose of the Study:
- To explore the potential therapeutic benefits of ketosis and betaOHB in various neurological disorders.
- To investigate the broader physiological effects of betaOHB, including energy metabolism and oxidative stress reduction.
- To identify necessary advancements in synthetic betaOHB delivery and metabolic phenotyping for clinical application.
Main Methods:
- Review of existing literature on ketosis, beta-hydroxybutyrate metabolism, and neuroprotection.
- Analysis of betaOHB's effects on neuronal cell death in Alzheimer's and Parkinson's disease models.
- Consideration of betaOHB's impact on cellular energy (ATP hydrolysis) and oxidative processes (CoQ, NADP+).
Main Results:
- Ketosis provides essential non-glucose substrate for the brain, sparing muscle during starvation.
- BetaOHB demonstrates potential as a more efficient brain energy source and exhibits neuroprotective properties.
- BetaOHB influences cellular energy dynamics and may reduce free radical damage.
Conclusions:
- Ketosis and elevated betaOHB levels show promise for treating a range of neurological conditions, including epilepsy, injury, and anoxic states.
- Clinical application requires development of oral synthetic betaOHB formulations and advanced metabolic analysis technologies.
- Characterizing polygenic disorders may be enhanced by integrating metabolic phenotyping with genetic analysis.
More Related Videos
05:42Elevated Plus Maze Test Combined with Video Tracking Software to Investigate the Anxiolytic Effect of Exogenous Ketogenic Supplements
Published on: January 7, 2019
11:44Cellular Membrane Affinity Chromatography Columns to Identify Specialized Plant Metabolites Interacting with Immobilized Tropomyosin Kinase Receptor B
Published on: January 19, 2022
Related Concept Videos
01:11Direct-Acting Cholinergic Agonists: Therapeutic Uses
Direct-acting cholinergic agonists have many therapeutic uses in various medical fields. Choline esters, including acetylcholine, have limited clinical utility due to their non-selectivity and short duration of action. Still, acetylcholine and carbachol are applied topically during ophthalmologic surgery to induce miosis. Pilocarpine, a muscarinic and ganglionic stimulator, effectively treats open-angle glaucoma and alleviates xerostomia and dry mouth caused by radiotherapy or Sjögren syndrome.
01:31Skeletal Muscle Relaxants: Therapeutic Uses
Skeletal muscle relaxants are used to relax muscle tone and alleviate painful muscle contractions. However, the choice of skeletal muscle relaxants depends on the duration of the surgical procedure in order to minimize potential side effects. Skeletal muscle relaxants like neuromuscular blocking agents [NMBAs] are commonly employed as adjuvants alongside general anesthetics in clinical settings. NMBAs are also used to maintain controlled ventilation during surgery of the larynx or pharynx as...
01:24Metabolic States of the Body: Fasting and Starvation
During the initial hours of fasting, the body uses up its glycogen stores as an energy source. Once these glycogen reserves are depleted, the body begins breaking down stored triglycerides and structural proteins. During this stage, glycerol becomes a key substrate for gluconeogenesis, while free fatty acids undergo beta-oxidation to provide energy for tissues, such as skeletal muscle. In the fasting state, the body spares protein breakdown as much as possible to conserve muscle and structural...
01:24Glucagon-like Receptor Agonists
Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
01:25Diabetic Ketoacidosis l: Introduction
DefinitionDiabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus, characterized by a triad of hyperglycemia (blood glucose >250 mg/dL), ketonemia or ketonuria, and metabolic acidosis (arterial pH <7.30 and serum bicarbonate <18 mEq/L). It results from insulin deficiency combined with elevated levels of counterregulatory hormones—glucagon, catecholamines, cortisol, and growth hormone—leading to increased lipolysis, hepatic ketone production, and...
01:22Diabetic Ketoacidosis ll: Pathophysiology
Diabetic ketoacidosis (DKA) is a metabolic emergency characterized by hyperglycemia, ketonemia, and metabolic acidosis. It results from severe insulin deficiency and an excess of counterregulatory hormones, leading to uncontrolled lipolysis, ketogenesis, and widespread electrolyte and fluid disturbances.Pathophysiology The central event in DKA is a profound loss of insulin action. Without insulin, glucose uptake in insulin-dependent tissues is impaired, while hepatic glucose production...