Etudes sur les hormones

Les protéines laitières rapides ont un impact à court et à long terme sur la glycémie

05/11/2017 | Etudes sur les hormones et Etudes Compléments alimentaires et Etudes Perte de poids et Etudes Anti-âge

 

Cela explique que l’on peut ne pas le sentir au début puis y devenir sensible

Comparison between pre–exercise casein peptide and intact casein supplementation on glucose tolerance in high–fat diet–fed mice

Yutaka Matsunaga         Applied Physiology, Nutrition, and Metabolism, 2017

We hypothesized that along with exercise, casein peptide supplementation would have a higher impact on improving glucose tolerance than intact casein. Male six–week–old ICR mice were provided a high–fat diet to induce obesity and glucose intolerance. The mice were randomly divided into four treatment groups: control (Con), endurance training (Tr), endurance training with intact casein supplementation (Cas+Tr), and endurance training with casein peptide supplementation (CP+Tr). The mice in each group were orally administrated water, intact casein, or casein peptide (1.0 mg/g BW, everyday), and then subjected to endurance training (15–25 m/min, 60 min, 5 times/week for 4 weeks) on a motor–driven treadmill 30 min after ingestion. Our results revealed that total intra–abdominal fat was significantly lower in CP+Tr than in Con (p<0.05). Following an oral glucose tolerance test, the blood glucose area under the curve (AUC) was found to be significantly smaller for CP+Tr than for Con (p<0.05). Moreover, in the soleus muscle, GLUT4 protein levels were significantly higher in CP+Tr than in Con (p<0.01). However, intra–abdominal fat, blood glucose AUC, and GLUT4 protein content in the soleus muscle did not alter in Tr and Cas+Tr when compared with Con. These observations suggest that pre–exercise casein peptide supplementation has a higher effect on improving glucose tolerance than intact casein does in high–fat diet–fed mice.

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.

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.

Angiotensine et catabolisme

20/04/2017 | Etudes sur les hormones

 

Skeletal muscle wasting: new role of nonclassical reninangiotensin system
Cabello-Verrugio           Current Opinion in Clinical Nutrition & Metabolic Care: May 2017 - Volume 20 - Issue 3 - p 158–163

Purpose of review: Skeletal muscle can be affected by many physiological and pathological conditions that contribute to the development of muscle weakness, including skeletal muscle loss, inflammatory processes, or fibrosis. Therefore, research into therapeutic treatment alternatives or alleviation of these effects on skeletal muscle is of great importance.

Recent findings: Recent studies have shown that angiotensin (1–7) [Ang-(1–7)] – a vasoactive peptide of the nonclassical axis in the renin–angiotensin system (RAS) – and its Mas receptor are expressed in skeletal muscle. Ang-(1–7), through its Mas receptor, prevents or diminishes deleterious effects induced by skeletal muscle disease or injury. Specifically, the Ang-(1–7)–Mas receptor axis modulates molecular mechanisms involved in muscle mass regulation, such as the ubiquitin proteasome pathway, the insulin-like growth factor type 1/Akt (protein kinase B) pathway, or myonuclear apoptosis, and also inflammation and fibrosis pathways.

Summary: Although further research into this topic and the possible side effects of Ang-(1–7) is necessary, these findings are promising, and suggest that the Ang-(1–7)–Mas axis can be considered a possible therapeutic target for treating patients with muscular disorders.

Effets de l’énanthate de testostérone sur les reins

21/03/2017 | Etudes sur les hormones

 

Effets de l’énanthate de testostérone sur les reins de rats mâles Wistar soumis à un entraînement en résistance
S. Karbasia         Science & Sports Available online 17 March 2017

Les Stéroïdes Anabolisants Androgéniques (AAS) sont les produits dopants les plus utilisés dans le sport et sont susceptibles d’exercer des effets secondaires sur le rein. Le but de cette étude était de déterminer les effets d’une injection d’énanthate de testostérone (TE) lors d’un entrainement en résistance (RT) de 8 semaines chez des rats Wistar mâles.

