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Gene Therapy and Testosterone Enhancement
#1
What would be a potential application of gene therapy for raising the body's baseline testosterone levels in men????
I was thinking whether it would be possible in the near future for gene therapy to work on the hippocampus in increasing the amount of GnRH released and thus LH and testosterone. Any thoughts?????
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#2
I'm doing a project on gene therapy and I'm having difficulties for seeking the information on what all the illnesses Gene therapy snacks and how it treats the disease.Any new idea?
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#3
Low testosterone level and SNPs

Testosterone is steroid hormone that could be found in numerous vertebrates (mammals, reptiles, birds…). It is produced in both males and females, but it is considered to be a typical male hormone, because its concentration is much higher and effects more pronounced in male gender. Testosterone regulates development of male reproductive organs and promotes development of secondary sexual characteristic during puberty. Testosterone regulates sperm production, increases strength and mass of muscles and bones, increases libido, but it is also vital for other (not that obvious) processes, such as platelet aggregation, regulation of physical and cognitive capacities… Level of testosterone is dropping with age (andropause in males), but decreased hormone level could be seen in younger males due to primary or secondary hypogonadism. Classic symptoms of low testosterone level include loss of bone and muscle mass, delayed puberty (in younger individuals), anxiety, depression, increased abdominal fat, cognitive problems… Besides these effects, low testosterone is associated with diabetes type 2, cardiovascular disorders, dyslipidemia, stroke, Alzheimer’s disease….Currently available medical solutions for low hormone level include testosterone replacement therapies via patches, injections or pallets.

Testosterone production is regulated via hypothalamus-pituitary-testes axis. Low testosterone level triggers release of gonadotropin-releasing hormone (GnRH) that induces release of follicle-stimulating (FSH) and luteinizing hormone (LH) from the pituitary gland. These two hormones stimulate synthesis of testosterone in the Leydig cells in testes. Similarly, high testosterone level blocks release of GnRH, FSH and LH and suppresses further testosterone production. These loops are targeted by GnRH antagonists in patients diagnosed with disorders associated with increased testosterone level. 5-alpha reductase inhibitors prevent conversion of testosterone into dihydrotestosterone, more potent form of the hormone, associated with benign prostatic hyperplasia, prostate cancer and androgenic alopecia.

7% of synthesized testosterone will be converted to dihydrotestosterone and 0,3% in estradiol. Both testosterone and dihydrotestosterone will circulate throughout the blood bound to the sex hormone binding globulin (SHBG) and albumin, and 1-2% of testosterone will circulate freely (unbound). This portion of free testosterone is biologically active and able to enter the cell and induce final effect. Testosterone exerts its effect by binding to the specific regions of DNA where it induces expression of genes associated with final androgenic effects. Since SHBG inhibits action of sex hormones, level of SHBG will determine bioavailability of testosterone. Recent study examined connection between SHBG gene polymorphism and testosterone level.

14 429 Caucasians were enrolled in study that investigated a link between testosterone level and genetic variability; other goal of the study was to establish if single nucleotide polymorphisms (SNPs) can be a risk factor for low testosterone level. Significant SNPs were found on the chromosome 17, in the SHBG gene. Better known as SNP rs12150660 and SNP rs6258, these two forms of SHBG (independently) showed strong correlation between serum levels of SHBG and testosterone. Both variants of SHBG gene showed decreased affinity for binding with testosterone. Besides these SNPs, locus associated with low testosterone level was identified on the X chromosome. SNP rs593405 near the FAM9B (family with sequence similarity 9, member B) and KAL1 (Kallmann syndrome 1 sequence) genes on chromosome Xp22 increases risk of androgen deficiency. Observed effect is unrelated to the polymorphism in the SHBG gene. Lower free serum testosterone level was noted in T genotype carriers compared with those having C genotype in rs5934505 locus. Genetic variability near KAL1 gene may not be accidental. Kallmann syndrome is a type of hypogonadotropic hypogonadism; genetic mutation in KAL1 gene was noted in 11-14% of Caucasians diagnosed with the disease. Exact molecular mechanism and significance of newly discovered genetic variation in SNPs rs12150660, rs6258, and rs5934505 still need to be examined, but this experiment provides valuable information about possible genetic factors associated with low testosterone level and provides directions for the future experiments. For now, these polymorphic regions should be considered as risk factors, rather than causative agents.

Until ideal gene candidate for gene treatment for the low testosterone level is identified, men can change at least some environmental factors that negatively affect hormone level. Vitamin D and magnesium can increase testosterone level. Zinc deficiency is well known factor that contributes to the low testosterone level, but extreme intake of zinc (much over recommended dose) can't increase hormone level more than it is normal for the organism. Increased body mass index and smoking decrease hormone level significantly while increased physical activity increases testosterone level (and reduces body mass - solves two problems at once).
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