Description:

As its name suggests, human growth hormone is an important mediator of the human growth process. This hormone is produced endogenously by the anterior. pituitary gland, and exists at especially high levels during childhood Its growth-promoting effects are broad, and can be separated into three distinct areas: bone, skeletal muscle, and internal organs. It also supports protein, carbohydrate, lipid, and mineral metabolism, and can stimulate the growth of connective tissues. Although vital to early development, human growth hormone is produced throughout adulthood. Its levels and biological role decline with age, but continue to support metabolism, muscle tissue growth/maintenance, and the management (reduction) of adipose tissue throughout life. Somatropin specifically describes pharmaceutical human growth hormone that was synthesized with the use of recombinant DNA technology. Somatropin (rhGH) is biologically equivalent to human growth hormone (hGH) of pituitary origin

In a medical setting, somatropin used to help treat a variety of health conditions. It is most notably prescribed in cases of childhood growth disorders that are characterized by insufficient growth hormone production. While usually not fully corrective, somatropin use is often capable of substantially increasing the linear growth rate and overall height before further growth is halted in adolescence. This medication is also used to accelerate growth in children that were born small and failed to catch up by the age of two. Other uses include the treatment of short bowel syndrome, growth failure due to renal insufficiency, muscle wasting associated with HIV infection, and adult growth hormone deficiency.

Somatropin is also sometimes prescribed to healthy men and women who are aging. Growth hormone levels tend to decline as we get older, and many physicians believe that its supplementation to more youthful levels can help slow some of the damage of aging. Given its beneficial metabolic effects on muscle mass, strength, energy, cell regeneration, and fat loss, there are many supporters of this use, even if hGH may not specifically retard the aging process. Note that in order to prescribe hGH for adult hormone deficiency in the US, the patient must have a diagnosed pituitary disease or history of childhood GH deficiency, it is specifically illegal according to Federal law to prescribe hormone for any off-label use, which includes anti-aging and bodybuilding purposes.

Somatropin may be given by either subcutaneous of intramuscular injection. During clinical studies, the pharmacokinetic properties of somatropin following bo methods of use were determined. When given by subcutaneous injection, somatropin has a similar bu moderately higher level of bioavailability (75% vs 63 The rate of drug metabolism following both routes w also very similar, with somatropin displaying a half-life of approximately 3.8 hours and 49 hours after subcutaneous and intramuscular injection, respectively. Baseline hormone levels are usually reached between 12 hours and 18 hours following injection, with the slower times seen with intramuscular use. Given the delayed rise in IGF-1 levels, however, which can remain elevated 24 hours after hGH injection, the metabolic activity of human growth hormone will outlast its actual levels in the body. Although drug absorption is acceptable by both methods of use daily subcutaneous administration is generally regarded as the preferred method of using somatropin.

A specific analysis of somatropin activity shows a hormone with a diverse set of effects. It is anabolic to skeletal muscle, shown to increase both the size and number of cells (processes referred to as hypertrophy and hyperplasia respectively). The hormone also seems to have growth promoting effects on all organs of the body excluding the eyes and brain. Somatropin has a diabetogenic effect on carbohydrate metabolism, which means that it causes blood sugar levels to rise (a process normally associated with diabetes). Excessive administration of somatropin over time may induce a state of type-2 (insulin resistant) diabetes. This hormone also supports triglyceride hydrolysis in adipose tissue, and may reduce body fat stores. Coinciding with this tends to be a reduction in serum cholesterol. The drug also tends to reduce levels of potassium, phosphorous, and sodium, and may cause a decrease in levels of the thyroid hormone triiodothyronine (T3). The latter effect marks a reduction in thyroid supported metabolism, and can interfere with the effectiveness of extended therapy with somatropin.

Growth hormone has both direct and indirect effects. On the direct side, the hGH protein attaches to receptors in muscle, bone, and adipose tissues, sending messages to support anabolism and lipolysis (fat loss). Growth hormone also directly increases glucose synthesis (gluconeogenesis) in the liver, and induces insulin resistance by blocking its activity in target cells. The indirect effects of growth hormone are largely mediated by IGF-1 (insulin-like growth factor), which is produced in the liver and virtually all other tissues in response to growth hormone. IGF-1 is also anabolic to both muscle and bone, augmenting growth hormone’s activity, IGF-1, however, also has effects that are strongly antagonistic to growth hormone.

This includes increased lipogenesis (fat retention), increased gcse consumption, and decreased gluconeogenesis. The synergistic and antagonists effects of these two hormones combine to form the character of hGH Lewise they also dictate the effects of somatropin administration, which include the support lipolysis, increased serum glucose levels, and reduced insulin sitivity.

