Activation of the mitogen-activated protein kinase (MAPK) signalling pathway in the liver of mice is related to plasma glucose levels after acute exercise

Hoene, Miriam; Franken, Holger; Fritsche, Louise; Lehmann, Rainer; Pohl, A; Häring, Hans‐Ulrich; Zell, Andreas; Schleicher, Erwin; Weigert, Cora

doi:10.1007/s00125-010-1666-3

Cited by 34 publications

(35 citation statements)

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“…In C57BL/6 mice fed CD, Cdkn1a gene expression was significantly increased during the recovery phase. Similar results showing increased p53 protein levels in the liver of exercised mice, particularly immediately after cessation of the exercise bout, were obtained by Hoene et al . This effect was absent in our NAFLD models, probably because of the ambivalent role of p53 in liver diseases.…”

Section: Discussionsupporting

confidence: 91%

“…Twenty‐four male C57BL/6J mice were purchased from Charles River Laboratories (Wilmington, MA, USA) and randomly assigned to either the HFD (45% kcal fat, high fat diet n. 2126; Kliba Nafag, Kaiseraugst, Switzerland) or CD (10% kcal fat, control diet n. 2125; Kliba Nafag). Twelve male hepatocyte‐specific PTEN ‐deficient model ( AlbCrePten flox/flox ‐Pten‐KO) mice were obtained from our own animal facility and were fed the CD. Twelve male constitutive Fxr ‐KO model ( Fxr −/− ) mice were purchased from Jackson Laboratory (Bar Harbor, ME, USA) and were fed with CD.…”

Section: Methodsmentioning

confidence: 99%

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Hepatic gene expression in mouse models of non‐alcoholic fatty liver disease after acute exercise

Piguet

Guarino

Potaczek

et al. 2019

Hepatology Research

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Aim Non‐alcoholic fatty liver disease (NAFLD) patients benefit from physical exercise. This study aimed to investigate the effect of acute exercise on hepatic gene expression in different mouse models of NAFLD. Methods C57BL/6J mice were fed with a control (CD) or a high fat (HFD) diet. AlbCrePtenflox/flox (Pten‐KO) and Fxr−/− mice, two genetic models of NAFLD with insulin hypersensitivity and resistance, respectively, were fed with CD. After 4 weeks, mice were randomly assigned to exercise or sedentariness. Mice were killed 15 min or 3 h after the running/sedentary period. Genome‐wide hepatic gene expression was evaluated with the Illumina Micro‐array platform. Quantitative polymerase chain reaction confirmed changes in gene expression. Results Acute exercise transiently affected the expression of genes involved in the immune response in C57BL/6 mice fed with CD and this effect normalized in the recovery phase. Acute exercise affected genes involved in gluconeogenesis in the insulin resistant Fxr−/− model. Genes involved in lipid metabolism were affected in C57BL/6 mice fed with CD, but not in mouse models of NAFLD. Genes involved in DNA damage response pathways were deregulated only in C57BL/6 mice fed with CD and not in mouse models of NAFLD. Conclusion The simultaneous analysis of different NAFLD models revealed that an acute exercise bout affects hepatic gene expression differentially according to animal models and that most of the differentially expressed genes are involved in glucose and fatty acid metabolism, immune regulation, and DNA damage response.

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Section: Discussionsupporting

confidence: 91%

Section: Methodsmentioning

confidence: 99%

Hepatic gene expression in mouse models of non‐alcoholic fatty liver disease after acute exercise

Piguet

Guarino

Potaczek

et al. 2019

Hepatology Research

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“…Acetylcarnitine levels were decreased, while other acylcarnitines were not affected by exercise in the liver (Supplementary Table S-3). Data from a whole genome expression analysis of mouse liver after an acute bout of exercise 20 pointed towards an upregulation of the carnitine transporter solute carrier family (Slc)22a5 which encodes for the organic cation transporter 2 (OCTN2). To investigate whether the increase in hepatic carnitine could be related to a higher carnitine uptake or to an elevated synthesis, we determined the expression of Slc22a5 and of the biosynthetic enzymes gamma-butyrobetaine hydroxylase (Bbox)1 and aldehyde dehydrogenase (Aldh)9a1 (Fig.…”

Section: Resultsmentioning

confidence: 99%

Muscle- and liver-specific alterations in lipid and acylcarnitine metabolism after a single bout of exercise in mice

