Skeletal muscle mitochondria exhibit decreased pyruvate oxidation capacity and increased ROS emission during surgery-induced acute insulin resistance

Hagve, Martin; Gjessing, Petter Fosse; Fuskevåg, Ole-Martin; Larsen, Terje S.; Irtun, Øivind

doi:10.1152/ajpendo.00459.2014

Cited by 8 publications

(8 citation statements)

References 54 publications

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“…muscle is negatively affected. It has been reported that skeletal muscle mitochondrial alterations (decreased pyruvate oxidation and increased ROS) in postoperative patients result in insulin resistance (25). In addition, approximately 50% of patients with cancer develop cachexia, a severe musclewasting syndrome associated with weakness and fatigue (26)(27)(28).…”

Section: Metabolic Maladaptations and Disease Statesmentioning

confidence: 99%

Metabolism and Skeletal Muscle Homeostasis in Lung Disease

Ceco

Weinberg

Chandel

et al. 2017

Am J Respir Cell Mol Biol

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There is increased awareness that patients with lung diseases develop muscle dysfunction. Muscle dysfunction is a major contributor to a decreased quality of life in patients with chronic pulmonary diseases. Furthermore, muscle dysfunction exacerbates lung disease outcome, as a decrease in muscle mass and function are associated with increased morbidity, often long after critical illness or lung disease has been resolved. As we are learning more about the role of metabolism in health and disease, we are appreciating more the direct role of metabolism in skeletal muscle homeostasis. Altered metabolism is associated with numerous skeletal muscle pathologies and, conversely, skeletal muscle diseases are associated with significant changes in metabolic pathways. In this review, we highlight the role of metabolism in the regulation of skeletal muscle homeostasis. Understanding the metabolic pathways that underlie skeletal muscle wasting is of significant clinical interest for critically ill patients as well as patients with chronic lung disease, in which proper skeletal muscle function is essential to disease outcome.

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Section: Metabolic Maladaptations and Disease Statesmentioning

confidence: 99%

Metabolism and Skeletal Muscle Homeostasis in Lung Disease

Ceco

Weinberg

Chandel

et al. 2017

Am J Respir Cell Mol Biol

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“…Some authors have suggested that IR contributes to increased oxidative stress, probably due to an alteration of mitochondrial function, and this increase may also further aggravate IR [4,5]. It is well known that the oxidative stress caused by an imbalance in redox state, owing to either excessive production of reactive species or disturbance of the antioxidant system, can lead to the damage of cell membranes and other functional components such as proteins, lipids, and DNA.…”

Section: Introductionmentioning

confidence: 99%

Antioxidant, antihyperglycemic, and antidyslipidemic effects of Brazilian-native fruit extracts in an animal model of insulin resistance

et al. 2017

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“…Study design and surgical intervention. Group sizes were estimated with power analysis on glucose clamp data from pilot experiments with GLP-1, as well as considering required group sizes in earlier clamp protocols (32). The pigs were examined in two consecutive experiments on separate experimental days (see figure 1).…”

Section: Methodsmentioning

confidence: 99%

Perioperative Infusion of Glucagon-Like Peptide-1 Prevents Insulin Resistance After Surgical Trauma in Female Pigs

et al. 2019

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Insulin resistance is an independent negative predictor of outcome after elective surgery and increases mortality among surgical patients in intensive care. The incretin hormone glucagon-like peptide-1 (GLP-1) potentiates glucose-induced insulin release from the pancreas but may also increase insulin sensitivity in skeletal muscle and directly suppress hepatic glucose release. Here, we investigated whether a perioperative infusion of GLP-1 could counteract the development of insulin resistance after surgery. Pigs were randomly assigned to three groups; surgery/control, surgery/GLP-1, and sham/GLP-1. Both surgery groups underwent major abdominal surgery. Whole-body glucose disposal (WGD) and endogenous glucose release (EGR) were assessed preoperatively and postoperatively using D-[6,6-2H2]-glucose infusion in combination with hyperinsulinemic euglycemic step-clamping. In the surgery/control group, peripheral insulin sensitivity (i.e., WGD) was reduced by 44% relative to preoperative conditions, whereas the corresponding decline was only 9% for surgery/GLP-1 (P < 0.05). Hepatic insulin sensitivity (i.e., EGR) remained unchanged in the surgery/control group but was enhanced after GLP-1 infusion in both surgery and sham animals (40% and 104%, respectively, both P < 0.05). Intraoperative plasma glucose increased in surgery/control (∼20%) but remained unchanged in both groups receiving GLP-1 (P < 0.05). GLP-1 diminished an increase in postoperative glucagon levels but did not affect skeletal muscle glycogen or insulin signaling proteins after surgery. We show that GLP-1 improves intraoperative glycemic control, diminishes peripheral insulin resistance after surgery, and suppresses EGR. This study supports the use of GLP-1 to prevent development of postoperative insulin resistance.

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Skeletal muscle mitochondria exhibit decreased pyruvate oxidation capacity and increased ROS emission during surgery-induced acute insulin resistance

Cited by 8 publications

References 54 publications

Metabolism and Skeletal Muscle Homeostasis in Lung Disease

Metabolism and Skeletal Muscle Homeostasis in Lung Disease

Antioxidant, antihyperglycemic, and antidyslipidemic effects of Brazilian-native fruit extracts in an animal model of insulin resistance

Perioperative Infusion of Glucagon-Like Peptide-1 Prevents Insulin Resistance After Surgical Trauma in Female Pigs

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