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Related Concept Videos

Histone Modification02:32

Histone Modification

The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
Acetylation
The enzyme histone acetyltransferase adds acetyl group to the histones. Another enzyme, histone deacetylase,...
Histone Modification02:32

Histone Modification

The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
Acetylation
The enzyme histone acetyltransferase adds acetyl group to the histones. Another enzyme, histone deacetylase,...
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are co-secreted in...
Hyperglycemia01:29

Hyperglycemia

Hyperglycemia is an abnormally high blood glucose level. It is diagnosed by fasting glucose ≥126 mg/dL, 2-hour oral glucose tolerance test (or OGTT) ≥200 mg/dL, random glucose ≥200 mg/dL with symptoms, or HbA1c ≥6.5%. However, HbA1c results may be unreliable in certain conditions, such as anemia or hemoglobinopathies, and the diagnosis should be confirmed unless classic symptoms are present. Postprandial hyperglycemia is typically considered significant when glucose levels exceed 180 mg/dL two...
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...

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Related Experiment Video

Updated: May 27, 2026

Global Level Quantification of Histone Post-Translational Modifications in a 3D Cell Culture Model of Hepatic Tissue
08:12

Global Level Quantification of Histone Post-Translational Modifications in a 3D Cell Culture Model of Hepatic Tissue

Published on: May 5, 2022

Global histone modification pattern predicts poor prognosis in organic hyperinsulinism.

A Raffel1, M Krausch, K Roushan

  • 1Department of General, Visceral and Pediatric Surgery, Heinrich-Heine, University of Düsseldorf, Germany

Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme
|November 23, 2011
PubMed
Summary

Low histone H3 K18 acetylation levels independently predict poor survival in organic hyperinsulinism. This finding may lead to new diagnostic tests for managing insulinoma patients.

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Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
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Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice

Published on: November 16, 2011

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Last Updated: May 27, 2026

Global Level Quantification of Histone Post-Translational Modifications in a 3D Cell Culture Model of Hepatic Tissue
08:12

Global Level Quantification of Histone Post-Translational Modifications in a 3D Cell Culture Model of Hepatic Tissue

Published on: May 5, 2022

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
11:10

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice

Published on: November 16, 2011

Area of Science:

  • Endocrinology and Oncology
  • Epigenetics and Cancer Biomarkers

Background:

  • Organic hyperinsulinism is a condition characterized by excessive insulin secretion.
  • Distinguishing benign from malignant insulinoma and predicting patient survival are critical clinical challenges.
  • Histone modifications are increasingly recognized as potential epigenetic biomarkers in various cancers.

Purpose of the Study:

  • To investigate if global histone modifications predict survival in organic hyperinsulinism.
  • To determine if histone modification patterns can differentiate benign from malignant primary insulinoma.
  • To identify potential prognostic biomarkers for insulinoma patients.

Main Methods:

  • A tissue microarray (TMA) was constructed from 63 organic hyperinsulinism patient samples.
  • Immunohistochemistry was performed using antibodies against specific histone modifications (H3K9Ac, H3K18Ac, H4K12Ac, H3K4diMe, H4R3diMe).
  • Staining results were correlated with WHO classification and clinical follow-up data using survival analysis (Cox proportional hazards model).

Main Results:

  • Significant differences in histone modification distribution were observed across tissue types (except H3K4diMe).
  • Lower levels of histone H3 K18 acetylation (H3K18Ac) were significantly associated with decreased relapse-free survival.
  • Low H3K18Ac levels were identified as an independent prognostic factor for organic hyperinsulinism.

Conclusions:

  • Reduced histone H3 K18 acetylation is a novel, independent prognostic biomarker in organic hyperinsulinism.
  • This finding suggests potential for developing standardized diagnostic tests to improve insulinoma patient management.
  • Further validation in independent cohorts is warranted to confirm the clinical utility of H3K18Ac.