Other search tools

About this data

The publication data currently available has been vetted by Vanderbilt faculty, staff, administrators and trainees. The data itself is retrieved directly from NCBI's PubMed and is automatically updated on a weekly basis to ensure accuracy and completeness.

If you have any questions or comments, please contact us.

Results: 1 to 10 of 39

Publication Record

Connections

Beneficial Effects of Exercise on Subendothelial Matrix Stiffness are Short-Lived.
Kohn JC, Bordeleau F, Miller J, Watkins HC, Modi S, Ma J, Azar J, Putnam D, Reinhart-King CA
(2018) J Biomech Eng 140:
MeSH Terms: Animals, Aorta, Biomechanical Phenomena, Collagen, Endothelium, Vascular, Glycation End Products, Advanced, Male, Mechanical Phenomena, Mice, Mice, Inbred C57BL, Physical Conditioning, Animal, Pulse Wave Analysis, Rest, Stroke Volume
Show Abstract · Added April 10, 2019
Aerobic exercise helps to maintain cardiovascular health in part by mitigating age-induced arterial stiffening. However, the long-term effects of exercise regimens on aortic stiffness remain unknown, especially in the intimal extracellular matrix layer known as the subendothelial matrix. To examine how the stiffness of the subendothelial matrix changes following exercise cessation, mice were exposed to an 8 week swimming regimen followed by an 8 week sedentary rest period. Whole vessel and subendothelial matrix stiffness were measured after both the exercise and rest periods. After swimming, whole vessel and subendothelial matrix stiffness decreased, and after 8 weeks of rest, these values returned to baseline. Within the same time frame, the collagen content in the intima layer and the presence of advanced glycation end products (AGEs) in the whole vessel were also affected by the exercise and the rest periods. Overall, our data indicate that consistent exercise is necessary for maintaining compliance in the subendothelial matrix.
0 Communities
1 Members
0 Resources
14 MeSH Terms
Reduced Nonexercise Activity Attenuates Negative Energy Balance in Mice Engaged in Voluntary Exercise.
Lark DS, Kwan JR, McClatchey PM, James MN, James FD, Lighton JRB, Lantier L, Wasserman DH
(2018) Diabetes 67: 831-840
MeSH Terms: Animals, Behavior, Animal, Calorimetry, Indirect, Energy Intake, Energy Metabolism, Male, Mice, Mice, Inbred C57BL, Motor Activity, Obesity, Physical Conditioning, Animal, Weight Loss
Show Abstract · Added March 26, 2019
Exercise alone is often ineffective for treating obesity despite the associated increase in metabolic requirements. Decreased nonexercise physical activity has been implicated in this resistance to weight loss, but the mechanisms responsible are unclear. We quantified the metabolic cost of nonexercise activity, or "off-wheel" activity (OWA), and voluntary wheel running (VWR) and examined whether changes in OWA during VWR altered energy balance in chow-fed C57BL/6J mice ( = 12). Energy expenditure (EE), energy intake, and behavior (VWR and OWA) were continuously monitored for 4 days with locked running wheels followed by 9 days with unlocked running wheels. Unlocking the running wheels increased EE as a function of VWR distance. The metabolic cost of exercise (kcal/m traveled) decreased with increasing VWR speed. Unlocking the wheel led to a negative energy balance but also decreased OWA, which was predicted to mitigate the expected change in energy balance by ∼45%. A novel behavioral circuit involved repeated bouts of VWR, and roaming was discovered and represented novel predictors of VWR behavior. The integrated analysis described here reveals that the weight loss effects of voluntary exercise can be countered by a reduction in nonexercise activity.
© 2018 by the American Diabetes Association.
1 Communities
1 Members
0 Resources
MeSH Terms
Loss of hepatic AMP-activated protein kinase impedes the rate of glycogenolysis but not gluconeogenic fluxes in exercising mice.
