Mitochondrial Function and Diabetes: Consequences for Skeletal and Cardiac Muscle Metabolism
Vera B Schrauwen-Hinderling1,2,3, Marianne Eline Kooi1,3,4, Patrick Schrauwen2,3
11 Department of Radiology, Maastricht University Medical Center , Maastricht, The Netherlands .
Significance:
An early hallmark in the development of type 2 diabetes is the resistance to the effect of insulin in skeletal muscle and in the heart. Since mitochondrial function was found to be diminished in patients with type 2 diabetes, it was suggested that this defect might be involved in the etiology of insulin resistance. Although several hypotheses were suggested, yet unclear is the mechanistic link between these two phenomena.
Recent Advances:
Herein, we review the evidence for disturbances in mitochondrial function in skeletal muscle and the heart in the diabetic state. Also the mechanisms involved in improving mitochondrial function are considered and, whenever possible, human data is cited.
Critical Issues:
Reported evidence shows that interventions that improve skeletal muscle mitochondrial function also improve insulin sensitivity in humans. In the heart, available data from animal studies suggests that enhancement of mitochondrial function can reverse aging-induced changes in heart function, and can be protective against cardiomyopathy and heart failure.
Future Directions:
Mitochondria and their functions can be targeted with the aim of improving skeletal muscle insulin sensitivity and cardiac function. However, human clinical intervention studies are needed to fully substantiate the potential of mitochondria as a target to prevent cardiometabolic disease.
Insights
Mitochondrial dysfunction is linked to type 2 diabetes and insulin resistance. Improving mitochondrial function may enhance insulin sensitivity and protect the heart, but human studies are needed.
Area of Science:
- Cardiovascular Biology
- Metabolic Disease Research
- Mitochondrial Medicine
Background:
- Insulin resistance in skeletal muscle and heart is an early sign of type 2 diabetes.
- Diminished mitochondrial function is observed in type 2 diabetes patients, potentially contributing to insulin resistance.
- The precise mechanistic link between mitochondrial defects and insulin resistance remains unclear.
Purpose of the Study:
- To review evidence on mitochondrial dysfunction in the diabetic heart and skeletal muscle.
- To explore mechanisms for improving mitochondrial function, citing human data where available.
- To discuss the therapeutic potential of targeting mitochondria for cardiometabolic diseases.
Main Methods:
- Literature review of studies on mitochondrial function in diabetes.
- Analysis of mechanisms influencing mitochondrial health.
- Inclusion of human data where applicable.
Main Results:
- Interventions improving skeletal muscle mitochondrial function enhance insulin sensitivity in humans.
- Animal studies indicate enhanced mitochondrial function can reverse age-related heart changes and protect against heart failure.
- Mitochondrial health is a potential therapeutic target for improving cardiac function.
Conclusions:
- Targeting mitochondria could improve skeletal muscle insulin sensitivity and cardiac function.
- Further human clinical trials are necessary to confirm mitochondria's role in preventing cardiometabolic diseases.
- Mitochondrial interventions show promise for managing type 2 diabetes and related cardiovascular complications.
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