Etudes sur les hormones : page 19.2

L’adiponectine : une hormone anti-carcinogène

11/05/2013 | Etudes sur les hormones et Etudes Perte de poids et Etudes Anti-âge

 

L’adiponectine : une adipokine anti-carcinogène ?
Annales d’Endocrinologie Vol 74 - N° 2   P. 102-105 - mai 2013

Le tissu adipeux a longtemps été considéré comme un simple organe de stockage énergétique. Bien que de nombreux travaux aient auparavant identifié la nature sécrétoire de l’adipocyte, le tissu endocrine n’a véritablement acquis son statut endocrine que lors de la découverte de la leptine en 1994. Il était à l’époque révolutionnaire de découvrir qu’une hormone synthétisée et sécrétée par le tissu adipeux, était capable de dialoguer avec le système nerveux central pour contrôler la satiété et l’équilibre énergétique de l’organisme. En fait, c’est presque à la même époque qu’a été découverte une autre adipokine majeure produite par l’adipocyte, l’adiponectine. Il a fallu attendre plusieurs années pour que soient mises en évidence les propriétés insulino-sensibilisantes, anti-inflammatoires et anti-athérogènes de cette hormone. Plus récemment, plusieurs données épidémiologiques, génétiques et expérimentales sont venues suggérer le rôle anti-carcinogène de l’adiponectine. Dans cette brève revue nous évoquerons les arguments en faveur d’une fonction protectrice de l’adiponectine dans la survenue ou la progression tumorale, en particulier dans le cadre du cancer mammaire. Le déficit en adiponectine couramment observé au cours de l’obésité pourrait contribuer à l’histoire naturelle de certains cancers, au même titre que l’élévation de la leptine ou d’autres perturbations hormonales associées à une adiposité excessive.

Le point sur les inhibiteurs de prise de muscle

11/05/2013 | Etudes sur les hormones

 

Rôle de l’Activine A et de la Myostatine dans la cachexie cancéreuse Role of Activin A and Myostatin in cancer cachexia
Jean-Paul Thissen       Annales d’Endocrinologie Vol 74 - N° 2   P. 79-81 - mai 2013

Des travaux récents suggèrent que l’Activine A (ActA) et la Myostatine (Mstn), deux membres de la superfamille du TGFβ, pourraient contribuer à l’atrophie musculaire induite par certains cancers. Ainsi, plusieurs lignées de cellules tumorales humaines produisent et sécrètent de l’ActA et de la Mstn. Ensuite, l’administration systémique d’ActA et de Mstn chez la souris cause une atrophie musculaire. De même, les souris KO Inhibine-α, qui sont caractérisées par des taux circulants élevés d’ActA, présentent une atrophie musculaire et meurent de cachexie. Enfin, l’administration d’antagonistes de l’ActA et de la Mstn prévient l’atrophie musculaire et la mortalité causées par certaines tumeurs chez l’animal. L’ensemble de ces observations suggère que la production d’ActA ou de Mstn par certaines tumeurs cancéreuses pourrait contribuer à la cachexie et donc à la mortalité associées à certains cancers chez l’homme. Cette hypothèse est d’autant plus intéressante que de nouvelles molécules, en particulier le sActRIIB, capables d’inhiber l’action de l’ActA et de la Mstn sont en cours de développement.

Comment l’absence de myostatine aide t’elle à perdre du gras ?

