Role of PGC-1α in exercise and fasting-induced adaptations in mouse liver

Haase, Tobias N.; Ringholm, Stine; Leick, Lotte; Biensø, Rasmus S.; Kiilerich, Kristian; Johansen, Sune; Nielsen, Maja Munk; Wojtaszewski, Jørgen F. P.; Hidalgo, Juan; Pedersen, Per Amstrup; Pilegaard, Henriette

doi:10.1152/ajpregu.00775.2010

Cited by 54 publications

(50 citation statements)

References 41 publications

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“…Alterations in the protein content of this transcription factor have been specifically associated with exercise traininginduced improvements in oxidative capacity of several tissues, including the liver [16]. In the present study, the content of both PGC-1α and mtTFA in the liver as well as citrate synthase activity were augmented by chronic exercise (particularly higher in the VPA group, Fig.…”

Section: Discussionsupporting

confidence: 59%

Exercise modulates liver cellular and mitochondrial proteins related to quality control signaling

et al. 2015

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Section: Discussionsupporting

confidence: 59%

Exercise modulates liver cellular and mitochondrial proteins related to quality control signaling

et al. 2015

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“…Other markers such as Cpt-1 activity, β-Had activity, citrate synthase activity, Tr4 protein, and cytochrome c oxidase component levels are increased suggesting an increase in mitochondrial function and/or content, 79,80,85–87 which may be dependent on presence of Pgc-1α . 86 Alterations in mitochondrial FA oxidation have typically been accompanied by a decrease in extramitochondrial palmitate oxidation in the OLETF rat model. 79,81,87 This decrease in extramitochondrial palmitate oxidation is hypothesized to represent a decrease in peroxisomal contributions to oxidation.…”

Section: Hepatic Adaptations To Regular Physical Activitymentioning

confidence: 99%

Exercise and the Regulation of Hepatic Metabolism

Trefts

Williams

Wasserman

2015

Progress in Molecular Biology and Translational Science

136

117

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The accelerated metabolic demands of the working muscle cannot be met without a robust response from the liver. If not for the hepatic response, sustained exercise would be impossible. The liver stores, releases, and recycles potential energy. Exercise would result in hypoglycemia if it were not for the accelerated release of energy as glucose. The energetic demands on the liver are largely met by increased oxidation of fatty acids mobilized from adipose tissue. Adaptations immediately following exercise facilitate the replenishment of glycogen stores. Pancreatic glucagon and insulin responses orchestrate the hepatic response during and immediately following exercise. Like skeletal muscle and other physiological systems, liver adapts to repeated demands of exercise by increasing its capacity to produce energy by oxidizing fat. The ability of regular physical activity to increase fat oxidation is protective and can reverse fatty liver disease. Engaging in regular physical exercise has broad ranging positive health implications including those that improve the metabolic health of the liver.

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“…We first wanted to ensure the effectiveness of VWR; thus, we assessed differences in body mass, glucose homeostasis, and levels of gluconeogenic enzymes previously shown to be increased with exercise (13). Mice in the VWR group averaged ϳ3-5 km/night over the 10-wk period (Fig.…”

Section: Vwr Attenuates Body Mass and Adipose Tissue Gain Improves Gmentioning

confidence: 99%

Voluntary wheel running attenuates lipopolysaccharide-induced liver inflammation in mice

Peppler

Anderson

Sutton

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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Peppler WT, Anderson ZG, Sutton CD, Rector RS, Wright DC. Voluntary wheel running attenuates lipopolysaccharide-induced liver inflammation in mice. Am J Physiol Regul Integr Comp Physiol 310: R934 -R942, 2016. First published February 17, 2016 doi:10.1152/ajpregu.00497.2015.-Sepsis induces an acute inflammatory response in the liver, which can lead to organ failure and death. Given the anti-inflammatory effects of exercise, we hypothesized that habitual physical activity could protect against acute sepsis-induced liver inflammation via mechanisms, including heat shock protein (HSP) 70/72. Male C57BL/6J mice (n ϭ 80, ϳ8 wk of age) engaged in physical activity via voluntary wheel running (VWR) or cage control (SED) for 10 wk. To induce sepsis, we injected (2 mg/kg ip) LPS or sterile saline (SAL), and liver was harvested 6 or 12 h later. VWR attenuated increases in body and epididymal adipose tissue mass, improved glucose tolerance, and increased liver protein content of PEPCK (P Ͻ 0.05). VWR attenuated increases in LPS-induced IL-6 signaling and mRNA expression of other inflammatory markers (TNF-␣, chemokine C-C motif ligand 2, inducible nitric oxide synthase, IL-10, IL-1␤) in the liver; however, this was not reflected at the whole body level, as systemic markers of inflammation were similar between SED and VWR. Insulin tolerance was greater in VWR compared with SED at 6 but not 12 h after LPS. The protective effect of VWR occurred in parallel with increases in the liver protein content of HSP70/72, a molecular chaperone that can protect against inflammatory challenges. This study provides novel evidence that physical activity protects against the inflammatory cascade induced by LPS in the liver and that these effects may be mediated via HSP70/72. lipopolysaccharide; inflammation; liver; physical activity; exercise SEPSIS IS A CONTINUUM OF CLINICAL events defined by the presence of infection and systemic inflammation (18). The worldwide incidence of sepsis was recently estimated at 437 cases per 100,000 person years between 2003 and 2015, with an associated fatality rate of 17% (11). This puts a significant burden on the health care system, and in the United States alone, the direct hospital costs associated with sepsis are over $24 billion (17).The infiltration of a host with both gram-negative and gram-positive bacterial species is often considered to be the cause of acute sepsis (34). LPS from Escherichia coli, a component of gram-negative bacteria, is often used to produce these effects in rodent models. Upon exposure to LPS, an inflammatory cascade is activated both systemically and at a tissue-specific level (1). Initial signaling involves a Toll-like receptor 4 (TLR4)-myeloid differentiation primary response gene 88 (MyD88) interaction that then propagates the inflammatory response (24). Increases in circulating inflammatory factors, such as TNF-␣, IL-6, and IL-1␤, occur rapidly and are regulated by the dose and duration of exposure (21,29,40). Clearance of inflammatory markers begins as early as 8 h post...

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Role of PGC-1α in exercise and fasting-induced adaptations in mouse liver

Cited by 54 publications

References 41 publications

Exercise modulates liver cellular and mitochondrial proteins related to quality control signaling

Exercise modulates liver cellular and mitochondrial proteins related to quality control signaling

Exercise and the Regulation of Hepatic Metabolism

Voluntary wheel running attenuates lipopolysaccharide-induced liver inflammation in mice

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