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Fina's affect on DNA
- Thread starter IPSON
- Start date
Why don't you tell the good doctor WHY he is full of shit.IPSON said:
uhhhh.....your full of shit and you don't know shit so shut up.
Don't forget to add in any scientific references you may have to refute his statement. I for one would love to have you explain what binding to the AR receptors does to facilitate changes in the DNA.-Spidey
SeekerOfKnowledge
New member
So would I on this issue
While the genome may not be altered,there is evidence to suggest that certain steroids have the ability to increase myonucleonic populations over the long haul(testosterone in particular).That would certainly qualify as a shift in more favorable genetic potential(ability to utilize proteins).Just a thought.
Shaved Ape
New member
IPSON, you need to chill out and really evaluate who is REALLY full of shit and who doesn't know shit. There is nothing wrong with using the board to seek out knowledge and information, regardless of how vague or incoherent one's question may be. And there is no need to judge someone like you, who obviously doesn't know what they are talking about anyways. But here you have asked a question which clearly highlights your own ignorance on a subject, and then attacked Dr. X when he tries to give you an accurate response.
Dr. X and Huck both make very valid points here. IPSON, you need to learn how to shut up and listen, without getting defensive when someone offers you information that you cannot understand.
Dr. X and Huck both make very valid points here. IPSON, you need to learn how to shut up and listen, without getting defensive when someone offers you information that you cannot understand.
Shaved Ape
New member
IPSON, you need to chill out and really evaluate who is REALLY full of shit and who doesn't know shit. There is nothing wrong with using the board to seek out knowledge and information, regardless of how vague or incoherent one's question may be. And there is no need to judge someone like you, who obviously doesn't know what they are talking about anyways. But here you have asked a question which clearly highlights your own ignorance on a subject, and then attacked Dr. X when he tries to give you an accurate response.
Dr. X and Huck both make very valid points here. IPSON, you need to learn how to shut up and listen, without getting defensive when someone offers you information that you cannot understand.
Dr. X and Huck both make very valid points here. IPSON, you need to learn how to shut up and listen, without getting defensive when someone offers you information that you cannot understand.
Shaved Ape
New member
I'm the dumbfuck eh? So why don't you tell me all about the effects of AS on YOUR DNA, because apparently you were right. It seems that Fina has affected your genetically-programmed survival skills, causing you to call people that you do not know and who are much more informed on topics such as molecular biology than you dumbfucks.
flo0rida fah q
New member
tisk tisk tisk
lets fight some more over the internet
cause you know, it really does a lot of good :laugh:
lets fight some more over the internet
cause you know, it really does a lot of good :laugh:
Shaved Ape
New member
you're right florida, it is a waste of everyone's time. But members should be able to post intelligent responses without being insulted by those asking the questions, or anyone else for that matter. Just wanted to get that straight. I'm chill, IPSON.
Shaved Ape
New member
Fine IPSON, I will expand on the answers given by Dr.X and Huck. First, the question as STATED involved the effects of FINA/AR on DNA. Dr. X accurately answered that androgens do not alter your DNA, which functions as your genetic blueprint. All nucleated cells in your body contain a copy of your entire genome, in the form of billions of base pairs of DNA sequence. This blueprint encodes all the genes, which encode all the proteins, expressed in the body.
In any particular cell, only a subset of these genes will actually be expressed, or activated such that they are transcribed into RNA and then translated into protein. Androgens are likely to have an effect on the expression levels of particular proteins (such as myosin, etc) encoded by these genes. This is in part due to AS binding to the androgen receptors at the cell surface. These androgen-receptor complexes can then translocate to the cell nucleus and both directly and indirectly impact the transcription of certain genes. The DNA itself remains unaltered, as significant alterations in your genetic blueprint are likely to result in either cell death or transformation.