Somatropin is considered to be a controversial anabolic and performance-enhancing drug in the realm of bodybuilding and athletics. The main issue of debate is the exact level of potential benefit this substance carries While studies with HIV+ patients in a wasting state tend to support potentially strong anabolic and anticatabolic properties, studies demonstrating these same effects in Sealthy adults and athletes are lacking. During the 1980s, a large body of myth surrounded discussions of hGH in bodybuilding circles, which may have been fueled by the high cost of the drug and its very name (“growth bormone). It was once thought to be the most powerful anabolic substance you could buy. Today, recombinant human growth hormone is much more affordable and readily obtained. Most experienced individuals now tend to agree that it is the fat-loss-promoting properties of somatropin that are most obvious. The drug can support muscle growth, strength gains, and increased athletic performance, but its effects are generally milder than those of anabolic/androgenic steroids. For a highly advanced athlete or bodybuilder, however, somatropin can help push body and performance further than might have been possible with steroids alone.

How Supplied:

Somatropin most commonly supplied in multi-dose vials containing a white lyophilized powder that requires reconstitution with sterile or bacteriostatic water before use. Dosage may vary widely from 1mg to 24mg or more per vial Somatropin is also available as a stabile pre-mixed solution (Nutropin AQ) that is biologically equivalent to reconstituted somatropin.

Structural Characteristics:

Somatropin is human growth hormone protein manufactured by recombinant DNA technology. It has 191 amino acid residues and a molecular weight of 22.125 daltons. It is identical in structure to human growth hormone of pituitary origin

Storage:

Do not freeze. Follow package insert for storage information. Refrigeration (2 to 8°C. 35 to 46 Fl may be required before and after reconstitution Side Effects (General);

The most common adverse reactions to somatropin therapy are joint pain, headache, flu-like symptoms, peripheral edema (water retention), and back pain. Less common adverse reactions include inflammation of mucous membranes in the nose (rhinitis), dizziness, upper respiratory infection, bronchitis, tingling or numbness on the skin, reduced sensitivity to touch, general edema, nausea, sore bones, carpal tunnel syndrome, chest pain, depression, gynecomastia, hypothyroidism, and insomnia. The abuse of somatropin may cause diabetes, acromegaly (a visible thickening of the bones, most notably the feet, forehead, hands, jaw, and elbows), and enlargement of the internal organs. Due to the growth promotion effects of human growth hormone, this drug should not be used by individuals with active or recurring cancer.

Side Effects (Impaired glucose tolerance]:

Somatropin may reduce sensitivity to insulin and raise blood sugar levels. This may occur in individuals without preexisting diabetes or impaired glucose tolerance.

Side Effects (Injection site):

The administration of somatropin may cause redness, itching, or lumps at the site of injection. It may also cause a localized decrease of adipose tissue, which may be compounded by the repeated administration at the same site of injection.

Administration:

Somatropin is designed for subcutaneous or intramuscular administration. One milligram of somatropin is equivalent to approximately 3 International Units (3 IU). When used to treat adult onset growth hormone deficiency, the drug is commonly applied at a dosage of .005/mg/kg per day to .01mg/kg per day. This equates to roughly 1 IU to 3 IU per day for person of approximately 180-220 lbs. A long-term maintenance dosage is established after reviewing the patient’s IGF-1 levels and clinical response over time.

When used for physique- or performance-enhancing purposes, somatropin is usually administered at a dosage between 1 IU and 6 IU per day (2-4 IU being most common). The drug is commonly cycled in a similar manner to anabolic/androgenic steroids, with the length of intake generally being between 6 weeks and 24 weeks. The anabolic effects of this drug are less apparent than its lipolytic (fat loss) properties, and generally take longer periods of time and higher doses to manifest themselves.

Other drugs are commonly used in conjunction with somatropin in order to elicit a stronger response. Thyroid drugs (usually T3) are particularly common given the known effects of somatropin on thyroid levels, and may significantly enhance fat loss during therapy. Insulin is also commonly used with somatropin. Aside from countering

some of the effects somatropin has on glucose tolerance, insulin can increase receptor sensitivity to IGF-1, and reduce levels of IGF binding protein-1, allowing for IGF-1 activity9307 (growth hormone itself also lowers IGF binding protein levels).9318 Anabolic/androgenic steroids are also commonly taken with Somatropin, in an effort maximize potential muscle-building effects. steroids may also further increase free IGF-1 b lowering of IGF binding proteins. Note that the stacking of somatropin with thyroid drugs and/or insulin is usually approached with great care and caution, given that these are particularly strong medications with potentially serious or life threatening acute side effects.

Anabolic steroids are a class of medications that contain a synthetically manufactured form of the hormone testosterone, or a related compound that is derived from (or similar in structure and action to) this hormone. In order to fully grasp how anabolic steroids work, it is, therefore, important to understand the basic functioning of testosterone.

Testosterone is the primary male sex hormone. It is manufactured by the Leydig’s cells in the testes at varying amounts throughout a person’s life span. The effects of this hormone become most evident during the time of puberty, when an increased output of testosterone will elicit dramatic physiological changes in the male body. This includes the onset of secondary male characteristics such as a deepened voice, body and facial hair growth, increased oil output by the sebaceous glands, development of sexual organs, maturation of sperm, and an increased libido. Indeed the male reproductive system will not function properly if testosterone levels are not significant. All such effects are considered the masculinizing or “androgenic” properties of this hormone.

