Faculty Collaboration Database

Effect of exercise on mouse liver and brain bioenergetic infrastructures. Exp Physiol 2013 Jan;98(1):207-19

Date

05/23/2012

Pubmed ID

22613742

Pubmed Central ID

PMC3540163

DOI

10.1113/expphysiol.2012.066688

Scopus ID

2-s2.0-84872173552 (requires institutional sign-in at Scopus site)   34 Citations

Abstract

To assess the effects of exercise on liver and brain bioenergetic infrastructures, we exposed C57BL/6 mice to 6 weeks of moderate-intensity treadmill exercise. During the training period, fasting blood glucose was lower in exercised mice than in sedentary mice, but serum insulin levels were not reduced. At week 6, trained mice showed a paradoxical decrease in plasma lactate during exercise, which was accompanied by an increase in the liver monocarboxylate transporter 2 protein level (∼30%, P < 0.05). Exercise increased liver peroxisomal proliferator-activated receptor-γ coactivator 1α expression (approximately twofold, P < 0.001), NAD-dependent deacetylase sirtuin-1 protein (∼30%, P < 0.05), p38 protein (∼15%, P < 0.05), cytochrome c oxidase subunit 4 isoform 1 protein (∼50%, P < 0.05) and AMP-activated protein kinase phosphorylation (∼40%, P < 0.05). Despite this, liver mitochondrial DNA copy number (∼30%, P = 0.05), mitochondrial transcription factor A expression (∼15%, P < 0.05), cytochrome c oxidase subunit 2 expression (∼10%, P < 0.05), cAMP-response element binding protein phosphorylation (∼60%, P < 0.05) and brain-derived neurotrophic factor expression (∼40%, P < 0.05) were all reduced, while cytochrome oxidase and citrate synthase activities were unchanged. The only altered brain parameter observed was a reduction in tumour necrosis factor α expression (∼35%, P < 0.05); tumour necrosis factor α expression was unchanged in liver. Our data suggest that lactate produced by exercising muscle modifies the liver bioenergetic infrastructure, and enhanced liver uptake may in turn limit the ability of exercise-generated lactate to modify brain bioenergetics. Also, it appears that, at least in the liver, a dissociated mitochondrial biogenesis, in which some components are strategically enhanced while others are minimized, can occur.

Author List

E L, Lu J, Burns JM, Swerdlow RH

Author

Lezi E PhD Assistant Professor in the Cell Biology, Neurobiology and Anatomy department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

AMP-Activated Protein Kinases
Animals
Blood Glucose
Brain
Brain-Derived Neurotrophic Factor
CREB-Binding Protein
Cyclic AMP Response Element-Binding Protein
DNA-Binding Proteins
Electron Transport Complex IV
Energy Metabolism
High Mobility Group Proteins
Lactic Acid
Liver
Male
Mice
Mice, Inbred C57BL
Mitochondria
Monocarboxylic Acid Transporters
Nuclear Respiratory Factor 1
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
Phosphorylation
Physical Conditioning, Animal
Sirtuin 1
Trans-Activators
Transcription Factors
Tumor Necrosis Factor-alpha
p38 Mitogen-Activated Protein Kinases