Huck also pointed out that AS may have an impact on the number and/or localization of muscle cell nuclei. Muscle cells are somewhat unique in that they are multinucleated (contain many nuclei distributed across the myofibers) and androgens may have an impact on the generation and/or distribution of myonuclei. An ongoing debate also exists as to whether AS and/or growth hormone primarily increase muscle mass through the hypertrophy of existing muscle fibers and/or through muscle cell hyperplasia, the generation of new muscle cells. But that is another long story.
In any particular cell, only a subset of these genes will actually be expressed, or activated such that they are transcribed into RNA and then translated into protein. Androgens are likely to have an effect on the expression levels of particular proteins (such as myosin, etc) encoded by these genes. This is in part due to AS binding to the androgen receptors at the cell surface. These androgen-receptor complexes can then translocate to the cell nucleus and both directly and indirectly impact the transcription of certain genes. The DNA itself remains unaltered, as significant alterations in your genetic blueprint are likely to result in either cell death or transformation.
Huck also pointed out that AS may have an impact on the number and/or localization of muscle cell nuclei. Muscle cells are somewhat unique in that they are multinucleated (contain many nuclei distributed across the myofibers) and androgens may have an impact on the generation and/or distribution of myonuclei. An ongoing debate also exists as to whether AS and/or growth hormone primarily increase muscle mass through the hypertrophy of existing muscle fibers and/or through muscle cell hyperplasia, the generation of new muscle cells. But that is another long story.
Hormonal effects are complex, but their functions can be divided into three broad categories. Some hormones change the permeability of the cell membrane. Other hormones can alter enzyme activity, and some hormones stimulate the release of other hormones.
Recent studies have shown that the more lasting effects of hormones ultimately result in the activation of specific genes. For example, when a steroid hormone enters a cell, it binds to a receptor in the cell’s cytoplasm. The receptor becomes activated and enters the cell’s nucleus, where it binds to specific sites in the deoxyribonucleic acid (DNA), the long molecules that contain individual genes. This activates some genes and inactivates others, altering the cell’s activity. Hormones have also been shown to regulate ribonucleic acids (RNA) in protein synthesiss.
A single hormone may affect one tissue in a different way than it affects another tissue, because tissue cells are programmed to respond differently to the same hormone. A single hormone may also have different effects on the same tissue at different times in life. To add to this complexity, some hormone-induced effects require the action of more than one hormone. This complex control system provides safety controls so that if one hormone is deficient, others will compensate.
Recent studies have shown that the more lasting effects of hormones ultimately result in the activation of specific genes. For example, when a steroid hormone enters a cell, it binds to a receptor in the cell’s cytoplasm. The receptor becomes activated and enters the cell’s nucleus, where it binds to specific sites in the deoxyribonucleic acid (DNA), the long molecules that contain individual genes. This activates some genes and inactivates others, altering the cell’s activity. Hormones have also been shown to regulate ribonucleic acids (RNA) in protein synthesiss.
A single hormone may affect one tissue in a different way than it affects another tissue, because tissue cells are programmed to respond differently to the same hormone. A single hormone may also have different effects on the same tissue at different times in life. To add to this complexity, some hormone-induced effects require the action of more than one hormone. This complex control system provides safety controls so that if one hormone is deficient, others will compensate.
drveejay11
New member
Hmmmmmmmm........
I found this interesting.
http://dayton.fsci.umn.edu/~bill/Po...le Growth.htm
Postnatal Muscle Growth
Postnatal muscle development
Muscle and Adipose Growth Curve
Limit to muscle growth appears to be reached — what is the biological mechanism or reason for this limit? Doesn’t happen for tissues such as adipose. We will try to understand why the plateau occurs and what, if anything, we can do about it.
Our goal in animal production is to lengthen the time of rapid muscle growth and put off the time when fat accretion becomes more significant.