Hughey CC, James FD, Bracy DP, Donahue EP, Young JD, Viollet B, Foretz M, Wasserman DH
(2017) J Biol Chem 292: 20125-20140
MeSH Terms: AMP-Activated Protein Kinases, Animals, Energy Metabolism, Gluconeogenesis, Glucose, Glycogenolysis, Homeostasis, Isotope Labeling, Liver, Mice, Mice, Knockout, Physical Conditioning, Animal
Show Abstract · Added March 14, 2018
Pathologies including diabetes and conditions such as exercise place an unusual demand on liver energy metabolism, and this demand induces a state of energy discharge. Hepatic AMP-activated protein kinase (AMPK) has been proposed to inhibit anabolic processes such as gluconeogenesis in response to cellular energy stress. However, both AMPK activation and glucose release from the liver are increased during exercise. Here, we sought to test the role of hepatic AMPK in the regulation of glucose-producing and citric acid cycle-related fluxes during an acute bout of muscular work. We used H/C metabolic flux analysis to quantify intermediary metabolism fluxes in both sedentary and treadmill-running mice. Additionally, liver-specific AMPK α1 and α2 subunit KO and WT mice were utilized. Exercise caused an increase in endogenous glucose production, glycogenolysis, and gluconeogenesis from phosphoenolpyruvate. Citric acid cycle fluxes, pyruvate cycling, anaplerosis, and cataplerosis were also elevated during this exercise. Sedentary nutrient fluxes in the postabsorptive state were comparable for the WT and KO mice. However, the increment in the endogenous rate of glucose appearance during exercise was blunted in the KO mice because of a diminished glycogenolytic flux. This lower rate of glycogenolysis was associated with lower hepatic glycogen content before the onset of exercise and prompted a reduction in arterial glucose during exercise. These results indicate that liver AMPKα1α2 is required for maintaining glucose homeostasis during an acute bout of exercise.
© 2017 by The American Society for Biochemistry and Molecular Biology, Inc.
1 Communities
1 Members
0 Resources
12 MeSH Terms
CETP Expression Protects Female Mice from Obesity-Induced Decline in Exercise Capacity.
Cappel DA, Lantier L, Palmisano BT, Wasserman DH, Stafford JM
(2015) PLoS One 10: e0136915
MeSH Terms: Animals, Cholesterol Ester Transfer Proteins, Diet, High-Fat, Female, Gene Expression Regulation, Glutamic Acid, Humans, Malates, Mice, Mitochondria, Muscle, Obesity, Oxidation-Reduction, Physical Conditioning, Animal
Show Abstract · Added September 28, 2015
Pharmacological approaches to reduce obesity have not resulted in dramatic reductions in the risk of coronary heart disease (CHD). Exercise, in contrast, reduces CHD risk even in the setting of obesity. Cholesteryl Ester Transfer Protein (CETP) is a lipid transfer protein that shuttles lipids between serum lipoproteins and tissues. There are sexual-dimorphisms in the effects of CETP in humans. Mice naturally lack CETP, but we previously reported that transgenic expression of CETP increases muscle glycolysis in fasting and protects against insulin resistance with high-fat diet (HFD) feeding in female but not male mice. Since glycolysis provides an important energy source for working muscle, we aimed to define if CETP expression protects against the decline in exercise capacity associated with obesity. We measured exercise capacity in female mice that were fed a chow diet and then switched to a HFD. There was no difference in exercise capacity between lean, chow-fed CETP female mice and their non-transgenic littermates. Female CETP transgenic mice were relatively protected against the decline in exercise capacity caused by obesity compared to WT. Despite gaining similar fat mass after 6 weeks of HFD-feeding, female CETP mice showed a nearly two-fold increase in run distance compared to WT. After an additional 6 weeks of HFD-feeding, mice were subjected to a final exercise bout and muscle mitochondria were isolated. We found that improved exercise capacity in CETP mice corresponded with increased muscle mitochondrial oxidative capacity, and increased expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α). These results suggest that CETP can protect against the obesity-induced impairment in exercise capacity and may be a target to improve exercise capacity in the context of obesity.
1 Communities
4 Members
0 Resources
13 MeSH Terms
AMPK controls exercise endurance, mitochondrial oxidative capacity, and skeletal muscle integrity.