30/04/2013 | Etudes sur les hormones et Etudes Perte de poids

 

Myostatin knockout drives browning of white adipose tissue through activating the AMPK-PGC1α-Fndc5 pathway in muscle
Tizhong Shan           The FASEB Journal vol. 27 no. 5 1981-1989

Myostatin (Mstn) is predominantly expressed in skeletal muscles and plays important roles in regulating muscle growth and development, as well as fat deposition. Mstn-knockout (Mstn−/−) mice exhibit increased muscle mass due to both hypertrophy and hyperplasia, and leaner body composition due to reduced fat mass. Here, we show that white adipose tissue (WAT) of Mstn−/− develops characteristics of brown adipose tissue (BAT) with dramatically increased expression of BAT signature genes, including Ucp1 and Pgc1α, and beige adipocyte markers Tmem26 and CD137. Strikingly, the observed browning phenotype is non-cell autonomous and is instead driven by the newly defined myokine irisin (Fndc5) secreted from Mstn−/− skeletal muscle. Within the muscle, Mstn−/− leads to increased expression of AMPK and its phosphorylation, which subsequently activates PGC1α and Fndc5. Together, our study defines a paradigm of muscle-fat crosstalk mediated by Fndc5, which is up-regulated and secreted from muscle to induce beige cell markers and the browning of WAT in Mstn−/− mice. These results suggest that targeting muscle Mstn and its downstream signaling represents a therapeutic approach to treat obesity and type 2 diabetes

Rôles de l’IL-15 sur les muscles

26/03/2013 | Etudes sur les hormones et Echauffement et blessures

 

From Anabolic to Oxidative: Reconsidering the Roles of IL-15 and IL-15Rα in Skeletal Muscle
Exercise & Sport Sciences Reviews: April 2013 - Volume 41 - Issue 2 - p 100–106     Pistilli, Emidio

Interleukin 15 (IL-15) and its receptor IL-15 receptor-α (IL-15Rα) are suggested to function in the determination of skeletal muscle phenotypes, with IL-15 originally proposed as an anabolic cytokine. This review will focus on recent work demonstrating that manipulation of IL-15 and IL-15Rα in vivo promotes changes in exercise capacity, muscle fatigue, and gene expression indicative of a more oxidative skeletal muscle phenotype.

Plus de testo grâce à la gelée royale ?

22/09/2012 | Etudes sur les hormones et Etudes Compléments alimentaires et Etudes Perte de poids et Etudes Anti-âge et Etudes sur les boosters sexuels et la sexualité

 

Effect of royal jelly ingestion for six months on healthy volunteers
Hiroyuki Morita             Nutrition Journal 2012, 11:77

Royal jelly is a widely ingested supplement for health, but its effects on humans are not well known. The objective was to evaluate the effects of long-term royal jelly ingestion on humans.

Methods

We conducted a randomized placebo-controlled, double-blind trial. A total of 61 healthy volunteers aged 42-83 years were enrolled and were randomly divided into a royal jelly group (n = 31) and a control group (n = 30). Three hundred mg of royal jelly (RJ) or a placebo in 100 ml liquid/day were ingested for 6 months. The primary outcomes were changes in anthropometric measurements and biochemical indexes from baseline to 6 months after intervention.

Results

Thirty subjects in the RJ group and 26 in the control group were included in the analysis of endpoints. In an adjusted mean change of the variables from the baseline, significant differences between the two groups could be found in red blood cell counts (+0.16x106 /muL for the RJ group vs. -0.01x106 /muL for the control group, P = 0.0134), hematocrit (+0.9% vs. -0.8%, P = 0.0251), log (fasting plasma glucose) (+0.01 +/- 0.01 log mg/dL vs. +0.05 +/- 0.01 log mg/dL, P = 0.0297), log (insulinogenic index) (+0.25 vs. -0.13, P = 0.0319), log dehydroepiandrosterone sulfate (DHEA-S) (+0.08 log mug/dL vs. +0.20 log mug/dL, P = 0.0483), log testosterone (T) (+0.12 +/- 0.04 log ng/mL vs. -0.02 +/- 0.05 log ng/mL, P = 0.0416), log T/DHEA-S ratio (+0.05 +/- 0.05 vs. -0.23 +/- 0.59, P = 0.0015), and in one of the SF-36 subscale scores, mental health (MH) (+4 vs. -7, P = 0.0276).

Conclusions

Six-month ingestion of RJ in humans improved erythropoiesis, glucose tolerance and mental health. Acceleration of conversion from DHEA-S to T by RJ may have been observed among these favorable effects.

