Mitochondria in Obesity and Type 2 Diabetes

Mitochondria in Obesity and Type 2 Diabetes

Comprehensive Review on Mitochondrial Functioning and Involvement in Metabolic Diseases
2019, Pages 155-172
Mitochondria in Obesity and Type 2 Diabetes

Chapter 6 - Role of Mitochondria in the Skeletal Muscle Metabolism in Obesity and Type 2 Diabetes

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Abstract

Skeletal muscle, by virtue of its mass and high rate of metabolism, represents an important tissue in the context of impaired glucose homeostasis. Although the underlying mechanism(s) causing diabetes remain incompletely elucidated, skeletal muscle insulin resistance is a hallmark of diabetes, and has been attributed to reactive lipid accumulation and increased mitochondrial derived reactive oxygen species (ROS) production. Impaired mitochondrial bioenergetics have been implicated in both reactive lipid accumulation and increased ROS production; conversely, interventions that improve mitochondrial oxidative potential prevent the development of skeletal muscle insulin resistance. Therefore, compelling evidence exists to suggest a mechanistic link between compromised mitochondrial bioenergetics and the development of insulin resistance/diabetes. This chapter will outline these relationships in detail, while also highlighting the potential for exercise to improve skeletal muscle mitochondrial respiratory capacity/function in concert with improving insulin action.

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This chapter will focus on the involvement of mitochondria in the regulation of muscle metabolic flexibility and insulin resistance.

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