Crnh Auvergne

Clermont-Ferrand, France

Crnh Auvergne

Clermont-Ferrand, France
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Thivel D.,University of Auvergne | Doucet E.,University of Ottawa | Julian V.,CRNH Auvergne | Julian V.,Clermont Ferrand University Hospital | And 11 more authors.
Physiology and Behavior | Year: 2017

Background To compare the energy and macronutrient intake responses to equivalent energy deficits induced by diet (food restriction) and exercise in adolescents with obesity. Methods Fourteen 12–15 years old obese adolescents completed three experimental conditions (08:00 am to 07:30 pm) in a randomized crossover design: i) control session (CON); ii) diet-induced 25% energy depletion (Def-EI), iii) and an exercise-induced 25% energy depletion (Def-EX). The sessions order was either CON/Def-EI/Def-EX or CON/Def-EX/Def-EI as the deficit corresponded to 25% of the energy ingested at lunch on the control day (CON) and was imposed either by exercise (Def-EX) or diet (Def-EI). Ad libitum EI and macronutrients preferences were assessed at dinner and appetite sensations assessed using visual analogue scales. Results Mean BMI was 36.6 ± 5.0 kg/m2 (z-BMI: 2.40 ± 0.29). The individually calibrated 25% energy deficit represented 254 ± 92 kcal. Ad libitum EI was significantly higher during both Def-EX (971 ± 225 kcal) and Def-EI (949 ± 246 kcal) compared with CON (742 ± 297) (p < 0.05). The relative energy ingested derived from fat was significantly higher on both Def-EX (36.6 ± 10.9%) and Def-EI (36.9 ± 13.1%) compared with CON (21.6 ± 7.8%) (p < 0.05). The energy derived from carbohydrates was significantly lower on both Def-EX (48.3 ± 9.0%) and Def-EI (44.4 ± 17.3%) compare with CON (61.1 ± 10.1%) (p < 0.05). Appetite sensations were not different between conditions. The induced energy deficit was negatively correlated with the ad libitum EI difference between the exercise and the control session (EI Def-EX – EI CON) (r = − 0,643 p < 0.05) and positively correlated with the EI difference between the dietary restriction and the control session (EI Def-EI – EI CON) (r = 0,569 p < 0.05). Conclusion Equicaloric exercise- or diet-induced energy deficits could lead to similar EI compensation in obese adolescents but this EI compensation might be influenced by the magnitude of the deficit. © 2016 Elsevier Inc.


Fearnbach S.N.,Pennsylvania State University | Fearnbach S.N.,Biomedical Imaging Center | Silvert L.,University Blaise Pascal | Silvert L.,French National Center for Scientific Research | And 10 more authors.
Nutrition Research | Year: 2017

Acute exercise has been found to reduce subsequent energy intake in obese adolescents. Although it has been suggested that some neural pathways are involved in this post-exercise energy intake regulation, it remains unknown whether the post-exercise attentional response to food cues differs as a function of weight status. We hypothesize that there will be a reduction in the neural response to food cues as a result of exercise in obese adolescents, but not in their lean counterparts. Fourteen obese and 14 lean adolescent boys (12-15 years) were randomized (within-subjects design) to remain seated (CON) or to exercise 45 minutes at 65% of their maximal capacities (EX). After the exercise or sitting period, the adolescents' cognitive engagement in the processing of food vs. non-food cues was assessed during an attentional computer-based task with electroencephalography (EEG) recording. An ad libitum lunch meal was offered and appetite feelings were assessed (visual analog scales). There was no main effect of condition on energy intake in lean subjects, but obese adolescents ate significantly less following EX compared with CON (P <.05). There was no effect of condition or stimulus type (food vs. non-food) on the EEG-recorded amplitude of the P3b component in lean adolescents. However, the response to food cues was significantly reduced compared with non-food stimuli after exercise in obese participants (P <.01). Following EX, but not CON, total body weight, body mass index, and fat mass were inversely correlated with the EEG response to food–non-food stimuli (all P <.05). However, this response was not associated with ad libitum EI (both P >.1). Acute exercise favors decreased neural response to food cues compared with non-food cues in obese but not lean adolescents, suggesting differential effects of exercise on the neural processing of food cues based on weight status. © 2017 Elsevier Inc.