I. Postnatal muscle growth occurs through hypertrophy — increase in size of fibers — formed prenatally
· No significant increase in the number of fibers after birth in meat-producing animals or humans
· Increase in muscle length during postnatal growth
▪ Limbs of most species approximately double in length during postnatal growth
▪ May relate to greater efficiency and rate of gain of animals with a larger size because longitudinal growth of bone may stimulate muscle growth by stretching the growing muscle
▪ Increases in muscle length occur via increases in the length of the fibers making up the muscle
· Increase in muscle diameter
▪ Occurs via an increase in muscle fiber diameter
▪ Also can occur due to increase in fiber length which increases fiber overlap and causes the muscle diameter to increase
· Hypertrophy is stimulated by (these stimuli don’t necessarily involve the same mechanism):
▪ Hormones and growth factors (IGF-1, FGF, TGF beta)
▪ Passive stretch (long bone growth)
▪ Work (exercise)
To better understand postnatal muscle growth, we need to first understand the concept of the DNA unit.
▪ DNA unit is the volume of cytoplasm “managed” by a single nucleus. A measure of DNA unit size is the protein/DNA ratio in muscle. This can be determined experimentally.
# of DNA units is determined by total DNA
Size of DNA unit is indicated by the protein/DNA ratio
▪ More and smaller DNA units are consistent with the potential for faster growth rate
▪ DNA unit concept must be tempered by the fact that only 75-80% of nuclei in muscle tissue comes from muscle cells. The rest comes from connective tissue, vascular tissue, macrophages, adipocytes, etc.
▪ Can also alter DNA unit size by exercise but usually won’t be maintained once exercise is stopped.
In meat producing animals, DNA accumulation (accretion) is highly related to muscle growth rate.
Most rapid period of DNA accretion coincides with the most rapid period of muscle growth.
Fiber size is also highly related to DNA content of the fibers (the more DNA, the bigger the fiber).
More rapid DNA accretion means that the DNA unit is kept smaller so each nucleus has a smaller amount of sarcoplasm to control, and thus growth occurs more rapidly.
Preponderance of evidence shows that much of the DNA in muscle fibers is accumulated postnatally and that accretion of DNA in muscle is a key factor in limiting muscle growth.
60-90% of DNA in mature muscle fibers is accumulated during postnatal growth
Based on what we know, this seems inconsistent because:
▪ Number of muscle fibers is fixed at birth, and muscle fibers can’t divide
▪ The nuclei in the muscle fiber cannot divide
▪ Where does the increase in DNA come from?
Satellite Cells
· mononucleated cells located between the sarcolemma and basement membrane of each muscle fiber. Probably present from mid-gestation on, but it isn’t possible to identify them until all of the embryonic myoblasts have fused into the fibers prior to birth.
· Satellite cells are muscle cells that have the ability to proliferate and/or differentiate and fuse into adjacent fibers. This process adds the satellite cell nucleus to the muscle fiber and provides more nuclei to control protein synthesis in the growing fiber. Once a satellite cell has differentiated and fused with its fiber, that satellite cells is lost from the total satellite cell population. Thus in order to maintain a viable satellite cell population in growing muscle it is essential that a significant number of satellite cells continue to proliferate without differentiating and fusing with muscle fibers. As with embryonic development, postnatal growth is, in a sense, a tug-of-war between the competing processes of proliferation and terminal differentiation.
· Satellite cells are responsible for providing nuclei needed for postnatal muscle growth
· As we approach plateau of muscle growth, two things happen relative to satellite cells:
▪ Number of satellite cells has been decreasing throughout the growth of muscle
▪ As many as 30% of muscle nuclei in newborn are satellite cells
▪ By adulthood, only 2-10% are satellite cells.
▪ Can see that ability of satellite cells to contribute nuclei decreases during growth simply because the number of satellite cells decreases. This means more cells are fusing with fibers than are dividing.
· As animal grows, the satellite cells begin to withdraw from the proliferative cycle and enter a quiescent state known as Go. These cells don’t proliferate or fuse with fibers.
