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Related Concept Videos

Epigenetic Regulation01:37

Epigenetic Regulation

Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
Epigenetic Regulation01:46

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
Epigenetic Regulation01:46

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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...
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,...
Genomic Imprinting and Inheritance02:30

Genomic Imprinting and Inheritance

Diploid organisms inherit genetic material through chromosomes from both parents. Copies of the same gene are known as alleles. In most cases, both alleles are simultaneously expressed and allow various cellular processes to function optimally. If one of the alleles is missing or mutated, the expression of the other allele can compensate; however, this is not true for all genes.
The expression of some genes depends on which parent passed the gene to the offspring, through a phenomenon known as...

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Related Experiment Video

Updated: Jun 11, 2026

A Zebrafish Model of Diabetes Mellitus and Metabolic Memory
10:03

A Zebrafish Model of Diabetes Mellitus and Metabolic Memory

Published on: February 28, 2013

Glycemic memory associated epigenetic changes.

Andrew L Siebel1, Ana Z Fernandez, Assam El-Osta

  • 1Epigenetics in Human Health and Disease Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.

Biochemical Pharmacology
|July 6, 2010
PubMed
Summary
This summary is machine-generated.

Metabolic memory in diabetes causes lasting vascular damage. Transient hyperglycemia epigenetically activates the NFκB p65 gene via the Set7 enzyme, leading to persistent inflammation and diabetic vascular complications.

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Epigenetics

Background:

  • Metabolic memory causes persistent diabetic complications despite normal blood glucose.
  • Transient hyperglycemia induces lasting transcriptional changes in vascular endothelial cells.

Purpose of the Study:

  • Investigate if hyperglycemia epigenetically activates the NFκB p65 promoter.
  • Identify enzymes regulating gene expression during transient hyperglycemia and recovery.

Main Methods:

  • Analyzed gene expression and epigenetic modifications (H3K4me1) on the NFκB p65 promoter.
  • Utilized Set7 knockdown in vascular endothelial cells.

Main Results:

  • Previous hyperglycemia persistently increases NFκB p65 gene expression.
  • The histone methyltransferase Set7 is recruited as a co-activator and mediates glucose-induced p65 expression.
  • H3K4me1 marks, but not H3K4me2/3, are associated with increased NFκB p65 transcription.

Conclusions:

  • Transient hyperglycemia triggers epigenetic changes, leading to persistent NFκB p65 activation.
  • Set7-mediated H3K4me1 methylation is crucial for diabetic vascular injury pathways.
  • Understanding these epigenetic events can reveal new therapeutic targets for diabetic complications.