Mitochondrial dysfunction, insulin resistance, and type 2 diabetes mellitus

Muhammad A Abdul-ghani, Ralph A Defronzo

Research output: Contribution to journalArticle

89 Citations (Scopus)

Abstract

Insulin resistance is a characteristic feature of type 2 diabetes mellitus, obesity, and the metabolic syndrome. Increased intracellular fat content in skeletal muscle and liver associated with insulin resistance has led to the hypothesis that a mitochondrial defect in substrate oxidation exists in disorders of insulin resistance. In vivo measurements of metabolic fluxes through the tricarboxylic acid and oxidative phosphorylation with magnetic resonance spectroscopy have demonstrated multiple defects in mitochondrial function in skeletal muscle. A decrease in mitochondrial density and mitochondrial copy number has been reported in insulin-resistant individuals. However, these findings have not been a consistent observation in all studies. Similarly, an intrinsic functional defect in mitochondrial adenosine triphosphate production synthesis has been reported in some but not all studies, This review summarizes evidence that implicates a defect in mitochondrial oxidative phosphorylation and its relation hip to insulin resistance in common metabolic diseases characterized by impaired insulin action.

Original languageEnglish (US)
Pages (from-to)173-178
Number of pages6
JournalCurrent Diabetes Reports
Volume8
Issue number3
DOIs
StatePublished - Jun 2008

Fingerprint

Type 2 Diabetes Mellitus
Insulin Resistance
Oxidative Phosphorylation
Skeletal Muscle
Tricarboxylic Acids
Insulin
Metabolic Diseases
Hip
Magnetic Resonance Spectroscopy
Obesity
Adenosine Triphosphate
Fats
Observation
Liver

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Internal Medicine

Cite this

Mitochondrial dysfunction, insulin resistance, and type 2 diabetes mellitus. / Abdul-ghani, Muhammad A; Defronzo, Ralph A.

In: Current Diabetes Reports, Vol. 8, No. 3, 06.2008, p. 173-178.

Research output: Contribution to journalArticle

@article{75a7606e6a8042a7863c7b854c3317a3,
title = "Mitochondrial dysfunction, insulin resistance, and type 2 diabetes mellitus",
abstract = "Insulin resistance is a characteristic feature of type 2 diabetes mellitus, obesity, and the metabolic syndrome. Increased intracellular fat content in skeletal muscle and liver associated with insulin resistance has led to the hypothesis that a mitochondrial defect in substrate oxidation exists in disorders of insulin resistance. In vivo measurements of metabolic fluxes through the tricarboxylic acid and oxidative phosphorylation with magnetic resonance spectroscopy have demonstrated multiple defects in mitochondrial function in skeletal muscle. A decrease in mitochondrial density and mitochondrial copy number has been reported in insulin-resistant individuals. However, these findings have not been a consistent observation in all studies. Similarly, an intrinsic functional defect in mitochondrial adenosine triphosphate production synthesis has been reported in some but not all studies, This review summarizes evidence that implicates a defect in mitochondrial oxidative phosphorylation and its relation hip to insulin resistance in common metabolic diseases characterized by impaired insulin action.",
author = "Abdul-ghani, {Muhammad A} and Defronzo, {Ralph A}",
year = "2008",
month = "6",
doi = "10.1007/s11892-008-0030-1",
language = "English (US)",
volume = "8",
pages = "173--178",
journal = "Current Diabetes Reports",
issn = "1534-4827",
publisher = "Current Medicine Group",
number = "3",

}

TY - JOUR

T1 - Mitochondrial dysfunction, insulin resistance, and type 2 diabetes mellitus

AU - Abdul-ghani, Muhammad A

AU - Defronzo, Ralph A

PY - 2008/6

Y1 - 2008/6

N2 - Insulin resistance is a characteristic feature of type 2 diabetes mellitus, obesity, and the metabolic syndrome. Increased intracellular fat content in skeletal muscle and liver associated with insulin resistance has led to the hypothesis that a mitochondrial defect in substrate oxidation exists in disorders of insulin resistance. In vivo measurements of metabolic fluxes through the tricarboxylic acid and oxidative phosphorylation with magnetic resonance spectroscopy have demonstrated multiple defects in mitochondrial function in skeletal muscle. A decrease in mitochondrial density and mitochondrial copy number has been reported in insulin-resistant individuals. However, these findings have not been a consistent observation in all studies. Similarly, an intrinsic functional defect in mitochondrial adenosine triphosphate production synthesis has been reported in some but not all studies, This review summarizes evidence that implicates a defect in mitochondrial oxidative phosphorylation and its relation hip to insulin resistance in common metabolic diseases characterized by impaired insulin action.

AB - Insulin resistance is a characteristic feature of type 2 diabetes mellitus, obesity, and the metabolic syndrome. Increased intracellular fat content in skeletal muscle and liver associated with insulin resistance has led to the hypothesis that a mitochondrial defect in substrate oxidation exists in disorders of insulin resistance. In vivo measurements of metabolic fluxes through the tricarboxylic acid and oxidative phosphorylation with magnetic resonance spectroscopy have demonstrated multiple defects in mitochondrial function in skeletal muscle. A decrease in mitochondrial density and mitochondrial copy number has been reported in insulin-resistant individuals. However, these findings have not been a consistent observation in all studies. Similarly, an intrinsic functional defect in mitochondrial adenosine triphosphate production synthesis has been reported in some but not all studies, This review summarizes evidence that implicates a defect in mitochondrial oxidative phosphorylation and its relation hip to insulin resistance in common metabolic diseases characterized by impaired insulin action.

UR - http://www.scopus.com/inward/record.url?scp=52649149879&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=52649149879&partnerID=8YFLogxK

U2 - 10.1007/s11892-008-0030-1

DO - 10.1007/s11892-008-0030-1

M3 - Article

VL - 8

SP - 173

EP - 178

JO - Current Diabetes Reports

JF - Current Diabetes Reports

SN - 1534-4827

IS - 3

ER -