Related Experiment Video
Updated: May 17, 2026
12:32
High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds
Published on: January 23, 2018
Protection Against Periodontitis by Improving Mitochondrial Function in Diabetes
Satoru Onizuka1, Takanori Shinjo2, Atsushi Ishikado1
1Section of Vascular Cell Biology, Dianne Nunnally Hoppes Laboratory, Joslin Diabetes Center, Harvard Medical School, Boston, MA.
Diabetes
|May 15, 2026
Summary
Diabetes impairs wound healing and increases periodontitis risk. Enhancing mitochondrial function, particularly with pyruvate kinase M2 activation, can reverse these effects, offering potential therapies for diabetic chronic wounds.
Area of Science:
- Oral biology
- Metabolic disorders
- Mitochondrial function
Background:
- Diabetes mellitus is a significant risk factor for severe periodontitis, characterized by impaired wound healing, chronic inflammation, and infection.
- Protective factors have been observed in individuals with long-standing type 1 diabetes, delaying severe complications like periodontitis despite hyperglycemia.
Purpose of the Study:
- To investigate the role of mitochondrial function in periodontitis associated with diabetes.
- To identify potential therapeutic targets for mitigating periodontal inflammation and bone loss in diabetic patients.
Main Methods:
- Proteomic analysis of gingival tissues from individuals with and without periodontitis, considering diabetes duration and glycemic control.
- Validation of findings in diabetic mouse models of ligature-induced periodontitis, assessing mitochondrial enzyme expression, oxygen consumption, inflammatory cytokines, and osteoclast activity.
- Investigating the effect of pyruvate kinase M2 activation on mitochondrial function and periodontal parameters.
Main Results:
- Diabetes was associated with reduced mitochondrial enzyme expression and function in gingival tissues, correlating with increased periodontal bone loss, inflammation (Il-1b, Il-6, Il-17a), and osteoclast activation.
- Activation of pyruvate kinase M2 reversed diabetes-induced mitochondrial dysfunction, decreased inflammatory cytokine levels, and mitigated periodontal bone loss, even under hyperglycemic conditions.
- Enhanced mitochondrial protein expression and function demonstrated a protective effect against periodontal inflammation and bone loss in diabetes.
Conclusions:
- Mitochondrial dysfunction plays a key role in the pathogenesis of diabetic periodontitis.
- Targeting mitochondrial function, specifically through pyruvate kinase M2 activation, presents a promising therapeutic strategy for managing periodontitis and chronic wound healing in diabetes.
- These findings suggest that improving mitochondrial health can counteract detrimental effects of hyperglycemia on periodontal tissues.
Related Concept Videos
01:46Electron Transport Chain: Complex I and II
The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
ROS generation is regulated and maintained at moderate levels necessary...
01:27The Oral Microbiota
The oral microbiome includes a complex ecosystem comprising over 700 microbial species, identified through genomic sequencing and culture-based analyses to date. This community includes a core microbiome, found universally among individuals, and a variable component influenced by environmental factors such as diet, lifestyle, and host genetics. Site-specific conditions, including oxygen gradients, pH levels, and nutrient availability, determine the spatial distribution of these microorganisms...
01:22Diabetes Mellitus: Overview and Type I Subtype
Diabetes mellitus is a chronic metabolic disorder characterized by high blood glucose levels due to inadequate insulin production, insulin resistance, or both. The condition affects millions worldwide and can significantly impact their health and quality of life.
Type 1 diabetes is an autoimmune disease in which the immune system mistakenly attacks and destroys the insulin-producing beta cells in the pancreas. As a result, the body is unable to produce sufficient insulin, and individuals with...
Type 1 diabetes is an autoimmune disease in which the immune system mistakenly attacks and destroys the insulin-producing beta cells in the pancreas. As a result, the body is unable to produce sufficient insulin, and individuals with...
01:24Type 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.
01:37Mitochondria
Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...