Gladine C.,Clermont University | Gladine C.,French National Institute for Agricultural Research | Meunier N.,Crnh Auvergne | Blot A.,Crnh Auvergne | And 9 more authors.
Contemporary Clinical Trials | Year: 2011

Numerous micronutrients naturally abundant in oilseeds prevent the risk of cardiovascular diseases by reducing cholesterolemia and oxidative stress. These micronutrients include phytosterols and various antioxidants such as polyphenols, tocopherols and coenzyme Q10/Q9 but most of them are lost during the oilseed oil refining. The main objective of the Optim'Oil project was to modify the processes of oil refining in order to reduce the lost of micronutrients. Two clinical trials (cross-over, monocentric, randomized, double-blind and controlled) were designed to investigate the effect of an optimized rapeseed oil 1) on cardiovascular biomarkers (long-term study) and 2) on oxidative stress parameters (post-prandial study). For the long-term study, 59 volunteers ingested daily 20 g of oil and 22 g of margarine (optimized or standard) for 2 periods of 3 weeks separated by a 3-week wash-out period. Blood samples were collected at the beginning and at the end of each period. For the post-prandial study, a sub-group of 16 volunteers came fasted at the laboratory and took 300 mL of a test meal containing 60% of the optimized or standard oils. Blood samples were collected before and during 6 h after the test meal intake. In comparison with the standard oil and margarine, the optimized oil and margarine exhibit as expected an increased content of phytosterol (+. 22%), polyphenols (×11), tocopherols (+. 131%) and coenzyme Q10/Q9 (+. 165%). Overall, conditions of this study were relevant to investigate the effect of the optimized rapeseed oil and margarine on the cardiovascular risk and the oxidative stress. © 2010 Elsevier Inc.


Caillaud K.,University Blaise Pascal | Boisseau N.,University Blaise Pascal | Ennequin G.,University Blaise Pascal | Chavanelle V.,University Blaise Pascal | And 8 more authors.
Diabetes and Metabolism | Year: 2015

Aim: Studies both in vitro and ex vivo of rodent skeletal muscle have highlighted the potential involvement of neuregulin 1 (NRG1) in glucose metabolism regulation, yet nothing is known of the role of NRG1 in systemic glucose homoeostasis. For this reason, it was hypothesized that systemic delivery of NRG1 might improve glucose tolerance and that the effect might be age-dependent. Methods: Glucose tolerance tests were performed in 6-month-old (adult) and 22-month-old (old) male Wistar rats 15. min after a single injection of either NRG1 (50. μg/kg) or saline (controls). Skeletal muscle and liver samples were also collected 30. min after the acute NRG1 or saline treatment, while the phosphorylation status of ErbB receptors and AKT was assessed by Western blotting. Results: Acute NRG1 treatment decreased the glycaemic response to an oral glucose load in both adult and old rats. NRG1 injection did not activate ErbB receptors in skeletal muscle, whereas phosphorylation of ErbB3 and AKT was markedly increased in the liver of NRG1-treated adult and old rats compared with controls. Conclusion: This study shows that NRG1 has a possible glucose-lowering effect in the liver and via an ErbB3/AKT signaling pathway. This NRG1 effect is also maintained in old rats, suggesting that the NRG1/ErbB signaling pathway might represent a promising therapeutic target in insulin resistance states. © 2015 Elsevier Masson SAS.


