Etudes sur les hormones : page 3.8

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.

 

L’ibuprofène contre la fatigue?

28/09/2016 | Etudes cardio et Etudes sur les hormones et Echauffement et blessures

 

Ibuprofen intake increases exercise time to exhaustion: A possible role for preventing exercise-induced fatigue
F. D. Lima     Scandinavian Journal of Medicine & Science in Sports   volume 26, Issue 10 October 2016
Pages 1160–1170

Although the intake of nonsteroidal anti-inflammatory drugs (NSAIDs) intake by athletes prevents soreness, little is known concerning their role in exercise performance. This study assessed the effects of ibuprofen intake on an exhaustive protocol test after 6 weeks of swimming training in rats. Animals were divided into sedentary and training groups. After training, animals were subdivided into two subsets: saline or ibuprofen. Afterwards, three repeated swimming bouts were performed by the groups. Ibuprofen (15 mg/kg) was administered once a day. Pain measurements were performed and inflammatory and oxidative stress parameters were assayed in cerebral cortex and gastrocnemius muscle. Training, ibuprofen administration, or both combined (P 

< 0.05; 211 ± 18s, 200 ± 31s, and 279 ± 23s) increased exercise time to exhaustion.

Training decreased the acetylcholinesterase (AChE) activity (P 

< 0.05; 149 ± 11) in cerebral cortex.

Ibuprofen intake decreased the AChE activity after exhaustive protocol test in trained and sedentary rats (P < 0.05; 270 ± 60; 171 ± 38; and 273 ± 29). It also prevented neuronal tumor necrosis factor-α (TNF-α) and interleukin (IL 1β) increase. Fatigue elicited by this exhaustive protocol may involve disturbances of the central nervous system. Additive anti-inflammatory effects of exercise and ibuprofen intake support the hypothesis that this combination may constitute a more effective approach. In addition, ergogenic aids may be a useful means to prevent exercise-induced fatigue.

Tout sur la 11-kéto-testostérone

24/07/2016 | Etudes sur les hormones

 

11-ketotestosterone is a major androgen produced in human gonads
Yoshitaka Imamichi     The Journal of Clinical Endocrinology & Metabolism First Published Online: July 18, 2016

11-ketotestosterone (11-KT) is a novel class of active androgen. However, the detail of its synthesis remains unknown for humans.
Objective: The objective of this study was to clarify the production and properties of 11-KT in human.

Design, Participants and Methods: Expression of CYP11B1 and HSD11B2 (key enzymes involved in the synthesis of 11-KT) were investigated in human gonads. The production of 11-KT was investigated in Leydig cells. Plasma concentrations of testosterone and 11-KT were measured in 10 women and 10 men of reproductive age. Investigation of its properties was performed using breast cancer-derived MCF-7 cells.

Results: CYP11B1 and HSD11B2 were detected in Leydig cells and theca cells. Leydig cells produced 11-KT, and relatively high levels of plasma 11-KT were measured in both men and women. There was no sexual dimorphism in the plasma levels of 11-KT, even though testosterone levels were more than 20-times higher in men than in women. It is noteworthy that the levels of testosterone and 11-KT were similar in women. In a luciferase reporter system, 11-KT activated human androgen receptor (AR)-mediated transactivation. Conversely, 11-KT did not activate estrogen receptor (ER)-mediated transactivation in aromatase-expressed MCF-7 cells, whereas testosterone did following conversion to estrogen. 11-KT did not affect the estrogen/ER-mediated cell proliferation of MCF-7 cells. Furthermore, it significantly inhibited cell proliferation when AR was transfected into MCF-7 cells.

Conclusions: The current study indicates that 11-KT is produced in the gonads and represents a major androgen in human. It can potentially serve as a non-aromatizable androgen.

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