Mechanisms underlying skeletal muscle insulin resistance induced by fatty acids: importance of the mitochondrial function

Martins, Amanda Roque; Nachbar, Renato Tadeu; Gorjão, Renata; Vinolo, Marco Aurélio Ramirez; Festuccia, William T.; Lambertucci, Rafael Herling; Cury-Boaventura, Maria Fernanda; Silveira, Leonardo R.; Curi, Rui; Hirabara, Sandro Massao

doi:10.1186/1476-511x-11-30

Cited by 233 publications

(164 citation statements)

References 149 publications

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“…The physiopathology of insulin resistance remains difficult to apprehend since it results from a complex integration of diverse cellular disorders: inflammation [144], intra/extracellular lipids accumulation [145,146], mitochondrial dysfunction [147] and oxidative stress [8].…”

Section: Evidence For a Role Of Rons In Skeletal Muscle Insulin Resismentioning

confidence: 99%

From physical inactivity to immobilization: Dissecting the role of oxidative stress in skeletal muscle insulin resistance and atrophy

Pierre

Appriou

Gratas-Delamarche

et al. 2016

Free Radical Biology and Medicine

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In the literature, the terms physical inactivity and immobilization are largely used as synonyms. The present review emphasizes the need to establish a clear distinction between these two situations. Physical inactivity is a behavior characterized by a lack of physical activity, whereas immobilization is a deprivation of movement for medical purpose. In agreement with these definitions, appropriate models exist to study either physical inactivity or immobilization, leading thereby to distinct conclusions. In this review, we examine the involvement of oxidative stress in skeletal muscle insulin resistance and atrophy induced by, respectively, physical inactivity and immobilization. A large body of evidence demonstrates that immobilization-induced atrophy depends on the chronic overproduction of reactive oxygen and nitrogen species (RONS). On the other hand, the involvement of RONS in physical inactivity-induced insulin resistance has not been investigated. This observation outlines the need to elucidate the mechanism by which physical inactivity promotes insulin resistance.

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Section: Evidence For a Role Of Rons In Skeletal Muscle Insulin Resismentioning

confidence: 99%

From physical inactivity to immobilization: Dissecting the role of oxidative stress in skeletal muscle insulin resistance and atrophy

Pierre

Appriou

Gratas-Delamarche

et al. 2016

Free Radical Biology and Medicine

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“…Such hyperinsulinemia therefore facilitates fattening in insulin-resistant conditions. While obesity is a common correlate of insulin resistance, it is clear that exposure to high-saturated fat diets can induce insulin resistance long before obesity ensues and that such diet-precipitated insulin resistance actually facilitates further fattening [21][22][23][24]. How a westernized diet high in saturated fats (and simple sugars) induces insulin resistance has been the focus of much investigation in the past few decades during which time the prevalence of obesity and T2DM has risen dramatically worldwide.…”

Section: Evolution Of Insulin Resistance and Its Potentiation By The mentioning

confidence: 99%

Bromocriptine-QR therapy for the management of type 2 diabetes mellitus: developmental basis and therapeutic profile summary

Raskin

Cincotta

2016

Expert Review of Endocrinology & Metabolism

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An extended series of studies indicate that endogenous phase shifts in circadian neuronal input signaling to the biological clock system centered within the hypothalamic suprachiasmatic nucleus (SCN) facilitates shifts in metabolic status. In particular, a diminution of the circadian peak in dopaminergic input to the peri-SCN facilitates the onset of fattening, insulin resistance and glucose intolerance while reversal of low circadian peak dopaminergic activity to the peri-SCN via direct timed dopamine administration to this area normalizes the obese, insulin resistant, glucose intolerant state in high fat fed animals. Systemic circadian-timed daily administration of a potent dopamine D2 receptor agonist, bromocriptine, to increase diminished circadian peak dopaminergic hypothalamic activity across a wide variety of animal models of metabolic syndrome and type 2 diabetes mellitus (T2DM) results in improvements in the obese, insulin resistant, glucose intolerant condition by improving hypothalamic fuel sensing and reducing insulin resistance, elevated sympathetic tone, and leptin resistance. A circadian-timed (within 2 hours of waking in the morning) once daily administration of a quick release formulation of bromocriptine (bromocriptine-QR) has been approved for the treatment of T2DM by the U.S. Food and Drug Administration. Clinical studies with such bromocriptine-QR therapy (1.6 to 4.8 mg/day) indicate that it improves glycemic control by reducing postprandial glucose levels without raising plasma insulin. Across studies of various T2DM populations, bromocriptine-QR has been demonstrated to reduce HbA1c by -0.5 to -1.7. The drug has a good safety profile with transient mild to moderate nausea, headache and dizziness as the most frequent adverse events noted with the medication. In a large randomized clinical study of T2DM subjects, bromocriptine-QR exposure was associated with a 42% hazard ratio reduction of a pre-specified adverse cardiovascular endpoint including myocardial infarction, stroke, hospitalization for congestive heart failure, revascularization surgery, or unstable angina. Bromocriptine-QR represents a novel method of treating T2DM that may have benefits for cardiovascular disease as well. ARTICLE HISTORY

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“…10 In addition to increased cytokine and acute phase reactant (e.g., C-reactive protein) production, FFA levels commonly seen in the plasma of obese patients and patients with type 2 diabetes mellitus lead to macrophage accumulation and contribute to insulin resistance. 11 Supranormal levels of FFA also impair endothelial function and nitric oxide release, with chronic elevation impacting on pancreatic cell function and insulin secretion.…”

Section: A Primer On the Adipocytementioning

confidence: 99%

Perioperative management of the severely obese patient: a selective pathophysiological review

Cullen

Ferguson

2012

Can J Anesth/J Can Anesth

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Mechanisms underlying skeletal muscle insulin resistance induced by fatty acids: importance of the mitochondrial function

Cited by 233 publications

References 149 publications

From physical inactivity to immobilization: Dissecting the role of oxidative stress in skeletal muscle insulin resistance and atrophy

From physical inactivity to immobilization: Dissecting the role of oxidative stress in skeletal muscle insulin resistance and atrophy

Bromocriptine-QR therapy for the management of type 2 diabetes mellitus: developmental basis and therapeutic profile summary

Perioperative management of the severely obese patient: a selective pathophysiological review

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