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Lifespan News – Testosterone Benefits

Testosterone is linked to mitochondrial function in the brain.

LSN Testosterone BenefitsLSN Testosterone Benefits
 

This week on Lifespan News, Brent Nally discusses a testosterone study in rats, a ginseng compound that reduces a marker of cellular senescence in humans, and a way in which caloric restriction affects immunosenescence.

Further Reading

Testosterone Restores Brain Function in Old Male Rats

Ginseng Compound Reduces Senescent Marker in Humans

Caloric Restriction Attenuates Immunosenescence

Script

Testosterone supplements improve mitochondrial function in old mice, restoring their cognitive performance. You’ll find this story and more in this episode of Lifespan News.

Welcome to Lifespan News on X10, your source for longevity science updates. I’m your host, Brent Nally. We encourage you to check the description below for links to these stories.

For our first story, testosterone restores brain function in old male rats. Researchers from Hebei Medical University in China have found that testosterone supplementation ameliorates age-related brain dysfunction in male rats. The researchers used three groups of male rats in their experiment. One group was 6 months old, a second group was 24 months old and naturally had an average testosterone level one-third that of the 6-month-old rats, and the third group was 24 months old but were given testosterone supplements, which raised their average level slightly higher than that of the younger rats. Rats allowed to explore a chamber were tested for walking, climbing, rearing, and sniffing, and all four of these behaviors dramatically declined in older rats. Older rats given testosterone had their climbing, rearing, and sniffing behaviors partially restored, roughly to halfway between the results seen in younger rats and untreated older rats. The researchers then looked deeper to determine what testosterone was doing to mitochondria, examining both mitochondrial membrane potential and mitochondrial respiratory complex activities. These results largely mirrored what was seen in the other tests, although mitochondrial membrane potential was only slightly increased while many of the mitochondrial respiratory complex activities were substantially increased. Taken together, these results show a strong link between mitochondrial dysfunction, testosterone depletion, and cognitive decline in older rats. So the effects of testosterone on the neuronal mitochondria of older men are worth investigating with a human clinical trial.

Lifespan.io is excited to announce our fourth annual Ending Age-Related Diseases conference which is scheduled to take place August 19th to 22nd, 2021. We’ll be meeting virtually to learn the latest developments from leading bio rejuvenation experts.You can register at lifespan.io/conference which is also linked in the description below.

For our next story, a ginseng compound reduces a senescent marker in humans. A study conducted by researchers at the University of Taipei in Taiwan has shown that the ginseng derivative Rg1 decreases the cellular senescence marker p16INK4a in fitness-trained men 24 hours after exercise. This experiment was relatively simple to conduct. A dozen healthy men with experience in weight training participated in a double-blind test of 5 milligrams of Rg1 versus placebo, and they received muscle biopsies. An hour later, they performed squat exercises with barbells of roughly their own body weight. 24 hours after that, their muscles were biopsied again, and the cells were examined for biomarkers. In both the placebo and Rg1 groups, the number of cells visibly expressing p16INK4a remained largely the same. However, the amount that was expressed changed dramatically. 24 hours after exercise, members of the placebo group were shown to have their p16INK4a mRNA roughly halved, and this was further decreased in the Rg1 group. The number of endothelial progenitor cells, which aid in the regeneration of muscle tissue, was doubled in both groups 24 hours after exercise. Interestingly, these cells were, more often than not, co-located with p16INK4a cells, a fact that this study was not able to explain. The positive effects of Rg1 were corroborated by a perceived exertion questionnaire. Despite lifting similar amounts of weight, the men given Rg1 simply did not feel like they had worked as hard as the men in the placebo group reported. These results provide even more evidence that resistance-based exercise provides substantial benefits for muscle tissue while also showing that Rg1 provides significant benefits relating to inflammation and physical exertion.

For our final story, caloric restriction attenuates immunosenescence. Caloric restriction, or CR, and senolytics seem to have some similar effects. Scientists have shown in mice that long-term CR can attenuate age-related immunosenescence on par with antibody-mediated clearance of senescent T-cells, or SA-T cells. On top of that, CR predictably improved glucose tolerance and lowered inflammation. In previous studies, scientists were able to ameliorate metabolic disorders in obese mice on a high-fat diet by clearing out SA-T cells in visceral adipose tissue, or VAT. This time, the researchers tried to evaluate the effect of long-term CR on the SA-T cells’ subpopulation and on glucose tolerance, which is another important marker of health linked to chronic inflammation. The researchers found, rather unsurprisingly, that old mice weighed more and had more VAT than younger ones – the problem of age-related abdominal fat accumulation is well-known to humans. Aged mice also suffered from impaired glucose tolerance and insulin resistance. SA-T cells taken from the spleen and the VAT of aged mice and of younger obese mice on a high-fat diet exhibited the familiar senescence-associated phenotype. Aged mice and obese mice also had more of these cells than normally fed mice. In contrast, mice subjected to long-term CR had much lower body weight, less VAT, and improved glucose tolerance and insulin resistance than normally fed age-matched mice, not to mention obese mice. The researchers found that long-term CR in mice also significantly reduced the burden of SA-T cells in the VAT. To rule out a non-causative correlation, the researchers then depleted the number of SA-T cells in a new group of mice using PD-1 antibodies. The clearing out of SA-T cells largely recapitulated the effects of CR, improving glucose tolerance and attenuating insulin resistance. The antibody treatment also substantially decreased the expression levels of most proinflammatory cytokines in VAT.

That’s all the news for this episode. Is there a recent life extension story that you think we should have covered but haven’t yet? And what was your favorite story from this episode? Let us know what you think in the comments and we’ll see ya in the next episode.

CategoryLifespan News, News
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