Matériels et méthodes

Vingt-huit rats Wistar mâles ont été randomisés en en 4 groupes : C : contrôle, RT : exercice en résistance + placebo, TE : énanthate de testostérone, et l’association des deux (TE + RT). Le Protocole d’entrainement en résistance consiste en la montée d’une échelle (5 fois à 3 reprises) pendant huit semaines. Le TE et le placebo (20 mg/kg de poids corporel, en IM) ont été injectés deux fois par jour. A la fin, les rats ont été euthanasiés pour réaliser l’analyse biochimique du sérum et l’examen histopathologique du tissu rénal.

Résultats

Dans le groupe RT, une augmentation significative (p

< 0,05) de la créatinine sérique a été observée en comparaison avec les groupes TE et TE + RT. Une hyperémie modérée et une congestion du tissu ont été observées dans tous les groupes de traitement.

Conclusion

Nous ne mettons pas en évidence de détérioration de la filtration glomérulaire après 8 semaines de TE (20 mg/kg) mais d’autres études sont nécessaires pour préciser l’effet rénal de ce traitement.

Rôle de la sirtuine 1 dans l’hypertrophie

02/03/2017 | Etudes sur les hormones et Etudes Musculation et Etudes Anti-âge

 

SIRT1 may play a crucial role in overload induced hypertrophy of skeletal muscle
Erika Koltai J physiol 2017

Significant skeletal muscle mass guarantees functional wellbeing and is important for high level performance in many sports. Although the molecular mechanism for skeletal muscle hypertrophy has been well-studied, it still is not completely understood. In the present study, we used a functional overload model to induce plantaris muscle hypertrophy by surgically removing the soleus, and gastrocnemius muscles in rats. Two weeks of muscle ablation resulted in a 40% increase in muscle mass, which was associated with a significant increase in SIRT1 content and activity (P

< 0.001). SIRT1-regulated Akt, eNOS, GLUT4 levels were also induced in hypertrophied muscles, and SIRT1 levels correlated with muscle mass, paired box protein 7 (Pax7), proliferating cell nuclear antigen (PCNA) and nicotinamide phosphoribosyltransferase (Nampt) levels. Alternatively, decreased FOXO1 and increased K48 polyubiquitination also suggest that SIRT1 could also be involved in the catabolic process of hypertrophy. Furthermore, increased levels of K63 and muscle RING finger 2 (MuRF2) protein could also be important enhancers of muscle mass. We report here that the levels of miR1 and miR133a decrease in hypertrophy and negatively correlate with muscle mass, SIRT1, and Nampt levels. Our results reveal a strong agreement between SIRT1 levels and activity, SIRT1 regulated pathways, and overload-induced hypertrophy.

These findings, along with the well-known regulatory

roles that SIRT1 plays in modulating both anabolic and catabolic pathways, allow us to propose the hypothesis that SIRT1 may actually play a crucial causal role in overload induced hypertrophy of skeletal muscle. This hypothesis will now require rigorous direct and functional testing.

Le mystère des aliments riche en mélatonine

31/12/2016 | Etudes sur les hormones et Etudes Compléments alimentaires et Etudes Anti-âge

 

Are the proposed benefits of melatonin-rich foods too hard to swallow?
David J. Kennaway     Critical Reviews in Food Science and Nutrition   2016 Pages 958-962

Melatonin has been proposed as a potent anti-oxidant, and its presence in many plants and foods has been suggested to be beneficial for health. Indeed, the concentrations of melatonin in blood and the melatonin metabolite 6 sulphatoxymelatonin in urine have been found to increase significantly after ingestion of melatonin-rich foods. In this review, the studies have been critically evaluated in light of the reported plant melatonin concentrations and our knowledge of pharmacokinetics of orally administered pure melatonin. In the case of studies involving measurement of plasma melatonin following ingestion of beer or fruits, the reported increase in melatonin is not consistent with the amount of melatonin ingested. Similarly, the amount of melatonin metabolite excreted following ingestion of melatonin-rich foods greatly exceeded the amount of melatonin ingested.

It is concluded that studies reporting the appearance of melatonin in blood and its metabolites in urine following ingestion of melatonin-rich foods are flawed. While there may be health benefits for certain foods, it is difficult to accept that these are due to their low melatonin content.

 

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