scholarly journals Mitochondria, glycogen, and lipid droplets in skeletal muscle during testosterone treatment and strength training: a randomized, double-blinded, placebo-controlled trial

Andrology ◽  
2018 ◽  
Vol 6 (4) ◽  
pp. 547-555 ◽  
Author(s):  
R. C. Jensen ◽  
L. L. Christensen ◽  
J. Nielsen ◽  
H. D. Schrøder ◽  
T. Kvorning ◽  
...  
2016 ◽  
Vol 32 (1) ◽  
pp. 253-253
Author(s):  
Adriane Aver Vanin ◽  
Eduardo Foschini Miranda ◽  
Caroline Santos Monteiro Machado ◽  
Paulo Roberto Vicente de Paiva ◽  
Gianna Móes Albuquerque-Pontes ◽  
...  

2019 ◽  
Vol 104 (12) ◽  
pp. 6238-6246 ◽  
Author(s):  
Glenn R Cunningham ◽  
Susan S Ellenberg ◽  
Shalender Bhasin ◽  
Alvin M Matsumoto ◽  
J Kellogg Parsons ◽  
...  

Abstract Context Prostate-specific antigen (PSA) changes during testosterone treatment of older hypogonadal men have not been rigorously evaluated. Design Double-blinded, placebo-controlled trial. Setting Twelve US academic medical centers. Participants Seven hundred ninety hypogonadal men ≥65 years of age with average testosterone levels ≤275 ng/dL. Men at high risk for prostate cancer were excluded. Interventions Testosterone or placebo gel for 12 months. Main Outcomes Percentile changes in PSA during testosterone treatment of 12 months. Results Testosterone treatment that increased testosterone levels from 232 ± 63 ng/dL to midnormal was associated with a small but substantially greater increase (P < 0.001) in PSA levels than placebo treatment. Serum PSA levels increased from 1.14 ± 0.86 ng/mL (mean ± SD) at baseline by 0.47 ± 1.1 ng/mL at 12 months in the testosterone group and from 1.25 ± 0.86 ng/mL by 0.06 ± 0.72 ng/mL in the placebo group. Five percent of men treated with testosterone had an increase ≥1.7 ng/mL and 2.5% of men had an increase of ≥3.4 ng/mL. A confirmed absolute PSA >4.0 ng/mL at 12 months was observed in 1.9% of men in the testosterone group and 0.3% in the placebo group. Four men were diagnosed with prostate cancer; two were Gleason 8. Conclusions When hypogonadal older men with normal baseline PSA are treated with testosterone, 5% had an increase in PSA ≥1.7 ng/mL, and 2.5% had an increase ≥3.4 ng/mL.


2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
D. Glintborg ◽  
L. L. Christensen ◽  
T. Kvorning ◽  
R. Larsen ◽  
K. Brixen ◽  
...  

Background.The beneficial effects of testosterone treatment (TT) are debated.Methods.Double-blinded, placebo-controlled study of six months TT (gel) in 54 men aged 60–78 with bioavailable testosterone (BioT) <7.3 nmol/L and waist >94 cm randomized to TT (50–100 mg/day,n=20), placebo (n=18), or strength training (ST) (n=16) for 24 weeks. Moreover, the ST group was randomized to TT (n=7) or placebo (n=9) after 12 weeks.Outcomes. Chemokines (MIF, MCP-1, and MIP-1α) and lean body mass (LBM), total, central, extremity, visceral, and subcutaneous (SAT) fat mass established by DXA and MRI.Results. From 0 to 24 weeks, MIF and SAT decreased during ST + placebo versus placebo, whereas BioT and LBM were unchanged. TT decreased fat mass (total, central, extremity, and SAT) and increased BioT and LBM versus placebo. MIF levels increased during TT versus ST + placebo. ST + TT decreased fat mass (total, central, and extremity) and increased BioT and LBM versus placebo. From 12 to 24 weeks, MCP-1 levels increased during TT versus placebo and MCP-1 levels decreased during ST + placebo versus placebo.Conclusion. ST + placebo was associated with decreased MIF levels suggesting decreased inflammatory activity. TT may be associated with increased inflammatory activity. This trial is registered with ClinicalTrials.govNCT00700024.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Mary Ni Lochlainn ◽  
Ayrun Nessa ◽  
Alyce Sheedy ◽  
Rachel Horsfall ◽  
María Paz García ◽  
...  