Effets intracrines du sur-entraînement

22/09/2012 | Etudes sur les hormones et Etudes Musculation

 

Effects of Overtraining on Skeletal Muscle Growth and Gene Expression
Int J Sports Med 2012; 33(10): 846-853     W. Xiao

The aim of this study was to investigate the effects of overtraining on skeletal muscle growth and growth-related gene expression. The rats of overtraining group (OT) and overtraining recovery group (OTR) were subject to 11 experimental weeks of overtraining protocol. It was found that the absolute gastrocnemius muscle wet weight of the OT group was significantly lower than that of the sedentary group (23.6%, P<0.01). Serum creatine kinase was significantly higher in the OT and OTR groups than the sedentary group. CD68, CD163, MyoD, myogenin, IL-1β, TNF-α, IGF-I and MGF mRNA did not change in the OT group as compared with the sedentary group.

IL-6 and TGF-β1 mRNA in the OT group increased significantly as compared with the sedentary group (2.17 fold and 1.78 fold, respectively; P<0.01). IL-10 mRNA decreased significantly in the OT group (63%, P<0.01) and the OTR group (77%, P<0.01) compared to the sedentary group.

COX-2 mRNA decreased significantly in the OT group (60%, P<0.01) and the OTR group (69%, P<0.01) from the sedentary group. uPA mRNA in the OT group was significantly lower than that in the sedentary group (32%, P<0.01).

These data suggest that inflammatory cytokines, COX-2 and uPA may play roles in the inhibition of skeletal muscle growth induced by overtraining.

Protéine A plasmatique associée à la grossesse, vecteur d’anabolisme

23/08/2012 | Etudes sur les hormones

 

Transgenic overexpression of pregnancy-associated plasma protein-A in skeletal muscle of mice increases myofiber size and central nucleation in sedentary muscle and promotes muscle regeneration in the injured muscle

Growth Hormone & IGF Research Volume 22, Issue 5, October 2012, Pages 173–179
Chandra Deba

While there is compelling evidence for an anabolic role of PAPP-A, an IGFBP protease, in muscle development, its effect on dynamic regulation of muscle regeneration has not been investigated. In this study, we evaluated the effect of transgenic PAPP-A overexpression in skeletal muscle of mice on myofiber formation in intact and crush-injured tibialus anterior muscle.

Design

Skeletal muscle in transgenic mice overexpressing human PAPP-A in skeletal muscle was subjected to crush-injury. Myofiber formation and myogenic gene expression were then evaluated in injured or intact muscle of PAPP-A transgenic mice and wild-type mice.

Results

In the intact muscle, aging PAPP-A transgenic (Tg.) mice (age of 12 months) showed more than a 2-fold increase in both myofiber size and number of nuclei per myofiber compared with their wild-type (Wt.) littermates. Myofibers with centered nuclei, a hallmark of muscle regeneration, were increased from

< 1% in Wt. mice to 65% in Tg. muscle. In the injured muscle, reduced inflammatory cell infiltration and increased new myofiber size and the area occupied by new myofibers were observed in PAPP-A transgenic mice compared to wild-type littermates. MyoD and creatine kinase in the injured muscle was also significantly increased in the Tg. mice. Although TNF-α induced PAPP-A expression in skeletal myoblast culture and its expression increased upon injury, abrogation of TNF-α signaling in TNF-α receptor knockout mice had no impact on the extent of injury induction of PAPP-A. We also found that TGF-β expression was significantly increased following muscle injury in vivo and treatment with recombinant TGF-β in vitro significantly enhanced PAPP-A expression in skeletal myoblasts.

Conclusion

Our findings demonstrate that exogenous

PAPP-A can promote recovery of muscle injury in aging mice albeit the expression of endogenous PAPP-A had already been increased dramatically upon muscle injury.

Page 14 sur 15 pages « First  <  12 13 14 15 >