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Featured researches published by Scott P. Naples.


Journal of Hepatology | 2010

Mitochondrial dysfunction precedes insulin resistance and hepatic steatosis and contributes to the natural history of non-alcoholic fatty liver disease in an obese rodent model

R. Scott Rector; John P. Thyfault; Grace M. Uptergrove; E. Matthew Morris; Scott P. Naples; Sarah J. Borengasser; Catherine R. Mikus; Matthew J. Laye; M. Harold Laughlin; Frank W. Booth; Jamal A. Ibdah

BACKGROUND & AIMS In this study, we sought to determine the temporal relationship between hepatic mitochondrial dysfunction, hepatic steatosis and insulin resistance, and to examine their potential role in the natural progression of non-alcoholic fatty liver disease (NAFLD) utilising a sedentary, hyperphagic, obese, Otsuka Long-Evans Tokushima Fatty (OLETF) rat model. METHODS OLETF rats and their non-hyperphagic control Long-Evans Tokushima Otsuka (LETO) rats were sacrificed at 5, 8, 13, 20, and 40 weeks of age (n=6-8 per group). RESULTS At 5 weeks of age, serum insulin and glucose and hepatic triglyceride (TG) concentrations did not differ between animal groups; however, OLETF animals displayed significant (p<0.01) hepatic mitochondrial dysfunction as measured by reduced hepatic carnitine palmitoyl-CoA transferase-1 activity, fatty acid oxidation, and cytochrome c protein content compared with LETO rats. Hepatic TG levels were significantly elevated by 8 weeks of age, and insulin resistance developed by 13 weeks in the OLETF rats. NAFLD progressively worsened to include hepatocyte ballooning, perivenular fibrosis, 2.5-fold increase in serum ALT, hepatic mitochondrial ultrastructural abnormalities, and increased hepatic oxidative stress in the OLETF animals at later ages. Measures of hepatic mitochondrial content and function including beta-hydroxyacyl-CoA dehydrogenase activity, citrate synthase activity, and immunofluorescence staining for mitochondrial carbamoyl phosphate synthetase-1, progressively worsened and were significantly reduced at 40 weeks in OLETF rats compared to LETO animals. CONCLUSIONS Our study documents that hepatic mitochondrial dysfunction precedes the development of NAFLD and insulin resistance in the OLETF rats. This evidence suggests that progressive mitochondrial dysfunction contributes to the natural history of obesity-associated NAFLD.


Journal of the American College of Cardiology | 2013

Simvastatin impairs exercise training adaptations.

Catherine R. Mikus; Leryn J. Boyle; Sarah J. Borengasser; Douglas J. Oberlin; Scott P. Naples; Justin A. Fletcher; Grace M. Meers; Meghan L. Ruebel; M. Harold Laughlin; Kevin C. Dellsperger; Paul J. Fadel; John P. Thyfault

OBJECTIVES This study sought to determine if simvastatin impairs exercise training adaptations. BACKGROUND Statins are commonly prescribed in combination with therapeutic lifestyle changes, including exercise, to reduce cardiovascular disease risk in patients with metabolic syndrome. Statin use has been linked to skeletal muscle myopathy and impaired mitochondrial function, but it is unclear whether statin use alters adaptations to exercise training. METHODS This study examined the effects of simvastatin on changes in cardiorespiratory fitness and skeletal muscle mitochondrial content in response to aerobic exercise training. Sedentary overweight or obese adults with at least 2 metabolic syndrome risk factors (defined according to National Cholesterol Education Panel Adult Treatment Panel III criteria) were randomized to 12 weeks of aerobic exercise training or to exercise in combination with simvastatin (40 mg/day). The primary outcomes were cardiorespiratory fitness and skeletal muscle (vastus lateralis) mitochondrial content (citrate synthase enzyme activity). RESULTS Thirty-seven participants (exercise plus statins: n = 18; exercise only: n = 19) completed the study. Cardiorespiratory fitness increased by 10% (p < 0.05) in response to exercise training alone, but was blunted by the addition of simvastatin resulting in only a 1.5% increase (p < 0.005 for group by time interaction). Similarly, skeletal muscle citrate synthase activity increased by 13% in the exercise-only group (p < 0.05), but decreased by 4.5% in the simvastatin-plus-exercise group (p < 0.05 for group-by-time interaction). CONCLUSIONS Simvastatin attenuates increases in cardiorespiratory fitness and skeletal muscle mitochondrial content when combined with exercise training in overweight or obese patients at risk of the metabolic syndrome. (Exercise, Statins, and the Metabolic Syndrome; NCT01700530).


