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La follistatine agit aussi sur l’insuline

06/03/2019 | Etudes sur les hormones

 

Mechanisms involved in follistatin-induced increased insulin action in skeletal muscle
Xiuquing Han     bioRxiv posted 5 March 2019

Background: Skeletal muscle wasting is often associated with insulin resistance. A major regulator of muscle mass is the transforming growth factor beta (TGF-beta) superfamily, including activin A, which causes atrophy. TGF-beta superfamily ligands also negatively regulate insulin-sensitive proteins, but whether this pathway contributes to insulin action remains to be determined.

Methods: To elucidate if TGF-beta superfamily ligands regulate insulin action we used an adeno-associated virus gene editing approach to overexpress the activin A inhibitor, follistatin (Fst288) in mouse muscle of lean and diet-induced obese mice. We determined basal and insulin-stimulated 2 deoxy-glucose uptake using isotopic tracers in vivo. Furthermore, to evaluate whether circulating Fst and activin A concentrations are associated with obesity, insulin resistance, and weight loss in humans we analysed serum from morbidly obese subjects before, 1 week, and 1 year after Roux-en-Y gastric bypass (RYGB).

Results: Fst288 muscle overexpression markedly increased in vivo insulin-stimulated (but not basal) glucose uptake (+75 percent) and increased protein expression and intracellular insulin signalling of AKT, TBC1D4, PAK1, and p70S6K. Importantly, Fst288 completely normalized muscle glucose uptake in insulin-resistant diet-induced obese mice. RYGB surgery doubled circulating Fst and reduced Activin A (-24 percent) concentration 1 week after surgery before any significant weight loss in morbidly obese normoglycemic patients, while major weight loss after 1 year did not further change the concentrations.

Conclusions: We here present evidence that Fst is a potent regulator of insulin action in muscle and in addition to AKT and p70S6K, we identify TBC1D1, TBC1D4 and PAK1 as Fst targets. A possible role for Fst in regulating glycemic control is suggested because circulating Fst more than doubled post RYGB surgery, a treatment that markedly improved insulin sensitivity. These findings demonstrate the therapeutic potential of inhibiting TGF-beta superfamily ligands to improve insulin action and Fst s relevance to insulin resistant conditions in mice and humans.

Comment expliquer la mémoire musculaire (suite)?

17/02/2019 | Etudes Musculation

 

Comparative Transcriptome and Methylome Analysis in Human Skeletal Muscle Anabolism, Hypertrophy and Epigenetic Memory.
Daniel C Turner         bioRxiv posted 15 February 2019

Transcriptome wide changes in human skeletal muscle after acute (anabolic) and chronic resistance exercise (RE) induced hypertrophy have been extensively determined in the literature. We have also recently undertaken DNA methylome analysis (850,000 + CpG sites) in human skeletal muscle after acute and chronic RE, detraining and retraining, where we identified a role for DNA methylation in an epigenetic memory of exercise induced skeletal muscle hypertrophy. However, it is currently unknown as to whether all the genes identified in the transcriptome studies to date are also epigenetically regulated at the DNA level after acute, chronic or repeated RE exposure. We therefore aimed to undertake large scale bioinformatical analysis by pooling the publicly available transcriptome data after acute (110 samples) and chronic RE (181 samples) and comparing these large data sets with our genome-wide DNA methylation analysis in human skeletal muscle after acute and chronic RE, detraining and retraining. Indeed, after acute RE we identified 866 up- and 936 down-regulated genes at the expression level, with 270 (out of the 866 up-regulated) identified as being hypomethylated, and 216 (out of 936 downregulated) as hypermethylated. After chronic RE we identified 2,018 up- and 430 down-regulated genes with 592 (out of 2,018 upregulated) identified as being hypomethylated and 98 (out of 430 genes downregulated) as hypermethylated. After KEGG pathway analysis, genes associated with cancer pathways were significantly enriched in both bioinformatic analysis of the pooled transcriptome and methylome data after both acute and chronic RE. This resulted in 23 (out of 69) and 28 (out of 49) upregulated and hypomethylated and 12 (out of 37) and 2 (out of 4) downregulated and hypermethylated cancer genes following acute and chronic RE respectively. Within skeletal muscle tissue, these cancer genes predominant functions were associated with matrix/ actin structure and remodelling, mechano-transduction (including PTK2/Focal Adhesion Kinase and Phospholipase D- following chronic RE only), TGF-beta signalling and protein synthesis (GSK3B after acute RE only). Interestingly, 51 genes were also identified to be up/downregulated in both the acute and chronic RE pooled transcriptome analysis as well as significantly hypo/hypermethylated after acute RE, chronic RE, detraining and retraining.

Five genes; FLNB, MYH9, SRGAP1, SRGN, ZMIZ1 demonstrated increased gene expression in the acute and chronic RE transcriptome and also demonstrated hypomethylation in these conditions. Importantly, these 5 genes demonstrated retained hypomethylation even during detraining (following training induced hypertrophy) when exercise was ceased and lean mass returned to baseline (pre-training) levels, identifying them as novel epigenetic memory genes. Importantly, for the first time across the transcriptome and epigenome combined, this study identifies novel differentially methylated genes associated with human skeletal muscle anabolism, hypertrophy and epigenetic memory.

