Insulin Resistance and Mitochondrial Dysfunction.
Adv Exp Med Biol
; 982: 465-520, 2017.
Article
em En
| MEDLINE
| ID: mdl-28551803
ABSTRACT
Insulin resistance precedes and predicts the onset of type 2 diabetes (T2D) in susceptible humans, underscoring its important role in the complex pathogenesis of this disease. Insulin resistance contributes to multiple tissue defects characteristic of T2D, including reduced insulin-stimulated glucose uptake in insulin-sensitive tissues, increased hepatic glucose production, increased lipolysis in adipose tissue, and altered insulin secretion. Studies of individuals with insulin resistance, both with established T2D and high-risk individuals, have consistently demonstrated a diverse array of defects in mitochondrial function (i.e., bioenergetics, biogenesis and dynamics). However, it remains uncertain whether mitochondrial dysfunction is primary (critical initiating defect) or secondary to the subtle derangements in glucose metabolism, insulin resistance, and defective insulin secretion present early in the course of disease development. In this chapter, we will present the evidence linking mitochondrial dysfunction and insulin resistance, and review the potential for mitochondrial targets as a therapeutic approach for T2D.
Palavras-chave
Texto completo:
1
Bases de dados:
MEDLINE
Assunto principal:
Resistência à Insulina
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Músculo Esquelético
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Diabetes Mellitus Tipo 2
/
Metabolismo Energético
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Mitocôndrias Musculares
Tipo de estudo:
Etiology_studies
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Prognostic_studies
Limite:
Animals
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Humans
Idioma:
En
Revista:
Adv Exp Med Biol
Ano de publicação:
2017
Tipo de documento:
Article
País de afiliação:
Estados Unidos