The Journal of Physiology | 2009

Changes in visceral adipose tissue mitochondrial content with type 2 diabetes and daily voluntary wheel running in OLETF rats

Matthew J. Laye; R. Scott Rector; Shana O. Warner; Scott P. Naples; Aspen L. Perretta; Grace M. Uptergrove; M. Harold Laughlin; John P. Thyfault; Frank W. Booth; Jamal A. Ibdah

Using the hyperphagic, obese, Otsuka Long–Evans Tokushima Fatty (OLETF) rat, we sought to determine if progression to type 2 diabetes alters visceral white adipose tissue (WAT) mitochondrial content and if these changes are modified through prevention of type 2 diabetes with daily exercise. At 4 weeks of age, OLETF rats began voluntary wheel running (OLETF‐EX) while additional OLETF rats (OLETF‐SED) and Long–Evans Tokushima Otsuka (LETO‐SED) rats served as obese and lean sedentary controls, respectively, for 13, 20 and 40 weeks of age (n= 6–8 for each group at each age). OLETF‐SED animals displayed insulin resistance at 13 and 20 weeks and type 2 diabetes by 40 weeks. OLETF‐SED animals gained significantly (P < 0.001) more weight and omental fat mass compared with OLETF‐EX and LETO‐SED. Markers of WAT mitochondrial protein content (cytochrome c, COXIV‐subunit I, and citrate synthase activity) significantly increased (P < 0.05) from 13 to 40 weeks in the LETO‐SED, but were significantly attenuated in the OLETF‐SED rats. Daily exercise normalized WAT cytochrome c and COXIV‐subunit I protein content in the OLETF‐EX to the healthy LETO‐SED animals. In conclusion, increases in omental WAT mitochondrial content between 20 and 40 weeks of age in LETO control animals are attenuated in the hyperphagic, obese OLETF rat. These alterations occurred in conjunction with the progression from insulin resistance to type 2 diabetes and were prevented with daily exercise. Reduced ability to increase WAT mitochondrial content does not appear to be a primary cause of insulin resistance, but may play a key role in the worsening of the disease condition.


Journal of Applied Physiology | 2009

Cessation of daily wheel running differentially alters fat oxidation capacity in liver, muscle, and adipose tissue

Matthew J. Laye; R. Scott Rector; Sarah J. Borengasser; Scott P. Naples; Grace M. Uptergrove; Jamal A. Ibdah; Frank W. Booth; John P. Thyfault

Physical inactivity is associated with the increased risk of developing chronic metabolic diseases. To understand early alterations caused by physical inactivity, we utilize an animal model in which rats are transitioned from daily voluntary wheel running to a sedentary condition. In the hours and days following this transition, adipose tissue mass rapidly increases, due in part to increased lipogenesis. However, whether a concurrent decrease in fatty acid oxidative capacity (FAO) in skeletal muscle, liver, and adipose tissue occurs during this period is unknown. Following 6 wk of access to voluntary running wheels (average distance of approximately 6 km a night), rats were rapidly transitioned to a sedentary state by locking the wheels for 5 h (WL5) or 173 h (WL173). Complete ([(14)C]palmitate oxidation to (14)CO(2)) and incomplete ([(14)C]palmitate oxidation to (14)C-labeled acid soluble metabolites) was determined in isolated mitochondrial and whole homogenate preparations from skeletal muscle and liver and in isolated adipocytes. Strikingly, the elevated complete FAO in the red gastrocnemius at WL5 fell to that of rats that never ran (SED) by WL173. In contrast, hepatic FAO was elevated at WL173 above both WL5 and SED groups, while in isolated adipocytes, FAO remained higher in both running groups (WL5 and WL173) compared with the SED group. The alterations in muscle and liver fat oxidation were associated with changes in carnitine palmitoyl transferase-1 activity and inhibition, but not significant changes in other mitochondrial enzyme activities. In addition, peroxisome proliferator-activated receptor coactivator-1alpha mRNA levels that were higher in both skeletal muscle and liver at WL5 fell to SED levels at WL173. This study is the first to demonstrate that the transition from high to low daily physical activity causes rapid, tissue-specific changes in FAO.


Applied Physiology, Nutrition, and Metabolism | 2010

Skeletal muscle mitochondrial and metabolic responses to a high-fat diet in female rats bred for high and low aerobic capacity.