Ennequin G.,University Blaise Pascal | Boisseau N.,University Blaise Pascal | Caillaud K.,University Blaise Pascal | Chavanelle V.,University Blaise Pascal | And 19 more authors.
Journal of Physiology | Year: 2015

Some studies suggest that the signalling pathway of neuregulin 1 (NRG1), a protein involved in the regulation of skeletal muscle metabolism, could be altered by nutritional and exercise interventions. We hypothesized that diet-induced obesity could lead to alterations of the NRG1 signalling pathway and that chronic exercise could improve NRG1 signalling in rat skeletal muscle. To test this hypothesis, male Wistar rats received a high fat/high sucrose (HF/HS) diet for 16 weeks. At the end of this period, NRG1 and ErbB expression/activity in skeletal muscle was assessed. The obese rats then continued the HF/HS diet or were switched to a well-balanced diet. Moreover, in both groups, half of the animals also performed low intensity treadmill exercise training. After another 8 weeks, NRG1 and ErbB expression/activity in skeletal muscle were tested again. The 16 week HF/HS diet induced obesity, but did not significantly affect the NRG1/ErbB signalling pathway in rat skeletal muscle. Conversely, after the switch to a well-balanced diet, NRG1 cleavage ratio and ErbB4 amount were increased. Chronic exercise training also promoted NRG1 cleavage, resulting in increased ErbB4 phosphorylation. This result was associated with increased protein expression and phosphorylation ratio of the metalloprotease ADAM17, which is involved in NRG1 shedding. Similarly, in vitro stretch-induced activation of ADAM17 in rat myoblasts induced NRG1 cleavage and ErbB4 activation. These results show that low intensity endurance training and well-balanced diet activate the NRG1-ErbB4 pathway, possibly via the metalloprotease ADAM17, in skeletal muscle of diet-induced obese rats. © 2015 The Physiological Society.


Isacco L.,University of Franche Comte | Thivel D.,University Blaise Pascal | Pereira B.,Estaing University Hospital Center | Duclos M.,CRNH Auvergne | And 4 more authors.
European Journal of Applied Physiology | Year: 2015

Purpose: Synthetic ovarian hormones contained in oral contraceptives (OC) may alter the aerobic capacity and lipid metabolism in oral contraceptive users (OC+) compared with non-users (OC−). The aim of this study was thus to investigate the differences between OC− and OC+ (1) in cardiorespiratory parameters at the anaerobic threshold (AT) and at the maximal aerobic capacity and (2) in the exercise intensity (Lipoxmax) at which lipid oxidation rate is maximal (MLOR).Methods: Twenty-one healthy untrained women (22.0 ± 0.6 years old) who took OC (OC+; low-dose monophasic OC, n = 11) or not (OC−; n = 10) performed two experimental exercise sessions. In the first one, cardiorespiratory parameters at the AT and at the maximal aerobic capacity were assessed during a maximal incremental exercise session. In the second one, Lipoxmax and MLOR were measured during a submaximal incremental exercise session.Results: No significant difference was observed in cardiorespiratory parameters at the AT and at the maximal aerobic capacity between OC+ and OC− women. OC+ women showed higher MLOR (7.6 ± 1.9 vs 4.6 ± 1.0 mg min−1 kg FFM−1; p < 0.01) that was elicited by higher Lipoxmax (45.2 ± 5.2 vs 36.2 ± 4.1 % of VO2max; p < 0.001) compared to OC− women.Conclusions: OC+ and OC− women did not differ in cardiorespiratory parameters at the AT and at the maximal aerobic capacity. However, OC+ women show higher MLOR and Lipoxmax compared with OC− women. The hormonal status appears to be an important MLOR and Lipoxmax determinant in untrained women. © 2014, Springer-Verlag Berlin Heidelberg.