· Thus, the reason that we see the plateau in muscle growth curve may well relate directly to the fact that the number of satellite cells has decreased and those that are left are not actively proliferating or fusing with fibers. Thus the DNA needed to support muscle growth is not being provided to the fibers and muscle growth slows or stops.
· Need to find ways to stimulate satellite cell proliferation during growth so the number of satellite cells isn’t decreased so dramatically during this process and so that they do not enter the quiescent state. Satellite cells respond to growth factor in the same way the embryonic myoblasts do.
· Effects of growth factors on satellite cell proliferation and differentiation
▪ IGF-1
a) Stimulates proliferation
b) Stimulates differentiation
▪ FGF
a) Stimulates proliferation
b) Inhibits differentiation
▪ TGF-beta
a) Inhibits proliferation
b) Inhibits differentiation
▪ These growth factors are all produced by the muscle cells so regulation of satellite cell proliferation and differentiation may well be controlled by the levels of these growth factors produced in the muscle tissue — as well as by circulating level of IGF-1 which is also found in large quantities in the blood.
▪ None of these growth factors will activate quiescent satellite cells, however. Activating these cells is also important in maintaining growth of muscle during the latter stages of the muscle growth curve when many of the satellite cells have become quiescent.
a) Hepatocyte growth factor activates quiescent satellite cells and makes them responsive to the above growth factors. It is produced in muscle tissue. Prolonging the linear phase of muscle growth may involve activation of quiescent satellite cells by HGF. This will allow them to proliferate in response to other growth factors and ultimately contribute needed nuclei to growing muscle.
Studies suggesting that IGF-I stimulated satellite cell proliferation contributes to postnatal muscle growth:
Overexpression of IGF-I in selected skeletal muscles of the mouse
When IGF-I is introduced into mouse hindlimb muscles by viral-mediated gene transfer, local overexpression of IGF-I produces significant increases in muscle mass and strength compared with untreated controls. IGF-I expression promotes an average increase of 15% in muscle mass and a 14% increase in strength in young adult mice, and prevents aging-related muscle changes in old adult mice, resulting in a 27% increase in strength as compared with uninjected old muscles. In order to test if satellite cells are essential in mediating the hypertrophic effects of IGF-I, gamma radiation was used to destroy the proliferative capacity of satellite cells. Treatment with gamma radiation significantly prevented normal growth of the muscle. When combined with IGF-I treatment, approximately half of the IGF-I effect was prevented by gamma radiation treatment. This suggests that the remaining half of IGF-I induced hypertrophy was due to paracrine/autocrine effects on the adult muscle fibers. Thus, these data are consistent with a mechanism by which IGF-I induced muscle hypertrophy via a combination of satellite cell activation and increasing protein synthesis in differentiated muscle fibers.
Mechanism of action of anabolic steroid implants in feedlot steers
Implantation of feedlot steers with an anabolic steroid implant containing trenbolone acetate (a testosterone analog) and estrogen results in a 20% increase in rate of gain, a 15% increase in feed efficiency and an increase in lean muscle mass. At the same time the levels of circulating IGF-I are increased by as much as 40% and the level of IGF-I mRNA in the muscle tissue is approximately 60-75% higher in implanted steers than in unimplanted steers. Additionally, satellite cells isolated from muscles of implanted steers show increased proliferative capacity in comparison to satellite cells isolated from unimplanted steers. These data suggest that the increased muscle growth in implanted steers may be the result of an IGF-I-stimulated increase in the proliferation of muscle satellite cells.
http://dayton.fsci.umn.edu/~bill/Po...le Growth.htm
Postnatal Muscle Growth
Postnatal muscle development
Muscle and Adipose Growth Curve
Limit to muscle growth appears to be reached — what is the biological mechanism or reason for this limit? Doesn’t happen for tissues such as adipose. We will try to understand why the plateau occurs and what, if anything, we can do about it.
Our goal in animal production is to lengthen the time of rapid muscle growth and put off the time when fat accretion becomes more significant.
