Etudes Perte de poids

Rôle de l’entraînement sur la densité mitochondriale

09/06/2017 | Etudes cardio et Etudes Perte de poids

 

Exercise training increases skeletal muscle mitochondrial volume density by enlargement of existing mitochondria and not de novo biogenesis
Anne-Kristine Meinild Lundby       Acta physiol 2017

Aims

1) determine whether exercise induced increases in muscle mitochondrial volume density (MitoVD) is related to enlargement of existing mitochondria or de novo biogenesis, 2) establish if measures of mitochondrial-specific enzymatic activities are valid biomarkers for exercise induced increases in MitoVD.
Method

Skeletal muscle samples were collected from twenty-one healthy males prior to and following 6 weeks of endurance training. Transmission electron microscopy was used for estimation of mitochondrial densities and profiles. Biochemical assays, western blotting and high resolution respirometry were applied to detect changes in specific mitochondrial functions.
Result

MitoVD increased with 55 ± 9% (P

< 0.001), whereas the number of mitochondrial profiles per area of skeletal muscle remained unchanged following training

. Citrate synthase activity (CS) increased (44 ± 12%, P < 0.001) however, there were no functional changes in oxidative phosphorylation capacity (OXPHOS, CI+IIP) or cytochrome c oxidase (COX) activity. Correlations were found between MitoVD and CS (P=0.01; r=0.58), OXPHOS, CI+CIIP (P=0.01; R=0.58) and COX (P=0.02; R=0.52) before training, after training a correlation was found between MitoVD and CS activity only (P=0.04; R=0.49). Intrinsic respiratory capacities decreased (P < 0.05) with training when respiration was normalized to MitoVD. This was not the case when normalized to CS activity although the percentage change was comparable.
Conclusions

MitoVD was increased by inducing mitochondrial enlargement rather than de novo biogenesis. CS activity may be appropriate to track training induced changes in MitoVD.

Rôles des peptides mitochondriaux dans la perte de graisse

09/06/2017 | Etudes cardio et Etudes Perte de poids

 

Mitochondrial derived peptides as novel regulators of metabolism
Su-Jeong Kim             J Physiol 2017
         
Mitochondrial derived peptides represent a new class of circulating signalling molecules. Humanin, the first member of this class, has been shown to have several metabolic effects such as reducing weight gain and visceral fat and increasing glucose stimulated insulin release. The discovery of several other new members such as MOTS-c and SHLP1-6, have further added to this group. These new peptides have also been found to affect metabolism with MOTS-c potently decreasing weight gain in mice on a high fat diet. In this review, we will cover the basic biology of this class of peptides and discuss the relevance to organismal metabolism.

L’équilibre en sodium est plus compliqué qu’il n’y parait

09/05/2017 | Etudes sur les hormones et Etudes Compléments alimentaires et Etudes Perte de poids et Etudes Anti-âge

 

Increased salt consumption induces body water conservation and decreases fluid intake
Natalia Rakova       J Clin Invest April 17, 2017 - More info

The idea that increasing salt intake increases drinking and urine volume is widely accepted. We tested the hypothesis that an increase in salt intake of 6 g/d would change fluid balance in men living under ultra-long-term controlled conditions.

METHODS. Over the course of 2 separate space flight simulation studies of 105 and 205 days’ duration, we exposed 10 healthy men to 3 salt intake levels (12, 9, or 6 g/d). All other nutrients were maintained constant. We studied the effect of salt-driven changes in mineralocorticoid and glucocorticoid urinary excretion on day-to-day osmolyte and water balance.

RESULTS. A 6-g/d increase in salt intake increased urine osmolyte excretion, but reduced free-water clearance, indicating endogenous free water accrual by urine concentration. The resulting endogenous water surplus reduced fluid intake at the 12-g/d salt intake level. Across all 3 levels of salt intake, half-weekly and weekly rhythmical mineralocorticoid release promoted free water reabsorption via the renal concentration mechanism. Mineralocorticoid-coupled increases in free water reabsorption were counterbalanced by rhythmical glucocorticoid release, with excretion of endogenous osmolyte and water surplus by relative urine dilution. A 6-g/d increase in salt intake decreased the level of rhythmical mineralocorticoid release and elevated rhythmical glucocorticoid release. The projected effect of salt-driven hormone rhythm modulation corresponded well with the measured decrease in water intake and an increase in urine volume with surplus osmolyte excretion.

CONCLUSION. Humans regulate osmolyte and water balance by rhythmical mineralocorticoid and glucocorticoid release, endogenous accrual of surplus body water, and precise surplus excretion.

Vitamine P4 contre la fatigue

30/04/2017 | Etudes Compléments alimentaires et Etudes Perte de poids et Etudes Anti-âge

 

Short-term effects of troxerutin (vitamin P4) on muscle fatigue and gene expression of Bcl-2 and Bax in the hepatic tissue of rats

Mohammad Zamanian         Revue canadienne de physiologie et pharmacologie 2017

Dans les présents travaux, nous avons étudié l’effet de la troxérutine (TRX) sur la fatigue musculaire et l’expression des gènes Bcl-2 et Bax dans le tissu hépatique de rat. Nous avons réparti aléatoirement 40 rats Wistar mâles dans les quatre groupes suivants : témoin et administration de TRX à 75 (TRX75), 150 (TRX150) et 300 mg/kg par jour (TRX300). Les groupes TRX et placebo ont reçu pendant 7 jours de la TRX et de l’eau, respectivement. Le 7e jour, tous les animaux ont été euthanasiés immédiatement après un test de nage menant à l’épuisement, et nous avons mesuré plusieurs paramètres biochimiques liés à la fatigue et à l’expression des gènes Bcl-2 et Bax dans le tissu hépatique. Nos résultats ont montré que dans le groupe TRX300, le temps de nage écoulé avant l’épuisement était 1,2 fois plus élevé que dans le groupe témoin (résultats statistiquement significatifs : P < 0,001).

