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In addition, Akt regulates muscle mass by phosphorylating and deactivating glycogen synthase kinase (GSK) β1, followed by the GSK β1-dependent inhibition of the eukaryotic translation initiation factor 2B (eIF2B) (Manning and Cantley, 2007; Schiaffino and Mammucari, 2011). Even though the phenotypes of mTORC1-signaling deficient mice are similar in terms of skeletal muscle myopathies, mitochondrial and oxidative metabolism in these mice are distinct. MTOR knockout muscle also undergoes metabolic changes, resulting in glycogen accumulation due to increased glycogen synthesis and glucose uptake together with reduced glycogen breakdown through glycogenolysis and the glycolytic and oxidative pathways.
Testosterone is thought to contribute to the maintenance of muscle mass in males; therefore, we investigated the effect of 28 days of testosterone depletion on muscle mass in male mice at multiple ages across the lifespan. We hypothesized that phenotypic outcomes in skeletal muscle following testosterone depletion would differ between male mice of different ages and maturity, and be related to alterations to protein degradation. Therefore, the primary objective of this study was to investigate the role testosterone plays in the regulation of muscle mass by examining the effect of orchiectomy-induced testosterone depletion in male mice at ages ranging from early postnatal to old age.
Testosterone depletion significantly decreased the tibialis anterior mean fiber CSA in 1.5-month-old mice but had no significant effect in other age groups (Fig 2A and 2B). Testosterone depletion significantly decreased perirenal fat pad mass in 12-month-old animals and had no effect in other cohorts (Fig 1C). All data were analyzed using two-way ANOVA using GraphPad Prism software (GraphPad Software, Inc., La Jolla, CA) with Factor 1 being testosterone and Factor 2 being age. Aliquots of frozen and powdered quadriceps muscles were weighed in precooled RNase free 1.5 mL Eppendorf tubes to calculate the amount of RNA per milligram of wet muscle tissue. The foot was secured to a footplate attached to an Aurora Scientific 300C servomotor, and the plantar flexor muscles were stimulated by two needle electrodes inserted proximally to the peroneal nerve. To measure muscle function in vivo, six isometric contractions were used to determine the baseline in vivo isometric torque–frequency profile of the ankle plantar flexor muscles (gastrocnemius, plantaris, and soleus) as previously described . Serial cross sections (10 μm) were cut from the TA and GA muscles using a Leica CM 3050S cryostat (Leica Microsystems).
Therefore, we suggest this tool as a sensitive and specific diagnostic biomarker in patients with MFM and FLNC variants of unknown significance. In addition, we demonstrate a highly similar composition of protein aggregates in all MFM-filaminopathy subtypes, independent of the individual FLNC mutation causative for this disease. Because the introduced stop codon occurs in the last exon, NMD does not occur, as confirmed by our RT-PCR experiments, indicating that a misfolded and unstable FLNc variant is indeed expressed, which not only leads to protein aggregation but also results in the formation of numerous myofibrillar lesions. Both mutations result in the same mutation at the protein level (p.W2710X), indicating that this specific stretch of guanines indeed is a mutation hotspot. All patients with MFM-filaminopathy but only 1 of 96 patients with different MFM subtypes had an FLNc ratio above 5. Our analyses revealed that proteomic aggregate profiles in 7 patients with MFM-filaminopathy with 3 distinct FLNC mutations were highly similar. Another clinically relevant point is that proteomic analysis can be helpful in differential diagnostic workup of patients with MFM.
One 8-week study found that subjects training with the same intensity, one with primarily eccentric contractions, increased muscle fiber mass by approximately 40%, while the concentric contraction group showed no change.However, this difference might not be the same when the total load is matched between training types.When matched for load, the increase in muscle volume seems to be the same between concentric and eccentric training. Biological factors, such as DNA, gender, nutrition, and training variables, can affect muscle hypertrophy.medical citation needed Individual differences in genetics account for a substantial portion of the variance in existing muscle mass. Muscle hypertrophy or muscle building involves a hypertrophy or increase in size of skeletal muscle through a growth in size of its component cells. The expression of several miRNAs, such as miR-1, miR-133, miR-206, and miR-125b, are regulated by mTOR directly or indirectly (Sun et al., 2010; Ge et al., 2011), suggesting the additional regulation of mTOR in skeletal muscle mass. Several miRNAs are identified as myomiRNAs, which are enriched in skeletal muscle and known to modulate the cellular processes involved in muscle growth, development, and maintenance, including hypertrophy and atrophy.
Testosterone has been found to act as an antagonist of the TrkA and p75NTR, receptors for the neurotrophin nerve growth factor (NGF), with high affinity (around 5 nM). The bones and the brain are two important tissues in humans where the primary effect of testosterone is by way of aromatization to estradiol. 5α-DHT binds to the same androgen receptor even more strongly than testosterone, so that its androgenic potency is about 5 times that of T. Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5α-dihydrotestosterone (5α-DHT) by the cytoplasmic enzyme 5α-reductase. Androgens such as testosterone have also been found to bind to and activate membrane androgen receptors. Both the free fraction and the one bound to albumin are available at the tissue level (their sum constitutes the bioavailable testosterone), while SHBG effectively and irreversibly inhibits the action of testosterone.