Scott P. Naples; Sarah J. Borengasser; R. Scott Rector; Grace M. UptergroveG.M. Uptergrove; E. Matthew Morris; Catherine R. Mikus; Lauren G. Koch; Steve L. Britton; Jamal A. Ibdah; John P. Thyfault

Rats selected artificially to be low-capacity runners (LCR) possess a metabolic syndrome phenotype that is worsened by a high-fat diet (HFD), whereas rats selected to be high-capacity runners (HCR) are protected against HFD-induced obesity and insulin resistance. This study examined whether protection against, or susceptibility to, HFD-induced insulin resistance in the HCR-LCR strains is associated with contrasting metabolic adaptations in skeletal muscle. HCR and LCR rats (generation 20; n = 5-6; maximum running distance approximately 1800 m vs. approximately 350 m, respectively (p < 0.0001)) were divided into HFD (71.6% energy from fat) or normal chow (NC) (16.7% energy from fat) groups for 7 weeks (from 24 to 31 weeks of age). Skeletal muscle (red gastrocnemius) mitochondrial-fatty acid oxidation (FAO), mitochondrial-enzyme activity, mitochondrial-morphology, peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC-1alpha), and peroxisome proliferator-activated receptor delta (PPARdelta) expression and insulin sensitivity (intraperitoneal glucose tolerance tests) were measured. The HFD caused increased adiposity and reduced insulin sensitivity only in the LCR and not the HCR strain. Isolated mitochondria from the HCR skeletal muscle displayed a 2-fold-higher rate of FAO on NC, but both groups increased FAO following HFD. PGC-1alpha mRNA expression and superoxide dismutase activity were significantly reduced with the HFD in the LCR rats, but not in the HCR rats. PPARdelta expression did not differ between strains or dietary conditions. These results do not provide a clear connection between protection of insulin sensitivity and HFD-induced adaptive changes in mitochondrial function or transcriptional responses but do not dismiss the possibility that elevated mitochondrial FAO in the HCR may play a protective role.


American Journal of Physiology-endocrinology and Metabolism | 2010

Changes in skeletal muscle mitochondria in response to the development of type 2 diabetes or prevention by daily wheel running in hyperphagic OLETF rats

R. Scott Rector; Grace M. Uptergrove; Sarah J. Borengasser; Catherine R. Mikus; E. Matthew Morris; Scott P. Naples; Matthew J. Laye; M. Harold Laughlin; Frank W. Booth; Jamal A. Ibdah; John P. Thyfault

The temporal changes in skeletal muscle mitochondrial content and lipid metabolism that precede type 2 diabetes are largely unknown. Here we examined skeletal muscle mitochondrial fatty acid oxidation (MitoFAOX) and markers of mitochondrial gene expression and protein content in sedentary 20- and 40-wk-old hyperphagic, obese Otsuka Long-Evans Tokushima fatty (OLETF-SED) rats. Changes in OLETF-SED rats were compared with two groups of rats who maintained insulin sensitivity: age-matched OLETF rats given access to voluntary running wheels (OLETF-EX) and sedentary, nonobese Long-Evans Tokushima Otsuka (LETO-SED) rats. As expected, glucose tolerance tests revealed insulin resistance at 20 wk that progressed to type 2 diabetes at 40 wk in the OLETF-SED, whereas both the OLETF-EX and LETO-SED maintained whole body insulin sensitivity. At 40 wk, complete MitoFAOX (to CO(2)), beta-hydroxyacyl-CoA dehydrogenase activity, and citrate synthase activity did not differ between OLETF-SED and LETO-SED but were significantly (P < 0.05) higher in OLETF-EX compared with OLETF-SED rats. Genes controlling skeletal muscle MitoFAOX (PGC-1alpha, PPARdelta, mtTFA, cytochrome c) were not different between OLETF-SED and LETO-SED at any age. Compared with the OLETF-SED, the OLETF-EX rats had significantly (P < 0.05) higher skeletal muscle PGC-1alpha, cytochrome c, and mtTFA mRNA levels at 20 and 40 wk and PPARdelta at 40 wk; however, protein content for each of these markers did not differ between groups at 40 wk. Limited changes in skeletal muscle mitochondria were observed during the transition from insulin resistance to type 2 diabetes in the hyperphagic OLETF rat. However, diabetes prevention through increased physical activity appears to be mediated in part through maintenance of skeletal muscle mitochondrial function.