Dans le groupe TRX300, l’activité de l’ALT diminuait et l’activité hépatique de la SOD augmentait de façons nettement plus marquées que dans le groupe témoin (P < 0,05 et P < 0,01, respectivement). De plus, la TRX entraînait une diminution de l’expression de l’ARNm du gène Bax et une augmentation du rapport Bcl-2/Bax nettement plus marquées que dans le groupe témoin (P < 0,001 dans les deux cas).

D’après nos données, la TRX exerce une action anti-apoptotique et hépatoprotectrice à la suite d’un exercice de nage menant à l’épuisement.

PTH et catabolisme

20/04/2017 | Etudes sur les hormones et Etudes Perte de poids

 

Parathyroid hormone stimulates adipose tissue browning: a pathway to muscle wasting
Thomas, Sandhya         Current Opinion in Clinical Nutrition & Metabolic Care: May 2017 - Volume 20 - Issue 3 - p 153–157

Purpose of review: Studying organ-to-organ communications (i.e. crosstalk) uncovers mechanisms regulating metabolism in several tissues. What is missing is identification of mediators of different catabolic conditions contributing to losses of adipose and muscle tissues. Identifying mediators involved in organ-to-organ crosstalk could lead to innovative therapeutic strategies because several disorders such as chronic kidney disease (CKD), cancer cachexia, and other catabolic conditions share signals of worsening metabolism and increased risk of mortality.

Recent findings: A recent breakthrough published in Cell Metabolism leads to the conclusion that parathyroid hormone (PTH) and parathyroid hormone-related peptide (PTHrP) cause ‘browning’ of white adipose tissue plus energy production via activation of uncoupling protein-1. Browning was associated with muscle wasting in mouse models of cancer and CKD. The pathway to browning includes PTH/PTHrP activation of protein kinase A (PKA) and lost muscle mass via the ubiquitin proteasome proteolytic system (UPS).

Summary: The results suggest that crosstalk between muscle and fat contributes in a major way to tissue catabolism. The pathway initiated by PTH or PTHrP is novel and it suggests potential interrelationships that control metabolism in other catabolic conditions. Identifying how the parathyroid hormone–PKA–UPS axis relates to obesity, type 2 diabetes, and other insulin-resistant conditions remains unclear.

Le Viagra est-il aussi un anti-aromatase?

01/12/2016 | Etudes Perte de poids et Etudes Anti-âge et Etudes sur les boosters sexuels et la sexualité

 

Effect of sildenafil on human aromatase activity: From in vitro structural analysis to catalysis and inhibition in cells
The Journal of Steroid Biochemistry and Molecular Biology Volume 165, Part B, January 2017, Pages 438–447       Roberta Baravalle

Highlights
• Human aromatase binds the drug sildenafil showing a Type II spectrum.
• EPR spectroscopy shows that sildenafil does not directly bind heme iron.
• Sildenafil acts as a mixed and partial inhibitor on human aromatase.
• Aromatase inhibition by sildenafil is confirmed in ST14A and MCF-7 cells.

Aromatase catalyses the conversion of androgens into estrogens and is a well-known target for breast cancer therapy. As it has been suggested that its activity is affected by inhibitors of phosphodiesterase-5, this work investigates the potential interaction of sildenafil with aromatase. This is carried out both at molecular level through structural and kinetics assays applied to the purified enzyme, and at cellular level using neuronal and breast cancer cell lines.

Sildenafil is found to bind to aromatase with a KD of 0.58 ± 0.05 μM acting as a partial and mixed inhibitor with a maximal inhibition of 35 ± 2%. Hyperfine sublevel correlation spectroscopy and docking studies show that sildenafil binds to the heme iron via its 6th axial water ligand.

These results also provide information on the starting molecular scaffold for the development of new generations of drugs designed to inhibit aromatase as well as phosphodiesterase-5, a new emerging target for breast cancer therapy.

Quels impacts des corps cétoniques chez le sportif?

18/11/2016 | Etudes Compléments alimentaires et Etudes Perte de poids

 

Metabolism of ketone bodies during exercise and training: physiological basis for exogenous supplementation
Mark Evans                   J Physiol 2016

Optimising training and performance through nutrition strategies is central to supporting elite sportspeople, much of which has focussed on manipulating the relative intake of carbohydrate and fat and their contributions as fuels for energy provision. The ketone bodies, namely acetoacetate, acetone, and β-hydroxybutyrate (βHB), are produced in the liver during conditions of reduced carbohydrate availability and serve as an alternative fuel source for peripheral tissues including brain, heart and skeletal muscle.

Ketone bodies are oxidised as a fuel source during exercise, are markedly elevated during the post-exercise recovery period, and the ability to utilise ketone bodies is higher in exercise-trained skeletal muscle. The metabolic actions of ketone bodies can alter fuel selection through attenuating glucose utilisation in peripheral tissues, anti-lipolytic effects on adipose tissue, and attenuation of proteolysis in skeletal muscle. Moreover, ketone bodies can act as signalling metabolites with βHB acting as an inhibitor of histone deacetylases, an important regulator of the adaptive response to exercise in skeletal muscle.

Recent development of ketone esters facilitates acute ingestion of βHB that results in nutritional ketosis without necessitating restrictive dietary practices. Initial reports suggest this strategy alters the metabolic response to exercise and improves exercise performance, while other lines of evidence suggest roles in recovery from exercise.

The present review focuses on the physiology of ketone bodies during and after exercise and in response to training, with specific interest in exploring the physiological basis for exogenous ketone supplementation and potential benefits for performance and recovery in athletes.

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