Lantier L, Fentz J, Mounier R, Leclerc J, Treebak JT, Pehmøller C, Sanz N, Sakakibara I, Saint-Amand E, Rimbaud S, Maire P, Marette A, Ventura-Clapier R, Ferry A, Wojtaszewski JF, Foretz M, Viollet B
(2014) FASEB J 28: 3211-24
MeSH Terms: AMP-Activated Protein Kinases, Animals, Glucose, Interleukin-6, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Mitochondria, Muscle Contraction, Muscle Fatigue, Muscle Fibers, Skeletal, Oxidation-Reduction, Phosphorylation, Physical Conditioning, Animal, Physical Endurance
Show Abstract · Added April 17, 2014
AMP-activated protein kinase (AMPK) is a sensor of cellular energy status that plays a central role in skeletal muscle metabolism. We used skeletal muscle-specific AMPKα1α2 double-knockout (mdKO) mice to provide direct genetic evidence of the physiological importance of AMPK in regulating muscle exercise capacity, mitochondrial function, and contraction-stimulated glucose uptake. Exercise performance was significantly reduced in the mdKO mice, with a reduction in maximal force production and fatigue resistance. An increase in the proportion of myofibers with centralized nuclei was noted, as well as an elevated expression of interleukin 6 (IL-6) mRNA, possibly consistent with mild skeletal muscle injury. Notably, we found that AMPKα1 and AMPKα2 isoforms are dispensable for contraction-induced skeletal muscle glucose transport, except for male soleus muscle. However, the lack of skeletal muscle AMPK diminished maximal ADP-stimulated mitochondrial respiration, showing an impairment at complex I. This effect was not accompanied by changes in mitochondrial number, indicating that AMPK regulates muscle metabolic adaptation through the regulation of muscle mitochondrial oxidative capacity and mitochondrial substrate utilization but not baseline mitochondrial muscle content. Together, these results demonstrate that skeletal muscle AMPK has an unexpected role in the regulation of mitochondrial oxidative phosphorylation that contributes to the energy demands of the exercising muscle.-Lantier, L., Fentz, J., Mounier, R., Leclerc, J., Treebak, J. T., Pehmøller, C., Sanz, N., Sakakibara, I., Saint-Amand, E., Rimbaud, S., Maire, P., Marette, A., Ventura-Clapier, R., Ferry, A., Wojtaszewski, J. F. P., Foretz, M., Viollet, B. AMPK controls exercise endurance, mitochondrial oxidative capacity, and skeletal muscle integrity.
© FASEB.
0 Communities
1 Members
0 Resources
16 MeSH Terms
β-Aminoisobutyric acid induces browning of white fat and hepatic β-oxidation and is inversely correlated with cardiometabolic risk factors.
Roberts LD, Boström P, O'Sullivan JF, Schinzel RT, Lewis GD, Dejam A, Lee YK, Palma MJ, Calhoun S, Georgiadi A, Chen MH, Ramachandran VS, Larson MG, Bouchard C, Rankinen T, Souza AL, Clish CB, Wang TJ, Estall JL, Soukas AA, Cowan CA, Spiegelman BM, Gerszten RE
(2014) Cell Metab 19: 96-108
MeSH Terms: Adipocytes, Brown, Adipocytes, White, Adipose Tissue, Brown, Adipose Tissue, White, Aminoisobutyric Acids, Animals, Cardiovascular Diseases, Cell Differentiation, Exercise, Gene Expression Regulation, Glucose Tolerance Test, Humans, Induced Pluripotent Stem Cells, Liver, Metabolic Diseases, Mice, Organ Specificity, Oxidation-Reduction, PPAR alpha, Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Phenotype, Physical Conditioning, Animal, Risk Factors, Transcription Factors, Transcription, Genetic, Weight Gain
Show Abstract · Added February 28, 2014
The transcriptional coactivator peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α) regulates metabolic genes in skeletal muscle and contributes to the response of muscle to exercise. Muscle PGC-1α transgenic expression and exercise both increase the expression of thermogenic genes within white adipose. How the PGC-1α-mediated response to exercise in muscle conveys signals to other tissues remains incompletely defined. We employed a metabolomic approach to examine metabolites secreted from myocytes with forced expression of PGC-1α, and identified β-aminoisobutyric acid (BAIBA) as a small molecule myokine. BAIBA increases the expression of brown adipocyte-specific genes in white adipocytes and β-oxidation in hepatocytes both in vitro and in vivo through a PPARα-mediated mechanism, induces a brown adipose-like phenotype in human pluripotent stem cells, and improves glucose homeostasis in mice. In humans, plasma BAIBA concentrations are increased with exercise and inversely associated with metabolic risk factors. BAIBA may thus contribute to exercise-induced protection from metabolic diseases.
Copyright © 2014 Elsevier Inc. All rights reserved.
1 Communities
1 Members
0 Resources
26 MeSH Terms
SIRT3 deacetylates ATP synthase F1 complex proteins in response to nutrient- and exercise-induced stress.
