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Related Concept Videos

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...
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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.
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Hepatic Encephalopathy01:29

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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In clinical practice, the direct measurement of hepatic blood flow to evaluate liver function presents significant challenges due to the intricate and specialized nature of the necessary techniques. Consequently, healthcare professionals often rely on empirical estimates derived from thorough patient examinations and liver function tests to gauge liver health. Among the tools at their disposal, the Child–Pugh and MELD scoring systems stand out for their ability to categorize and assess the...
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Related Experiment Video

Updated: Jun 2, 2026

Mouse Model of Metabolic Dysfunction-Associated Steatotic Liver Disease with Fibrosis
06:26

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Published on: July 18, 2025

Focal hepatic glycogenosis.

P Bannasch1, U Jahn, H Hacker

  • 1UNIV HEIDELBERG, INST PATHOL, D-6900 HEIDELBERG, GERMANY. UNIV HANNOVER, DEPT SURG, HANNOVER, GERMANY. UNIV HEIDELBERG, DEPT SURG, D-6900 HEIDELBERG, GERMANY.

International Journal of Oncology
|May 3, 2011
PubMed
Summary
This summary is machine-generated.

Foci of altered hepatocytes (FAH) with focal hepatic glycogenosis are found in human livers, particularly in patients with liver cancer and cirrhosis. These lesions show reduced glycogen breakdown enzymes, suggesting a role in hepatocyte neoplastic transformation.

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Area of Science:

  • Hepatology and Cancer Research
  • Biochemistry and Molecular Biology

Background:

  • Foci of altered hepatocytes (FAH), including those with focal hepatic glycogenosis, are recognized preneoplastic lesions in animal models of liver cancer.
  • Their presence and characteristics in human livers, especially in relation to liver diseases, require further investigation.

Purpose of the Study:

  • To investigate the occurrence and characteristics of FAH with focal hepatic glycogenosis in human livers.
  • To compare the enzyme histochemical profiles of FAH and hepatocellular carcinoma (HCC).

Main Methods:

  • Histological and histochemical analyses of 67 explanted and 2 resected human livers.
  • Enzyme histochemistry to assess the activity of various enzymes in FAH and HCC.

Main Results:

  • FAH were frequently detected in livers with HCC (14/14) and cirrhosis (21/42), but not in donor livers.
  • FAH showed significantly increased cell proliferation and consistent reductions in glycogen phosphorylase (98%) and glucose-6-phosphatase (95%) activity.
  • HCC exhibited distinct enzyme patterns, including increased mitochondrial glycerol-3-phosphate dehydrogenase activity, differing from FAH.

Conclusions:

  • Focal hepatic glycogenosis in humans is a putative preneoplastic lesion, mirroring findings in animal models.
  • This condition appears to be an early step in hepatocyte neoplastic transformation, involving metabolic shifts.