Hoene¹,

Li²,

Häring³

et al. 2015

Diabetologie und Stoffwechsel

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Intracellular lipid pools are highly dynamic and tissue-specific. Physical exercise is a strong physiologic modulator of lipid metabolism, but most studies focus on changes induced by long-term training. To assess the acute effects of endurance exercise, mice were subjected to one hour of treadmill running, and 13 C 16 -palmitate was applied to trace fatty acid incorporation in soleus and gastrocnemius muscle and liver. The amounts of carnitine, FFA, lysophospholipids and diacylglycerol and the post-exercise increase in acetylcarnitine were pronouncedly higher in soleus than in gastrocnemius. In the liver, exercise increased the content of lysophospholipids, plasmalogens and carnitine as well as transcript levels of the carnitine transporter.13 C 16 -palmitate was detectable in several lipid and acylcarnitine species, with pronounced levels of tracer-derived palmitoylcarnitine in both muscles and a strikingly high incorporation into triacylglycerol and phosphatidylcholine in the liver. These data illustrate the high lipid storing activity of the liver immediately after exercise whereas in muscle, fatty acids are directed towards oxidation. The observed muscle-specific differences accentuate the need for singlemuscle analyses as well as careful consideration of the particular muscle employed when studying lipid metabolism in mice. In addition, our results reveal that lysophospholipids and plasmalogens, potential lipid signalling molecules, are acutely regulated by physical exercise.Certain lipids such as ceramides, diacylglycerols, and acylcarnitines have been shown to activate intracellular signalling cascades and to regulate metabolic pathways [1][2][3][4] . Intracellular accumulation of these lipids in liver and skeletal muscle is frequently related to a chronic inflammatory state and to the development of metabolic diseases 5,6 . However, lipid bioactivity per se is a physiological event and it is only the deregulated production and storage of lipids that leads to a non-physiological activation of signalling pathways 7 . Physical exercise induces tissue-specific alterations in substrate supply and utilization that are evident as increased turnover of fatty acids 8 and elevated levels of acylcarnitines 9 . Previous studies addressed the hepatic lipid response to long-term training 10 or the exercise-dependent regulation of the intramyocellular triglyceride pools in skeletal muscle 11 , but the acute regulation of other lipid species by one bout of exercise is less well understood. Thus, changes in the levels of individual lipid signaling molecules could play a role in the acute response to physiological challenges that affect lipid metabolism.While it is reasonable to expect differences in the regulation of lipid species between organs such as liver and muscle, less attention is usually paid to the distinct metabolism of individual skeletal muscles. Muscles contain different myofibres with specific metabolic and contractile properties. The main classification for different types of muscle fibres is into "slow"...

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“…Exercise represents a physical stress that transiently disrupts homeostasis [1], and the working skeletal muscle is clearly the organ most directly affected during physical activity [2]. Studies indicate that exercise may induce structural damage to muscle cells [3], and the production of metabolic by-products, such as lactate [4], and reactive oxygen species (ROS) [5], [6].…”

Section: Introductionmentioning

confidence: 99%

Swimming Training Induces Liver Mitochondrial Adaptations to Oxidative Stress in Rats Submitted to Repeated Exhaustive Swimming Bouts

et al. 2013

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Background and AimsAlthough acute exhaustive exercise is known to increase liver reactive oxygen species (ROS) production and aerobic training has shown to improve the antioxidant status in the liver, little is known about mitochondria adaptations to aerobic training. The main objective of this study was to investigate the effects of the aerobic training on oxidative stress markers and antioxidant defense in liver mitochondria both after training and in response to three repeated exhaustive swimming bouts.MethodsWistar rats were divided into training (n = 14) and control (n = 14) groups. Training group performed a 6-week swimming training protocol. Subsets of training (n = 7) and control (n = 7) rats performed 3 repeated exhaustive swimming bouts with 72 h rest in between. Oxidative stress biomarkers, antioxidant activity, and mitochondria functionality were assessed.ResultsTrained group showed increased reduced glutathione (GSH) content and reduced/oxidized (GSH/GSSG) ratio, higher superoxide dismutase (MnSOD) activity, and decreased lipid peroxidation in liver mitochondria. Aerobic training protected against exhaustive swimming ROS production herein characterized by decreased oxidative stress markers, higher antioxidant defenses, and increases in methyl-tetrazolium reduction and membrane potential. Trained group also presented higher time to exhaustion compared to control group.ConclusionsSwimming training induced positive adaptations in liver mitochondria of rats. Increased antioxidant defense after training coped well with exercise-produced ROS and liver mitochondria were less affected by exhaustive exercise. Therefore, liver mitochondria also adapt to exercise-induced ROS and may play an important role in exercise performance.

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Activation of the mitogen-activated protein kinase (MAPK) signalling pathway in the liver of mice is related to plasma glucose levels after acute exercise

Cited by 34 publications

References 50 publications

Hepatic gene expression in mouse models of non‐alcoholic fatty liver disease after acute exercise

Hepatic gene expression in mouse models of non‐alcoholic fatty liver disease after acute exercise

Muscle- and liver-specific alterations in lipid and acylcarnitine metabolism after a single bout of exercise in mice

Swimming Training Induces Liver Mitochondrial Adaptations to Oxidative Stress in Rats Submitted to Repeated Exhaustive Swimming Bouts

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