Actions santé de la mélatonine

11/01/2019 | Etudes sur les hormones et Echauffement et blessures et Etudes Compléments alimentaires et Etudes Anti-âge

 

The multiple protective roles and molecular mechanisms of melatonin and its precursor N-acetylserotonin in targeting brain injury and liver damage and in maintaining bone health
ChengliangLuoa       Free Radical Biology and Medicine Volume 130, January 2019, Pages 215-233

Highlights
• Melatonin and NAS are protective agents for brain injury, liver damage and bone health.
• Melatonin and NAS are anti-oxidative stress and anti-inflammation.
• Melatonin and NAS are against autophagy dysfunction and anti-apoptosis.
• MT1/MT2 are needed for brain and liver injuries and MT2 is important for bone health.
• Melatonin and NAS will be likely to show utility in clinical trials.

Melatonin is a neurohormone associated with sleep and wakefulness and is mainly produced by the pineal gland. Numerous physiological functions of melatonin have been demonstrated including anti-inflammation, suppressing neoplastic growth, circadian and endocrine rhythm regulation, and its potent antioxidant activity as well as its role in regeneration of various tissues including the nervous system, liver, bone, kidney, bladder, skin, and muscle, among others.

In this review, we summarize the recent advances related to the multiple protective roles of melatonin receptor agonists, melatonin and N-acetylserotonin (NAS), in brain injury, liver damage, and bone health. Brain injury, including traumatic brain injury, ischemic stroke, intracerebral hemorrhage, subarachnoid hemorrhage, and newborn perinatal hypoxia-ischemia encephalopathy, is a major cause of mortality and disability. Liver disease causes serious public health problems and various factors including alcohol, chemical pollutants, and drugs induce hepatic damage. Osteoporosis is the most common bone disease in humans. Due in part to an aging population, both the cost of care of fracture patients and the annual fracture rate have increased steadily. Despite the discrepancy in the pathophysiological processes of these disorders, time frames and severity, they may share several common molecular mechanisms. Oxidative stress is considered to be a critical factor in these pathogeneses. We update the current state of knowledge related to the molecular processes, mainly including anti-oxidative stress, anti-apoptosis, autophagy dysfunction, and anti-inflammation as well as other properties of melatonin and NAS. Particularly, the abilities of melatonin and NAS to directly scavenge oxygen-centered radicals and toxic reactive oxygen species, and indirectly act through antioxidant enzymes are disscussed. In this review, we summarize the similarities and differences in the protection provided by melatonin and/or NAS in brain, liver and bone damage.

We analyze the involvement of melatonin receptor 1A (MT1), melatonin receptor 1B (MT2), and melatonin receptor 1C (MT3) in the protection of melatonin and/or NAS. Additionally, we evaluate their potential clinical applications. The multiple mechanisms of action and multiple organ-targeted properties of melatonin and NAS may contribute to development of promising therapies for clinical trials.

Combien de mélatonine pour la santé?

26/12/2018 | Etudes sur les hormones et Etudes Compléments alimentaires et Etudes Anti-âge

 

Melatonin as a chronobiotic/cytoprotector: its role in healthy aging
Daniel P. Cardinali         Biological Rhythm Research Volume 50, 2019 - Issue 1

Preservation of sleep, a proper nutrition and adequate physical exercise are key elements for healthy aging. Aging causes sleep alterations, and in turn, sleep disturbances lead to numerous pathophysiological changes that accelerates the aging process. In the central nervous system, sleep loss impairs the clearance of waste molecules like amyloid-β or tau peptides. Melatonin, a molecule of unusual phylogenetic conservation present in all known aerobic organisms, is effective both as a chronobiotic and a cytoprotective agent to maintain a healthy aging.

The late afternoon increase of melatonin “opens the sleep doors” every night and its therapeutic use to preserve slow wave sleep has been demonstrated. Melatonin reverses inflammaging via prevention of insulin resistance, suppression of inflammation and down regulation of proinflammatory cytokines. Melatonin increases the expression of α- and γ-secretase and decreases β-secretase expression. It also inhibits tau phosphorylation. Clinical data support the efficacy of melatonin to treat Alzheimer’s disease, particularly at the early stages of disease. From animal studies the cytoprotective effects of melatonin need high doses to become apparent (i.e. in the 40–100 mg/day range). The potentiality of melatonin as a nutraceutical is discussed.

Nouveau bénéfices de la mélatonine contre le cancer?

07/12/2018 | Etudes Compléments alimentaires et Etudes Perte de poids et Etudes Anti-âge

 

Adjuvant chemotherapy with melatonin for targeting human cancers: A review
Masoud Najafi         Journal of Cellular Physiology           07 September 2018

Melatonin is a multifunctional hormone that has long been known for its antitumoral effects. An advantage of the application of melatonin in cancer therapy is its ability to differentially influence tumors from normal cells. In this review, the roles of melatonin adjuvant therapy in human cancer are discussed.

