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TA-65 administration during 4 months significantly improved the capacity to uptake glucose after a glucose pulse
liver protective action of TA-65
A disadvantage of mTERT potentiation could be associated to its capacity to favor proliferation of cancerous cells in murine models
TA-65 treated mice presented a similar incidence of malignant cancers at time of death, with a tendency to show decreased sarcomas and slightly increased lymphomas
We demonstrate here that TA-65 leads to a significant rescue of short telomeres through telomerase activation
TA-65 treatment increases proliferation and mobilization potential of mouse keratinocytes in vitro, a situation mimicking telomerase overexpression
TAT2, a similar molecule, have beneficial effects in the activation of CD8+ T lymphocytes from HIV-infected patients where they observe an increase of the proliferative potential and enhancement of cytokine/chemokine production
TA-65 resulted in a similar rescue of short telomeres in leukocytes post-treatment as observed with humans, most likely through an activation of telomerase
we observe that TA-65 lead to 10 fold increase of telomerase RNA levels in the liver of treated mice comparing to the non-treated same-age cohorts
TA-65 regulates telomerase at the transcription level, probably through the regulation of the MAPK pathway
TA-65 dependent telomerase activation results in a better organ fitness as demonstrated by the improved scores at the glucose tolerance test and insulin levels at fasting
TA-65 supplemented mice also present modest enhancement of the subcutaneous and epidermal thickness, as well as higher bone density, representative of an overall fitness status improvemen
TA-65 treated mice present higher levels of RBC and hemoglobin comparing to the control cohorts
improved health-span of TA-65 treated mice is not accompanied by increased cancer incidence, which may be related to the fact that TERT levels are very modestly increased in all tissues tested except for the liver
systemic telomerase overexpression from the germline leads to protection from aging associated pathologies
similar situation could be mimicked expressing telomerase late in life in a telomerase deficient background
we observed a higher proliferation rate and a partial protection from cell death in some tissues of TA65 treated mice
Studies have shown pharmacological doses of testosterone to relax coronary arteries when injected intraluminally [39] and to produce modest but consistent improvement in exercise-induced angina and reverse associated ECG changes [40]. The mechanism of action is via blockade of calcium channels with effect of similar magnitude to nifedipine
Testosterone acts as a calcium channel blocker inducing vasodilation.
men with chronic stable angina pectoris, the ischaemic threshold increased after 4 weeks of TRT and a recent study demonstrates improvement continuing beyond 12 months [
Exercise capacity in men with chronic heart failure increased after 12 weeks
Studies have shown an inverse relationship between serum testosterone and fasting blood glucose and insulin levels
Medications such as chronic analgesics, anticonvulsants, 5ARIs, and androgen ablation therapy are associated with increased risk of testosterone deficiency and insulin resistance
Women with T2D or metabolic syndrome characteristically have low SHBG and high free testosterone
Hypogonadism is a common feature of the metabolic syndrome
The precise interaction between insulin resistance, visceral adiposity, and hypogonadism is, as yet, unclear but the important mechanisms are through increased aromatase production, raised leptin levels, and increase in inflammatory kinins
levels of testosterone are reduced in proportion to degree of obesity
Men should be encouraged to combine aerobic exercise with strength training. As muscle increases, glucose will be burned more efficiently and insulin levels will fall. A minimum of 30 minutes exercise three times weekly should be advised
Testosterone increases levels of fast-twitch muscle fibres
By increasing testosterone, levels of type 2 fibres increase and glucose burning improves
Weight loss will increase levels of testosterone
studies now clearly show that low testosterone leads to visceral obesity and metabolic syndrome and is also a consequence of obesity
In the case of MMAS [43], a baseline total testosterone of less than 10.4 nmol/L was associated with a greater than 4-fold incidence of type 2 diabetes over the next 9 years
There is high level evidence that TRT improves insulin resistance
Low testosterone predicts increased mortality and testosterone therapy improves survival in 587 men with type 2 diabetes
A similar retrospective US study involved 1031 men with 372 on TRT. The cumulative mortality was 21% in the untreated group versus 10% (
) in the treated group with the greatest effect in younger men and those with type 2 diabetes
the presence of ED has been shown to be an independent risk factor, particularly in hypogonadal men, increasing the risk of cardiac events by over 50%
A recent online publication on ischaemic heart disease mortality in men concluded optimal androgen levels are a biomarker for survival
inverse associations between low TT or FT (Table 2) and the severity of CAD
A recent 10 year study from Western Australia involving 3690 men followed up from 2001–2010 concluded that TT and FT levels in the normal range were associated with decreased all-cause and cardiovascular mortality, for the first time suggesting that both low and DHT are associated with all-cause mortality and higher levels of DHT reduced cardiovascular risk
TDS is associated with increased cardiovascular and all-cause mortality
The effect of treatment with TRT reduced the mortality rate of treated cohort (8.4%) to that of the eugonadal group whereas the mortality for the untreated remained high at 19.2%
hypogonadal men had slightly increased triglycerides and HDL
Men with angiographically proven CAD (coronary artery disease) have significantly lower testosterone levels [29] compared to controls (
) and there was a significant inverse relationship between the degree of CAD and TT (total testosterone) levels
TRT has also been shown to reduce fibrinogen to levels similar to fibrates
men treated with long acting testosterone showed highly significant reductions in TC, LDL, and triglycerides with increase in HDL, associated with significant reduction in weight, BMI, and visceral fat
Low androgen levels are associated with an increase in inflammatory markers
In the Moscow study, C-reactive protein was reduced by TRT at 30 weeks versus placebo
In some studies, a decline in diastolic blood pressure has been observed, after 3–9 months [24, 26] and in systolic blood pressure
A decline was noted in IL6 and TNF-alpha
No studies to date show an increase in LUTS/BPH symptoms with higher serum testosterone levels
TRT has been shown to upregulate PDE5 [65] and enhance the effect of PDE5Is (now an accepted therapy for both ED and LUTS), it no longer seems logical to advice avoidance of TRT in men with mild to moderate BPH.
What about just starting with normalization of Testosterone levels first.
Several meta-analyses have failed to show a link between TRT and development of prostate cancer [66] but some studies have shown a tendency for more aggressive prostate cancer in men with low testosterone
And if one would have looked at their estrogen levels, I guarantee they would have been found to be elevated.
low bioavailable testosterone and high SHBG were associated with a 4.9- and 3.2-fold risk of positive biopsy
Current EAU, ISSAM, and BSSM guidance [1, 2] is that there is “no evidence TRT is associated with increased risk of prostate cancer or activation of subclinical cancer.”
Men with prostate cancer, treated with androgen deprivation, develop an increase of fat mass with an altered lipid profile
Erectile dysfunction is an established marker for future cardiovascular risk and the major presenting symptom leading to a diagnosis of low testosterone
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