I. Postnatal muscle growth occurs through hypertrophy — increase in size of fibers — formed prenatally
· No significant increase in the number of fibers after birth in meat-producing animals or humans
· Increase in muscle length during postnatal growth
▪ Limbs of most species approximately double in length during postnatal growth
▪ May relate to greater efficiency and rate of gain of animals with a larger size because longitudinal growth of bone may stimulate muscle growth by stretching the growing muscle
▪ Increases in muscle length occur via increases in the length of the fibers making up the muscle
· Increase in muscle diameter
▪ Occurs via an increase in muscle fiber diameter
▪ Also can occur due to increase in fiber length which increases fiber overlap and causes the muscle diameter to increase
· Hypertrophy is stimulated by (these stimuli don’t necessarily involve the same mechanism):
▪ Hormones and growth factors (IGF-1, FGF, TGF beta)
▪ Passive stretch (long bone growth)
▪ Work (exercise)
To better understand postnatal muscle growth, we need to first understand the concept of the DNA unit.
▪ DNA unit is the volume of cytoplasm “managed” by a single nucleus. A measure of DNA unit size is the protein/DNA ratio in muscle. This can be determined experimentally.
# of DNA units is determined by total DNA
Size of DNA unit is indicated by the protein/DNA ratio
▪ More and smaller DNA units are consistent with the potential for faster growth rate
▪ DNA unit concept must be tempered by the fact that only 75-80% of nuclei in muscle tissue comes from muscle cells. The rest comes from connective tissue, vascular tissue, macrophages, adipocytes, etc.
▪ Can also alter DNA unit size by exercise but usually won’t be maintained once exercise is stopped.
In meat producing animals, DNA accumulation (accretion) is highly related to muscle growth rate.
Most rapid period of DNA accretion coincides with the most rapid period of muscle growth.
Fiber size is also highly related to DNA content of the fibers (the more DNA, the bigger the fiber).
More rapid DNA accretion means that the DNA unit is kept smaller so each nucleus has a smaller amount of sarcoplasm to control, and thus growth occurs more rapidly.
Preponderance of evidence shows that much of the DNA in muscle fibers is accumulated postnatally and that accretion of DNA in muscle is a key factor in limiting muscle growth.
60-90% of DNA in mature muscle fibers is accumulated during postnatal growth
Based on what we know, this seems inconsistent because:
▪ Number of muscle fibers is fixed at birth, and muscle fibers can’t divide
▪ The nuclei in the muscle fiber cannot divide
▪ Where does the increase in DNA come from?
Satellite Cells
· mononucleated cells located between the sarcolemma and basement membrane of each muscle fiber. Probably present from mid-gestation on, but it isn’t possible to identify them until all of the embryonic myoblasts have fused into the fibers prior to birth.
· Satellite cells are muscle cells that have the ability to proliferate and/or differentiate and fuse into adjacent fibers. This process adds the satellite cell nucleus to the muscle fiber and provides more nuclei to control protein synthesis in the growing fiber. Once a satellite cell has differentiated and fused with its fiber, that satellite cells is lost from the total satellite cell population. Thus in order to maintain a viable satellite cell population in growing muscle it is essential that a significant number of satellite cells continue to proliferate without differentiating and fusing with muscle fibers. As with embryonic development, postnatal growth is, in a sense, a tug-of-war between the competing processes of proliferation and terminal differentiation.
· Satellite cells are responsible for providing nuclei needed for postnatal muscle growth
· As we approach plateau of muscle growth, two things happen relative to satellite cells:
▪ Number of satellite cells has been decreasing throughout the growth of muscle
▪ As many as 30% of muscle nuclei in newborn are satellite cells
▪ By adulthood, only 2-10% are satellite cells.
▪ Can see that ability of satellite cells to contribute nuclei decreases during growth simply because the number of satellite cells decreases. This means more cells are fusing with fibers than are dividing.