Combination of melatonin with chemotherapy could provide synergistic antitumoral outcomes and resolve drug resistance in affected patients. This combination reduces the dosage for chemotherapeutic agents with the subsequent attenuation of side effects related to these drugs on normal cells around tumor and on healthy organs. The combination therapy increases the rate of survival and improves the quality of life in affected patients. Cancer cell viability is reduced after application of the combinational melatonin therapy.

Melatonin does all these functions by adjusting the signals involved in cancer progression, re‐establishing the dark/light circadian rhythm, and disrupting the redox system for cancer cells. To achieve effective therapeutic outcomes, melatonin concentration along with the time of incubation for this indoleamine needs to be adjusted. Importantly, a special focus is required to be made on choosing an appropriate chemotherapy agent for using in combination with melatonin. Because of different sensitivities of cancer cells for melatonin combination therapy, cancer‐specific targeted therapy is also needed to be considered. For this review, the PubMed database was searched for relevant articles based on the quality of journals, the novelty of articles published by the journals, and the number of citations per year focusing only on human cancers.

De la carnosine pour la régénération nerveuse?

07/12/2018 | Etudes sur les hormones et Echauffement et blessures et Etudes Compléments alimentaires et Etudes Anti-âge

 

Carnosine improves functional recovery and structural regeneration after sciatic nerve crush injury in rats
Navideh Mirzakhani             Life Sciences volume 215, 15 December 2018, Pages 22-30


Aims
Peripheral nerve injury represents a substantial clinical problem with insufficient or unsatisfactory treatment options. Current researches have extensively focused on the new approaches for the treatment of peripheral nerve injuries. Carnosine is a naturally occurring pleotropic dipeptide and has many biological functions such as antioxidant property. In the present study, we examined the regenerative ability of carnosine after sciatic nerve crush injury using behavioral, biochemical, histological and ultrastructural evaluations.

Materials and methods
Seventy-two rats were divided into six groups including control, sham, crush and carnosine (10, 20 and 40 mg/kg) groups. Crush injury in left sciatic nerve was induced by a small haemostatic forceps. Carnosine was administered for 15 consecutive days after induction of crush injury. Sciatic functional index (SFI) was recorded weekly. Histopathological and ultrastructural evaluations were made using light and electron microscopes, respectively. Sciatic nerve tissue malondialdehyde (MDA), superoxide dismutase (SOD) and tumor necrosis factor-alpha (TNF-α) levels were measured. Gastrocnemius muscle weight was determined.

Key findings
Carnosine at the doses of 20 and 40 mg/kg accelerated SFI recovery. Wallerian degeneration severity and myelinated fibers density, myelin sheath thickness and diameter as well as ultrastructural changes of myelinated axons were improved. It also recovered nerve tissue biochemical (MDA, SOD and TNF-α) changes induced by crush injury. Muscle weight ratio was reached to near normal values.

Our results suggest a regenerative effect of carnosine. Inhibition of oxidative stress and inflammatory pathways, along with provocation of myelination and prevention of muscular atrophy might be involved in this effect of carnosine.

Significance
Carnosine treatment might be considered as a therapeutic agent for peripheral nerve regeneration and its functional recovery.

Peut-on perdre du muscle en gardant sa force au régime?

28/11/2018 | Etudes Musculation et Etudes Perte de poids

 

Si tu veux clacher tous les coachs à la mode

A Low-Carbohydrate Ketogenic Diet Reduces Body Mass Without Compromising Performance in Powerlifting and Olympic Weightlifting Athletes
Greene, David A       The Journal of Strength & Conditioning Research: December 2018 - Volume 32 - Issue 12 - p 3373–3382

There is evidence that low carbohydrate diets might offer specific advantages for weight reduction without the negative impact on strength and power previously hypothesized to accompany carbohydrate restriction. Therefore, the purpose of this study was to determine whether a low-carbohydrate ketogenic diet (LCKD) could be used as a weight reduction strategy for athletes competing in the weight class sports of powerlifting and Olympic weightlifting.

Fourteen intermediate to elite competitive lifting athletes (age 34 ± 10.5, n = 5 female) consumed an ad libitum usual diet (UD) (>250 g daily intake of carbohydrates) and an ad libitum LCKD (≤50 g or ≤10% daily intake of carbohydrates) in random order, each for 3 months in a crossover design. Lifting performance, body composition, resting metabolic rate, blood glucose, and blood electrolytes were measured at baseline, 3 months, and 6 months.

The LCKD phase resulted in significantly lower body mass (−3.26 kg, p = 0.038) and lean mass (−2.26 kg, p = 0.016) compared with the UD phase.

Lean mass losses were not reflected in lifting performances that were not different between dietary phases.

No other differences in primary or secondary outcome measures were found between dietary phases. Weight class athletes consuming an ad libitum LCKD decreased body mass and achieved lifting performances that were comparable with their UD. Coaches and athletes should consider using an LCKD to achieve targeted weight reduction goals for weight class sports.

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