It has been found that the prostate, the anterior pituitary, the submaxillary gland and the pancreas have a rather elevated Sa-reductase activity. In conclusion, testosterone administration caused a decrease in the capacity for ACTH and corticosterone secretion in a rat model of the andropause. Both untreated groups of animals achieved significantly higher body weight and length of tibia than estradiol treated animals. Blood samples for serum growth hormone assay were collected via cardiac puncture. The body weight and the length of the rats were recorded for calculation of the body mass index. Normal saline was administered intramuscularly to the control group, while 2.5 and 6.25 mg/d of testosterone propionate were administered intramuscularly to the low-dose and high-dose groups, respectively, for fourteen (14) days. Testosterone is a steroid hormone from the androgen groups, secreted primarily in the testicles of males.
The culminating phase of ageing in males-andropause is characterized by enhanced activity of the hypothalamic-pituitary-adrenal axis and frequent glucocorticoid excess. The results of the present study show that the inhibitory effect of estradiol on body growth of young male rats is not only the result of decreased food intake and that testosterone can improve the skeletal growth of male rats altered by previously given estradiol. Moreover, testosterone was given to a half of these animals at 45, 50 and 55 days of age. The influence of estradiol and testosterone on body growth of young male Wistar rats was investigated. Plasma levels of testosterone have been measured in adult male Sprague-Dawley rats using a gas-chromatographic procedure.
Fat-free mass, fat mass, muscle strength, sexual function, mood, visuospatial cognition, hormone levels, and safety measures were evaluated before, during, and after treatment. The participants in this randomized, double-blind trial were 60 ambulatory, healthy, older men, yr of age, who had normal serum testosterone levels. Although this might suggest that testosterone has an indirect effect on muscle turnover through changes in growth rate, this parallelism was not confirmed by studies on adrenalectomized-castrated rats. that consistent anaerobic strength training will produce hypertrophy over the long term, in addition to its effects on muscular strength and endurance. This method has been shown to induce hypertrophy comparable to traditional high-load training, likely due to mechanical tension and muscle fiber recruitment.|Approximately 5 to 7% of testosterone is converted by 5α-reductase into 5α-DHT, with circulating levels of 5α-DHT about 10% of those of testosterone, and approximately 0.3% of testosterone is converted into estradiol by aromatase. The plasma protein binding of testosterone is 98.0 to 98.5%, with 1.5 to 2.0% free or unbound. Finally, increasing levels of testosterone through a negative feedback loop act on the hypothalamus and pituitary to inhibit the release of GnRH and FSH/LH, respectively. When testosterone levels are low, gonadotropin-releasing hormone (GnRH) is released by the hypothalamus, which in turn stimulates the pituitary gland to release FSH and LH.|Amplicons were cloned into the prokaryotic expression vectors pET23-EEF, pET23-T7, or pGEX-6P3 for expression of fusion proteins carrying a C-terminal His-tag and either a C-terminal EEF- or N-terminal T7-immunotag or an N-terminal GST-tag, respectively. Informed consent was obtained from all patients (approval of Ruhr-University Bochum ethics committee #4078–11). Individuals with proven mutation and deceased family members who had muscle weakness are represented by filled symbols. A German family with 9 patients representing 3 generations was included in this study (table e-1, links.lww.com/NXG/A410, figure 1A). We characterize the clinical and histopathologic phenotype of a German family with MFM-filaminopathy caused by a novel FLNc mutation in Ig-like domain 24, analyze the molecular pathogenesis, and provide new data about the composition of intramyoplasmic protein aggregates in MFM-filaminopathy. FLNc contains an N-terminal actin-binding domain followed by 24 Ig-like domains that serve as versatile protein interaction interfaces. MRI reveals a typical pattern of lower limb muscle involvement helpful in differential diagnostics.6,10-12 Mutations in FLNC may also lead to a distal myopathy with histopathologic features distinct from MFM13,14 or may cause different types of cardiomyopathies.15|Conclusion All together our data indicate that testosterone through the activation of non-genomic pathways, participates in skeletal muscle glucose metabolism by inducing insulin-related effects. The present study was carried out to study the effect of short-term administration of testosterone on serum growth hormone concentration, body mass index (BMI) and body weight in adult male rats. Unexpectedly, OrxϩT mice had increased fatigue resistance of SOL muscle compared with OrxϩC mice (P Ͻ 0.001).|In the in vitro study, testosterone caused a marked decrease of aldosterone secretion by zona glomerulosa (ZG) cells, but failed to alter the accumulation of intracellular adenosine 3',5'-cyclic monophosphate (cAMP). Orchidectomized rats were injected subcutaneously with oil or testosterone propionate (TP 2 mg/kg) for 7 days. The activity of the 3a-hvdroxysteroid-dehydrogenase was found to be totally unrelated to the Sa-redicing capacit; of each stru&re. The kidney has a limited capacity to form Sa-reduced metabolites of testosterone.}
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