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Related Concept Videos

Type II Diabetes I: Introduction01:26

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Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
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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.
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Related Experiment Video

Updated: Jun 4, 2026

Three-dimensional Imaging and Analysis of Mitochondria within Human Intraepidermal Nerve Fibers
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Published on: September 29, 2017

Tissue-specific differences in mitochondrial DNA content in type 2 diabetes.

Ching-Jung Hsieh1, Shao-Wen Weng, Chia-Wei Liou

  • 1Department of Internal Medicine, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung, Taiwan.

Diabetes Research and Clinical Practice
|February 2, 2011
PubMed
Summary

Hyperglycemia impacts mitochondrial DNA (mtDNA) differently across tissues. Diabetic patients show reduced muscle mtDNA due to oxidative stress and increased apoptosis, despite stimulated mitochondrial biogenesis.

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Area of Science:

  • Mitochondrial biology and diabetes research.
  • Cellular and molecular medicine.

Background:

  • Hyperglycemia's effect on mitochondrial DNA (mtDNA) content may vary by tissue.
  • Understanding tissue-specific mtDNA changes is crucial in diabetes.

Purpose of the Study:

  • To investigate the tissue-specific impact of hyperglycemia on mitochondrial DNA content.
  • To explore the relationship between oxidative stress, mitochondrial biogenesis, and apoptosis in diabetic tissues.

Main Methods:

  • Compared mtDNA content in leg muscle, blood vessel, and leucocytes between type 2 diabetes patients and controls.
  • Assessed oxidative stress markers (8-OHdG, TBARS) and apoptosis (TUNEL).
  • Examined expression of PGC1-α and Tfam in muscle tissue via immunohistochemistry.

Main Results:

  • mtDNA content was highest in muscle, intermediate in blood vessels, and lowest in leucocytes across all subjects.
  • Diabetic patients exhibited significantly lower muscle mtDNA and higher leucocyte mtDNA compared to controls.
  • Increased oxidative stress (8-OHdG) correlated positively with muscle mtDNA content.

Conclusions:

  • Oxidative stress in diabetes stimulates mitochondrial biogenesis but also increases apoptosis.
  • This dual effect leads to a net decrease in mitochondrial DNA content within muscle tissue.
  • Tissue-specific responses to hyperglycemia highlight the complexity of mitochondrial dysfunction in diabetes.