Vassilopoulos A, Pennington JD, Andresson T, Rees DM, Bosley AD, Fearnley IM, Ham A, Flynn CR, Hill S, Rose KL, Kim HS, Deng CX, Walker JE, Gius D
(2014) Antioxid Redox Signal 21: 551-64
MeSH Terms: ATP Synthetase Complexes, Acetylation, Adenosine Triphosphatases, Adenosine Triphosphate, Animals, Carrier Proteins, Cell Line, Enzyme Activation, Humans, Membrane Proteins, Mice, Mice, Knockout, Mitochondrial Proton-Translocating ATPases, Muscle, Skeletal, Physical Conditioning, Animal, Protein Binding, Sirtuin 3, Stress, Physiological
Show Abstract · Added October 5, 2015
AIMS - Adenosine triphosphate (ATP) synthase uses chemiosmotic energy across the inner mitochondrial membrane to convert adenosine diphosphate and orthophosphate into ATP, whereas genetic deletion of Sirt3 decreases mitochondrial ATP levels. Here, we investigate the mechanistic connection between SIRT3 and energy homeostasis.
RESULTS - By using both in vitro and in vivo experiments, we demonstrate that ATP synthase F1 proteins alpha, beta, gamma, and Oligomycin sensitivity-conferring protein (OSCP) contain SIRT3-specific reversible acetyl-lysines that are evolutionarily conserved and bind to SIRT3. OSCP was further investigated and lysine 139 is a nutrient-sensitive SIRT3-dependent deacetylation target. Site directed mutants demonstrate that OSCP(K139) directs, at least in part, mitochondrial ATP production and mice lacking Sirt3 exhibit decreased ATP muscle levels, increased ATP synthase protein acetylation, and an exercise-induced stress-deficient phenotype.
INNOVATION - This work connects the aging and nutrient response, via SIRT3 direction of the mitochondrial acetylome, to the regulation of mitochondrial energy homeostasis under nutrient-stress conditions by deacetylating ATP synthase proteins.
CONCLUSION - Our data suggest that acetylome signaling contributes to mitochondrial energy homeostasis by SIRT3-mediated deacetylation of ATP synthase proteins.
0 Communities
1 Members
0 Resources
18 MeSH Terms
Exercise prevents hyperhomocysteinemia in a dietary folate-restricted mouse model.
Neuman JC, Albright KA, Schalinske KL
(2013) Nutr Res 33: 487-93
MeSH Terms: Absorption, Animals, Betaine-Homocysteine S-Methyltransferase, Diet, Disease Models, Animal, Female, Folic Acid, Homocysteine, Hyperhomocysteinemia, Methylenetetrahydrofolate Reductase (NADPH2), Mice, Physical Conditioning, Animal
Show Abstract · Added August 2, 2016
Hyperhomocysteinemia is a condition that results from altered methyl group metabolism and is associated with numerous pathological conditions. A number of nutritional and hormonal factors have been shown to influence circulating homocysteine concentrations; however, the impact of exercise on homocysteine and methyl group balance is not well understood. Our hypothesis was that exercise represents an effective means to prevent hyperhomocysteinemia in a folate-independent manner. The purpose of this study was to determine the influence of exercise on homocysteine metabolism in a dietary folate-restricted mouse model characterized by moderate hyperhomocysteinemia. Female outbred mice (12 weeks old) were assigned to either a sedentary or free-access wheel exercise group. Following a 4-week acclimation period, half of the mice in each group were provided a folate-restricted diet for 7-weeks prior to euthanasia and tissue collection. As expected, folate-restricted sedentary mice exhibited a 2-fold increase in plasma total homocysteine concentrations; however, exercise completely prevented the increase in circulating homocysteine concentrations. Moreover, exercise reduced plasma homocysteine concentrations 36% within the group fed only the control diet. The prevention of hyperhomocysteinemia by exercise appears, at least in part, to be the result of increased folate-independent homocysteine remethylation owing to a 2-fold increase in renal betaine homocysteine S-methyltransferase. To our knowledge, this is the first report demonstrating the prevention of hyperhomocysteinemia by exercise in a dietary folate-restriction model. Future research will be directed at determining if exercise can have a positive impact on other nutritional, hormonal, and genetic models of hyperhomocysteinemia relevant to humans.
Copyright © 2013 Elsevier Inc. All rights reserved.
0 Communities
1 Members
0 Resources
12 MeSH Terms
Synergistic effect of exercise and statins on femoral strength in rats.