· As animal grows, the satellite cells begin to withdraw from the proliferative cycle and enter a quiescent state known as Go. These cells don’t proliferate or fuse with fibers.
· Thus, the reason that we see the plateau in muscle growth curve may well relate directly to the fact that the number of satellite cells has decreased and those that are left are not actively proliferating or fusing with fibers. Thus the DNA needed to support muscle growth is not being provided to the fibers and muscle growth slows or stops.
· Need to find ways to stimulate satellite cell proliferation during growth so the number of satellite cells isn’t decreased so dramatically during this process and so that they do not enter the quiescent state. Satellite cells respond to growth factor in the same way the embryonic myoblasts do.
· Effects of growth factors on satellite cell proliferation and differentiation
▪ IGF-1
a) Stimulates proliferation
b) Stimulates differentiation
▪ FGF
a) Stimulates proliferation
b) Inhibits differentiation
▪ TGF-beta
a) Inhibits proliferation
b) Inhibits differentiation
▪ These growth factors are all produced by the muscle cells so regulation of satellite cell proliferation and differentiation may well be controlled by the levels of these growth factors produced in the muscle tissue — as well as by circulating level of IGF-1 which is also found in large quantities in the blood.
▪ None of these growth factors will activate quiescent satellite cells, however. Activating these cells is also important in maintaining growth of muscle during the latter stages of the muscle growth curve when many of the satellite cells have become quiescent.
a) Hepatocyte growth factor activates quiescent satellite cells and makes them responsive to the above growth factors. It is produced in muscle tissue. Prolonging the linear phase of muscle growth may involve activation of quiescent satellite cells by HGF. This will allow them to proliferate in response to other growth factors and ultimately contribute needed nuclei to growing muscle.
Studies suggesting that IGF-I stimulated satellite cell proliferation contributes to postnatal muscle growth:
Overexpression of IGF-I in selected skeletal muscles of the mouse
When IGF-I is introduced into mouse hindlimb muscles by viral-mediated gene transfer, local overexpression of IGF-I produces significant increases in muscle mass and strength compared with untreated controls. IGF-I expression promotes an average increase of 15% in muscle mass and a 14% increase in strength in young adult mice, and prevents aging-related muscle changes in old adult mice, resulting in a 27% increase in strength as compared with uninjected old muscles. In order to test if satellite cells are essential in mediating the hypertrophic effects of IGF-I, gamma radiation was used to destroy the proliferative capacity of satellite cells. Treatment with gamma radiation significantly prevented normal growth of the muscle. When combined with IGF-I treatment, approximately half of the IGF-I effect was prevented by gamma radiation treatment. This suggests that the remaining half of IGF-I induced hypertrophy was due to paracrine/autocrine effects on the adult muscle fibers. Thus, these data are consistent with a mechanism by which IGF-I induced muscle hypertrophy via a combination of satellite cell activation and increasing protein synthesis in differentiated muscle fibers.
Mechanism of action of anabolic steroid implants in feedlot steers
Implantation of feedlot steers with an anabolic steroid implant containing trenbolone acetate (a testosterone analog) and estrogen results in a 20% increase in rate of gain, a 15% increase in feed efficiency and an increase in lean muscle mass. At the same time the levels of circulating IGF-I are increased by as much as 40% and the level of IGF-I mRNA in the muscle tissue is approximately 60-75% higher in implanted steers than in unimplanted steers. Additionally, satellite cells isolated from muscles of implanted steers show increased proliferative capacity in comparison to satellite cells isolated from unimplanted steers. These data suggest that the increased muscle growth in implanted steers may be the result of an IGF-I-stimulated increase in the proliferation of muscle satellite cells.
IPSON said:
Look fuckface, do you see the smile after the posts....use your fucking imagination....Now I'm calling you a dumbfuck without the smile. Chill bro, I was just fucking with him. If I knew the answer to the question then i would never had asked.
Gee, this Ipson guy sounds just like Johnboy. Wonder if they're related.
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