Abstract Background Loss of skeletal muscle mass and strength occurs with increasing age and is associated with loss of function, disability, and the development of sarcopenia and frailty. Dietary protein is essential for skeletal muscle function, but older adults do not anabolise muscle in response to protein supplementation as well as younger people, so called ‘anabolic resistance’. The aetiology and molecular mechanisms for this are not understood, however the gut microbiome is known to play a key role in several of the proposed mechanisms. Thus, we hypothesise that the gut microbiome may mediate anabolic resistance and therefore represent an exciting new target for ameliorating muscle loss in older adults. This study aims to test whether modulation of the gut microbiome using a prebiotic, in addition to protein supplementation, can improve muscle strength (as measured by chair-rise time) versus protein supplementation alone. Methods The study is a randomised, double-blinded, placebo-controlled trial, with two parallel arms; one will receive prebiotic and protein supplementation, and the other will receive placebo (maltodextrin) and protein supplementation. Participants will be randomised as twin pairs, with one twin from each pair in each arm. Participants will be asked to take supplementation once daily for 12 weeks in addition to resistance exercises. Every participant will receive a postal box, containing their supplements, and the necessary equipment to return faecal, urine, saliva and capillary blood samples, via post. A virtual visit will be performed using online platform at the beginning and end of the study, with measures taken over video. Questionnaires, food diary and cognitive testing will be sent out via email at the beginning and end of the study. Discussion This study aims to provide evidence for the role of the gut microbiome in anabolic resistance to dietary protein. If those who take the prebiotic and protein supplementation have a greater improvement in muscle strength compared with those who take protein supplementation alone, this would suggest that strategies to modify the gut microbiome may reduce anabolic resistance, and therefore potentially mitigate sarcopenia and frailty in older adults. Trial registration Clinicaltrials.gov: NCT04309292. Registered on the 2nd May 2020. 


2018 ◽  
Vol 178 (3) ◽  
pp. 277-283 ◽  
Author(s):  
Husam Ghanim ◽  
Sandeep Dhindsa ◽  
Sanaa Abuaysheh ◽  
Manav Batra ◽  
Nitesh D Kuhadiya ◽  
...  

Aims One-third of males with type 2 diabetes (T2DM) have hypogonadism, characterized by low total and free testosterone concentrations. We hypothesized that this condition is associated with a compensatory increase in the expression of androgen receptors (AR) and that testosterone replacement reverses these changes. We also measured estrogen receptor and aromatase expression. Materials and methods This is a randomized double-blind placebo-controlled trial. Thirty-two hypogonadal and 32 eugonadal men with T2DM were recruited. Hypogonadal men were randomized to receive intramuscular testosterone or saline every 2 weeks for 22 weeks. We measured AR, ERα and aromatase expression in peripheral blood mononuclear cells (MNC), adipose tissue and skeletal muscle in hypogonadal and eugonadal males with T2DM at baseline and after 22 weeks of treatment in those with hypogonadism. Results The mRNA expression of AR, ERα (ESR1) and aromatase in adipose tissue from hypogonadal men was significantly lower as compared to eugonadal men, and it increased significantly to levels comparable to those in eugonadal patients with T2DM following testosterone treatment. AR mRNA expression was also significantly lower in MNC from hypogonadal patients compared to eugonadal T2DM patients. Testosterone administration in hypogonadal patients also restored AR mRNA and nuclear extract protein levels from MNC to that in eugonadal patients. In the skeletal muscle, AR mRNA and protein expression are lower in men with hypogonadism. Testosterone treatment restored AR expression levels to that comparable to levels in eugonadal men. Conclusions We conclude that, contrary to our hypothesis, the expression of AR, ERα and aromatase is significantly diminished in hypogonadal men as compared to eugonadal men with type 2 diabetes. Following testosterone replacement, there is a reversal of these deficits.


2016 ◽  
Vol 31 (8) ◽  
pp. 1555-1564 ◽  
Author(s):  
Adriane Aver Vanin ◽  
Eduardo Foschini Miranda ◽  
Caroline Santos Monteiro Machado ◽  
Paulo Roberto Vicente de Paiva ◽  
Gianna Móes Albuquerque-Pontes ◽  
...  

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