Pujos-Guillot E.,French National Institute for Agricultural Research | Pickering G.,French Institute of Health and Medical Research | Lyan B.,French National Institute for Agricultural Research | Ducheix G.,French Institute of Health and Medical Research | And 8 more authors.
Age | Year: 2012

Sulfur amino acids are determinant for the detoxification of paracetamol (N-acetyl-p-aminophenol) through sulfate and glutathione conjugations. Long-term paracetamol treatment is common in the elderly, despite a potential cysteine/glutathione deficiency. Detoxification could occur at the expense of anti-oxidative defenses and whole body protein stores in elderly. We tested how older persons satisfy the extra demand in sulfur amino acids induced by long-term paracetamol treatment, focusing on metabolic and nutritional aspects. Effects of 3 g/day paracetamol for 14 days on fasting blood glutathione, plasma amino acids and sulfate, urinary paracetamol metabolites, and urinary metabolomic were studied in independently living older persons (five women, five men, mean (±SEM) age 74 ± 1 years). Dietary intakes were recorded before and at the end of the treatment and ingested sulfur amino acids were evaluated. Fasting blood glutathione, plasma amino acids, and sulfate were unchanged. Urinary nitrogen excretion supported a preservation of whole body proteins, but large-scale urinary metabolomic analysis revealed an oxidation of some sulfur-containing compounds. Dietary protein intake was 13% higher at the end than before paracetamol treatment. Final sulfur amino acid intake reached 37 mg/kg/day. The increase in sulfur amino acid intake corresponded to half of the sulfur excreted in urinary paracetamol conjugates. In conclusion, older persons accommodated to long-term paracetamol treatment by increasing dietary protein intake without any mobilization of body proteins, but with decreased anti-oxidative defenses. The extra demand in sulfur amino acids led to a consumption far above the corresponding population-safe recommendation. © 2011 American Aging Association.


PubMed | University of Texas Health Science Center at Houston, University Blaise Pascal and CRNH Auvergne
Type: Journal Article | Journal: The Journal of physiology | Year: 2015

Some studies suggest that neuregulin 1 (NRG1) could be involved in the regulation of skeletal muscle energy metabolism in rodents. Here we assessed whether unbalanced diet is associated with alterations of the NRG1 signalling pathway and whether exercise and diet might restore NRG1 signalling in skeletal muscle of obese rats. We show that diet-induced obesity does not impair NRG1 signalling in rat skeletal muscle. We also report that endurance training and a well-balanced diet activate the NRG1 signalling in skeletal muscle of obese rats, possibly via a new mechanism mediated by the protease ADAM17. These results suggest that some beneficial effects of physical activity and diet in obese rats could be partly explained by stimulation of the NRG1 signalling pathway.Some studies suggest that the signalling pathway of neuregulin 1 (NRG1), a protein involved in the regulation of skeletal muscle metabolism, could be altered by nutritional and exercise interventions. We hypothesized that diet-induced obesity could lead to alterations of the NRG1 signalling pathway and that chronic exercise could improve NRG1 signalling in rat skeletal muscle. To test this hypothesis, male Wistar rats received a high fat/high sucrose (HF/HS) diet for 16weeks. At the end of this period, NRG1 and ErbB expression/activity in skeletal muscle was assessed. The obese rats then continued the HF/HS diet or were switched to a well-balanced diet. Moreover, in both groups, half of the animals also performed low intensity treadmill exercise training. After another 8weeks, NRG1 and ErbB expression/activity in skeletal muscle were tested again. The 16week HF/HS diet induced obesity, but did not significantly affect the NRG1/ErbB signalling pathway in rat skeletal muscle. Conversely, after the switch to a well-balanced diet, NRG1 cleavage ratio and ErbB4 amount were increased. Chronic exercise training also promoted NRG1 cleavage, resulting in increased ErbB4 phosphorylation. This result was associated with increased protein expression and phosphorylation ratio of the metalloprotease ADAM17, which is involved in NRG1 shedding. Similarly, in vitro stretch-induced activation of ADAM17 in rat myoblasts induced NRG1 cleavage and ErbB4 activation. These results show that low intensity endurance training and well-balanced diet activate the NRG1-ErbB4 pathway, possibly via the metalloprotease ADAM17, in skeletal muscle of diet-induced obese rats.

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