Journal of Applied Physiology | 2012

Effects of voluntary running on oxygen consumption, RQ, and energy expenditure during primary prevention of diet-induced obesity in C57BL/6N mice

Jacob D. Brown; Scott P. Naples; Frank W. Booth

Diet-induced obesity (DIO) in C57BL/6 mice is the standard model for studying obesity in mice. The few reports of DIO utilizing voluntary running provide contradictory results with respect to prevention of obesity. However, total energy expenditures associated with voluntary running during DIO are unknown. We hypothesized that voluntary running would increase the amount of total energy expended during DIO. Female C57BL/6N mice were randomly assigned to one of three experimental groups [high-fat diet with voluntary running (HFRun); high-fat diet without running (HFSed); and low-fat diet without running (LFSed)] for a 10-wk period. We confirmed production of obesity in HFSed, and more importantly demonstrated primary prevention of obesity by voluntary running in a group of cohorts (HFRun). Indirect calorimetry was performed to determine oxygen consumption (Vo(2)) and respiratory quotient (RQ). The following novel mechanisms were identified in female C57BL/6N mice: 1) HFRun showed ∼2 times greater total energy expenditures during a day compared with HFSed and LFSed; 2) HFRun had increased Vo(2) compared with HFSed and LFSed, lower RQ in the light period than HFSed, and lower RQ in both light and dark periods than LFSed; and 3) in the HFRun group, the magnitude of change in Vo(2) and RQ differed in dark and light periods during voluntary running. Our data combined with existing literature point to a potential threshold of physical activity that would prevent DIO in this mouse model. These data give a mechanistic explanation to resolve contradictory reports on whether voluntary running can prevent obesity in the DIO mouse model. In conclusion, voluntary running rescues high-fat fed, female C57BL/6N mice from obesity in DIO by doubling energy expenditure during the dark period and significantly increasing energy expenditure during the light cycle.


Medicine and Science in Sports and Exercise | 2010

Effects of Statins on Metabolic Adaptations to Aerobic Exercise Training: Preliminary Findings: 2701

Leryn J. Boyle; Jessica L. Libla; Catherine R. Mikus; Sarah J. Borengasser; Scott P. Naples; Meghan L. Ruebel; Nicolas M. Szary; Paul J. Fadel; Tom R. Thomas; M. Harold Laughlin; John P. Thyfault

Results: Baseline age, body weight, and body mass index (BMI) of St+Ex and Ex were as follows: 41±2.5 and 40±4.7 yr, 98.2±7.0 and 84.7±4.0 kg, 33.6±1.6 and 30.3±1.0 kg·m-2, respectively. Body weight and BMI were unchanged in response to both therapies. Fasting insulin levels decreased significantly with Ex therapy (10.6±5.0 to 8.8±4.8 uIU·ml-1, p<0.05), while no difference was observed after St+Ex therapy (8.7±3.3 to 9.9±3.9 uIU·ml-1). Fasting blood glucose did not change in response to St+Ex (94.4±3.2 to 90.7±3.4 mg·dL-1) or Ex (83.7±3.6 to 85.5±3.8 mg·dL-1) therapy. Only exercise improved maximal oxygen consumption (fitness) (33.8±2.6 to 36.3±3.4 ml·kg-1·min-1) while no improvements were observed in response to combined St+Ex therapy (25.7±1.4 to 26.0±1.3 ml·kg-1·min-1).


Gastroenterology | 2011

Division I College Athletes of the Highest Intensity Sports Have More Functional GI Disorders

Eva H. Alsheik; Scott P. Naples; Thomas Coyne; Kashif S. Anwar; Xochiquetzal Martinez; Amir Prushani; Eugene Hong; Scott E. Myers; JulieAnne Hlavac Bruno; Asyia S. Ahmad


Archive | 2015

prevention of diet-induced obesity in C57BL/6N mice RQ, and energy expenditure during primary Effects of voluntary running on oxygen consumption,

Jacob D. Brown; Scott P. Naples; Frank W. Booth; Michael D. Roberts; Lauren P. Oberle; J Alexander; Jens J. Holst; Bente K. Pedersen; Seier Hansen; Kristian Karstoft; Louise Lehrskov-Schmidt; Maria Pedersen; Thomas P. J. Solomon; Sine H. Knudsen

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Sarah J. Borengasser

University of Arkansas for Medical Sciences

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