2009
DOI: 10.1073/pnas.0902380106
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Abstract: We know a great deal about the cellular response to starvation via AMPK, but less is known about the reaction to nutrient excess. Insulin resistance may be an appropriate response to nutrient excess, but the cellular sensors that link these parameters remain poorly defined. In the present study we provide evidence that mitochondrial superoxide production is a common feature of many different models of insulin resistance in adipocytes, myotubes, and mice. In particular, insulin resistance was rapidly reversible… Show more

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Cited by 444 publications
(434 citation statements)
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References 33 publications
(37 reference statements)
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“…Overactivation of stress pathways such as oxidative and endoplasmic reticulum stress have been linked with insulin resistance [36][37][38], though there is also evidence that reactive oxygen species production and the unfolded protein response can positively influence insulin action [39,40]. Obese, insulin-resistant individuals also exhibit a state of chronic low-grade inflammation, and as such activation of inflammatory pathways have also been proposed as a major driver of insulin resistance [1,2].…”
Section: Discussionmentioning
confidence: 99%
“…Overactivation of stress pathways such as oxidative and endoplasmic reticulum stress have been linked with insulin resistance [36][37][38], though there is also evidence that reactive oxygen species production and the unfolded protein response can positively influence insulin action [39,40]. Obese, insulin-resistant individuals also exhibit a state of chronic low-grade inflammation, and as such activation of inflammatory pathways have also been proposed as a major driver of insulin resistance [1,2].…”
Section: Discussionmentioning
confidence: 99%
“…Intermittent, low-level ROS production has been reported to enhance insulin action via improvements in insulin signal transduction [50]. However, other recent studies have shown that excessive or persistent generation of ROS in mitochondria contributes to the pathogenesis of insulin resistance [10,11]. The exact mechanism(s) by which excess ROS antagonises insulin action is currently unknown; however, this effect appears to be independent of changes in the canonical PI3K/Akt insulin-signalling pathway [10].…”
Section: Discussionmentioning
confidence: 99%
“…Another factor that has recently been implicated in the development of insulin resistance is oxidative stress [10][11][12]. Several groups, including our own, have demonstrated in cells and animals that insulin resistance is associated with excessive production of reactive oxygen species (ROS), particularly from the mitochondrial respiratory chain [10,11].…”
Section: Introductionmentioning
confidence: 99%
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“…91,92 366 367 From this perspective, a key benefit of 'maintenance' comprises protection against T2DM, 368 through glucose homeostasis at the level of tissues and organs, and the suppression of 369 oxidative stress at the molecular level. 93 Stresses during early life alter energy-allocation 370 patterns, potentially reducing investment in 'maintenance' and growth with long-term 371 detrimental effects on homeostasis. Such stresses may derive directly from inadequate 372 energy supply, or indirectly from allocating more energy to immune function.…”
mentioning
confidence: 99%