Starnes JW, Neidre DB, Nyman JS, Roy A, Nelson MJ, Gutierrez G, Wang X
(2013) Exp Gerontol 48: 751-5
MeSH Terms: Animals, Biomechanical Phenomena, Bone Density, Female, Femur, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Linear Models, Models, Animal, Physical Conditioning, Animal, Rats, Rats, Sprague-Dawley
Show Abstract · Added October 31, 2013
It is now widely recognized that in order to optimize bone health in the later years, bone healthy behaviors should begin at a young age and continue throughout life. Prescribed orally to lower lipid levels in adults of all ages, statins have also been shown to stimulate bone formation in vitro by promoting bone morphogenic protein-2 (BMP-2) activity and to stimulate bone formation in vivo. Weight bearing exercise is well known to stimulate bone formation through a mechanism whereby mechanical loading is 'sensed' by the mechano-sensors leading to a cascade of events involving the activation of osteoblasts. For individuals with high cholesterol levels, both of these interventions are recommended throughout adult life. Since statins and exercise stimulate bone formation via different mechanisms, we hypothesized that exercise in combination with oral simvastatin synergistically increases bone mineral density and strength. Mature adult female, Sprague Dawley rats were divided into 4 groups: control (n=9), statin only (n=8), exercise only (n=11), and statin plus exercise (n=11). Simvastatin was given to the two groups at a dose of 10 mg/kg/day in standard rat chow for the entire 5 week period. All rats ate the same mass of food. The two exercise groups ran on a treadmill with progressively greater speeds and time, ending on week 5 at 30 m/min for 60 min. After 5 weeks, rats were euthanized, and excised femurs were scanned for areal bone mineral density (BMD) and tested by three point bending to obtain the following performance measures: maximum force (strength), stiffness, and work-to-fracture. Only the group treated with statins and exercise showed a positive effect on the biomechanical performance of the femurs. Compared to controls, this group had increased maximum force, stiffness, moment of inertia, and BMD. Linear regression analysis revealed that the increased performance was related to increased BMD. We conclude that the combination of oral statins and appropriate exercise increases bone strength better than either individual treatment and may provide optimal protection against osteoporosis.
Copyright © 2013 Elsevier Inc. All rights reserved.
1 Communities
1 Members
0 Resources
11 MeSH Terms
Phenotypic and molecular differences between rats selectively bred to voluntarily run high vs. low nightly distances.
Roberts MD, Brown JD, Company JM, Oberle LP, Heese AJ, Toedebusch RG, Wells KD, Cruthirds CL, Knouse JA, Ferreira JA, Childs TE, Brown M, Booth FW
(2013) Am J Physiol Regul Integr Comp Physiol 304: R1024-35
MeSH Terms: Absorptiometry, Photon, Animals, Body Composition, DNA, Complementary, Eating, Female, Hindlimb, Male, Muscle Fibers, Skeletal, Muscle, Skeletal, NAD, Nucleus Accumbens, Organ Size, Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Phenotype, Physical Conditioning, Animal, RNA, Messenger, RNA-Binding Proteins, Rats, Rats, Wistar, Real-Time Polymerase Chain Reaction, Running, Sex Characteristics, Transcription Factors
Show Abstract · Added October 23, 2017
The purpose of the present study was to partially phenotype male and female rats from generations 8-10 (G8-G10) that had been selectively bred to possess low (LVR) vs. high voluntary running (HVR) behavior. Over the first 6 days with wheels, 34-day-old G8 male and female LVRs ran shorter distances (P < 0.001), spent less time running (P < 0.001), and ran slower (P < 0.001) than their G8 male and female HVR counterparts, respectively. HVR and LVR lines consumed similar amounts of standard chow with or without wheels. No inherent difference existed in PGC-1α mRNA in the plantaris and soleus muscles of LVR and HVR nonrunners, although G8 LVR rats inherently possessed less NADH-positive superficial plantaris fibers compared with G8 HVR rats. While day 28 body mass tended to be greater in both sexes of G9-G10 LVR nonrunners vs. G9-G10 HVR nonrunners (P = 0.06), body fat percentage was similar between lines. G9-G10 HVRs had fat mass loss after 6 days of running compared with their prerunning values, while LVR did not lose or gain fat mass during the 6-day voluntary running period. RNA deep sequencing efforts in the nucleus accumbens showed only eight transcripts to be >1.5-fold differentially expressed between lines in HVR and LVR nonrunners. Interestingly, HVRs presented less Oprd1 mRNA, which ties in to potential differences in dopaminergic signaling between lines. This unique animal model provides further evidence as to how exercise may be mechanistically regulated.
0 Communities
1 Members
0 Resources
24 MeSH Terms