Increased testosterone production will also cause growth promoting or “anabolic” in the body, including an enhanced rate of protein synthesis (leading to muscle accumulation). Testosterone is the reason males carry more muscle mass than women, as the two sexes have vastly contrasting amounts of this hormone. More specifically, the adult male body will manufacture between 2.5 and 11 mg per day’ while females only produce about 1/4mg. The dominant sex hormone for women is estrogen, which has a significantly different effect on the body. Among other things, a lower androgen and higher estrogen level will cause women to store more body fat, accumulate less muscle tissue, have a shorter stature, and become more apt to bone weakening with age (osteoporosis).

The actual mechanism in which testosterone elicits these changes is somewhat complex. When free in the blood stream, the testosterone molecule is available to interact with various cells in the body. This includes skeletal muscle cells, as well as skin, scalp, kidney, bone, central nervous system, and prostate tissues. Testosterone binds with a cellular target in order to exert its activity, and will, therefore, effect only those body cells that posses the proper hormone receptor site (specifically the androgen receptor). This process can be likened to a lock and key system, with each receptor (lock) only being activated by a particular type of hormone (key). During this interaction, the testosterone molecule will become bound to the intracellular receptor site (located in the cytosol, not on the membrane surface), forming a new “receptor complex.” This complex (hormone + receptor site) will then migrate to the cell’s nucleus, where it will attach to a specific section of the cell’s DNA, referred to as the hormone response element. This will activate the transcription of specific genes, which in the case of skeletal muscle cell will ultimately cause (among other things) an increase in the synthesis of the two primary contractile proteins, actin and myosin (muscular growth). Carbohydrate storage in muscle tissue may be increased due to androgen action as well.

Once this messaging process is completed, the complex will be released, and the receptor and hormone will disassociate. Both are then free to migrate back into the cytosol for further activity. The testosterone molecule is also free to diffuse back into circulation to interact with other cells. The entire receptor cycle, including hormone binding, receptor-hormone complex migration, gene transcription and subsequent return to cytosol is a slow process, taking hours, not minutes, to complete. For example, in studies using a single injection of nandrolone, it is measured to be 4 to 6 hours before free androgen receptors migrate back to the cytosol after activation. It is also suggested that this cycle includes the splitting and formation of new androgen receptors once returned to cytosol, a possible explanation for the many observations that androgens are integral in the formation of their own receptor sites.

In the kidneys, this same process works to allow androgens to augment erythropoiesis (red blood cell production). It is this effect that leads to an increase in red blood cell concentrations, and possibly increased oxygen transport capacity, during anabolic/androgenic steroid therapy. Many athletes mistakenly assume that oxymetholone and boldenone are unique in this ability, due to specific uses or mentions of this effect in drug literature. In fact, stimulation of erythropoiesis occurs with nearly all anabolic/androgenic steroids, as this effect is simply tied with activation of the androgen receptor in kidney cells. The only real exceptions might be compounds such as dihydrotestosterone and some of its derivatives,4 which are rapidly broken down upon interaction with the 3alpha-hydroxysteroid dehydrogenase enzymes (kidney tissue has a similar enzyme distribution to muscle tissue, see “anabolic/androgenic dissociation” section), and therefore display low activity in these tissues.

diagrama de celula

 

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Adipose (fat) tissues are also androgen responsive, and here these hormones support the lipolytic (fat mobilizing) capacity of cells. This may be accomplished by an androgen-tied regulation of beta-adrenergic receptor concentrations or general cellular activity (through adenylate cyclase). We also note that the level of androgens in the body will closely correlate (inversely) with the level of stored body fat. As the level of androgenic hormones drops, typically the deposition of body fat will increase. Likewise as we enhance the androgen level, body fat may be depleted at a more active rate. The ratio of androgen to estrogen action is in fact most important, as estrogen plays a counter role by acting to increase the storage of body fat in many sites of action. Likewise, if one wished to lose fat during steroid use, estrogen levels should be kept low. This is clearly evidenced by the fact that non-aromatizing steroids have always been favored by bodybuilders looking to increase the look of definition and muscularity while aromatizing compounds are typically relegated to bulking phases of training due to their tendency to increase body fat storage. Aromatization is discussed in more detail in a following section (see: Estrogen Aromatization).

As mentioned, testosterone also elicits androgenic activity, which occurs by its activating receptors in what are considered to be androgen responsive tissues (often through prior conversion to dihydrotestosterone. See: DHT Conversion). This includes the sebaceous glands, which are responsible for the secretion of oils in the skin. As the androgen level rises, so does the release of oils. As oil output increases, so does the chance for pores becoming clogged (we can see why acne is such a common side effect of steroid use). The production of body and facial hair is also linked to androgen receptor activation in skin and scalp tissues. This becomes most noticeable as boys mature into puberty, a period when testosterone levels rise rapidly, and androgen activity begins to stimulate the growth of hair on the body and face. Some time later in life, and with the contribution of a genetic predisposition, androgen activity in the scalp may also help to initiate male-pattern hair loss. It is a misconception that dihydrotestosterone is an isolated culprit in the promotion of hair loss, however; as in actuality it is the general activation of the androgen receptor that is to blame (see: DHT Conversion). The functioning of sex glands and libido are also tied to the activity of androgens, as are numerous
 

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