Related Experiment Video

Updated: Jul 20, 2026

One-step Metabolomics: Carbohydrates, Organic and Amino Acids Quantified in a Single Procedure
09:28

One-step Metabolomics: Carbohydrates, Organic and Amino Acids Quantified in a Single Procedure

Published on: June 26, 2010

Transient carnitine-responsive medium-chain dicarboxylic aciduria in an infant with cholestasis, hypoglycemia and

M Matsuo, K Saiki, T Momota

    Acta Paediatrica Japonica : Overseas Edition
    |April 1, 1989
    PubMed

    More Related Videos

    The Murine Choline-Deficient, Ethionine-Supplemented (CDE) Diet Model of Chronic Liver Injury07:27

    The Murine Choline-Deficient, Ethionine-Supplemented (CDE) Diet Model of Chronic Liver Injury

    Published on: October 21, 2017

    In Vitro Modeling of Fat Deposition in Metabolic Dysfunction-Associated Steatotic Liver Disease07:03

    In Vitro Modeling of Fat Deposition in Metabolic Dysfunction-Associated Steatotic Liver Disease

    Published on: July 19, 2024

    Related Concept Videos

    Protein Import into the Peroxisomes01:27

    Protein Import into the Peroxisomes

    Cells contain membrane-bound organelles called peroxisomes that oxidize organic molecules by transferring hydrogen atoms to oxygen, producing hydrogen peroxide. Peroxisomes enzymatically convert the released hydrogen peroxide into water and oxygen.
    Peroxisomal Protein Import:
    Peroxisomes lack the genetic machinery required to code for their own proteins. Hence, most peroxisomal membrane, lumenal and transmembrane proteins are synthesized in the cytoplasm or ER and transported to the peroxisome...
    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

    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...
    Lipid Catabolism01:25

    Lipid Catabolism

    Triglycerides serve as crucial long-term energy storage molecules in microorganisms, providing a dense source of metabolic energy. Their breakdown is mediated by lipases, which hydrolyze triglycerides into glycerol and free fatty acids. Each of these components follows distinct metabolic pathways, ultimately contributing to ATP synthesis and cellular energy homeostasis.Glycerol MetabolismGlycerol, released from triglyceride hydrolysis, is phosphorylated by glycerol kinase to form...
    Diabetic Ketoacidosis l: Introduction01:25

    Diabetic 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...
    Diabetic Ketoacidosis ll: Pathophysiology01:22

    Diabetic 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...