The short version of somatotroph fits in a sentence. The long version — which is the one that helps — is below.
Reviewed 2025-11-17. Anything still debated is marked as such rather than presented as settled.
Tesamorelin is a synthetic peptide that belongs to the growth hormone-releasing hormone family and contains the same forty-four amino acid sequence as endogenous GHRH, extended at the amino terminus by a trans-3-hexenoyl group. That small fatty acid modification protects the peptide from rapid cleavage by dipeptidyl peptidase-4, the enzyme that shortens the half-life of native GHRH to only a few minutes. Chemically the compound is produced by solid-phase peptide synthesis, purified by chromatography, and supplied as a sterile lyophilized powder for reconstitution.
Regulatory approval in the United States came in 2010, when the Food and Drug Administration cleared the peptide for the reduction of excess abdominal fat in adults with HIV infection and associated lipodystrophy. The decision rested mainly on two randomized phase 3 trials that enrolled roughly eight hundred patients and ran for twenty-six weeks. Participants receiving active drug showed substantially greater declines in visceral adipose tissue than those receiving placebo, while total body weight changed comparatively little. A reformulated presentation was later approved, and the product has remained a niche therapy rather than a general weight-loss agent.
Tesamorelin occupies a narrow position among agents that act on the growth hormone axis. Unlike growth hormone itself, which is given as replacement, it stimulates the pituitary to release the hormone in pulses, so the downstream increase in insulin-like growth factor 1 depends on intact somatotroph function. Other peptides in the same family include shorter GHRH fragments and synthetic secretagogues with different stability profiles. Several points remain unresolved, including whether the reduction in visceral fat translates into fewer cardiovascular events, what happens to metabolic markers after long-term use, and how the drug compares with lifestyle or surgical approaches.
Stimulated growth hormone release leads to hepatic production of insulin-like growth factor 1, a key mediator of many growth hormone effects. In clinical studies, tesamorelin increased IGF-1 levels in a dose-dependent manner, although the response varies among individuals. The drug's effect on visceral fat is thought to involve growth hormone-mediated lipolysis and altered adipocyte metabolism. Muscle mass and lean body mass have also been assessed as secondary outcomes, but changes are generally smaller and less consistent than fat reductions.
Pharmacodynamic studies show that tesamorelin reduces visceral adipose tissue more than subcutaneous adipose tissue in the studied population. This selectivity may relate to differences in blood flow and hormone sensitivity between fat depots. Effects on glucose metabolism and insulin sensitivity have been investigated, with some trials reporting modest changes and others showing stability. The precise relationship between growth hormone exposure, IGF-1 levels, and visceral fat loss remains an active area of analysis.
Tesamorelin binds to growth hormone-releasing hormone receptors on somatotroph cells in the anterior pituitary. Receptor activation increases intracellular cyclic AMP and promotes synthesis and secretion of growth hormone. Because the peptide mimics endogenous GHRH, it amplifies the normal pulsatile release of growth hormone rather than providing exogenous growth hormone directly. This upstream action distinguishes tesamorelin from recombinant growth hormone preparations and from growth hormone secretagogues that act at different receptors.
| Property | Value | Notes |
|---|---|---|
| Peptide class | Synthetic GHRH analogue | 44 residues; N-terminal trans-3-hexenoyl group |
| First approval year | 2010 | United States; HIV-associated abdominal fat accumulation |
| Administration route | Subcutaneous injection | Abdominal site; clinician-administered or self-injected |
| Common synonyms | TH9507; tesamorelin acetate | Development code and acetate salt form |
| Originator | Canadian biotechnology firm | Original developer and regulatory sponsor |
A documented effect of tesamorelin is a reduction in visceral adipose tissue in some study populations. Researchers have reported decreases in trunk fat measured by computed tomography alongside changes in lipid markers. The mechanism is thought to involve growth hormone-mediated lipolysis, though the precise contribution of direct versus indirect pathways is not fully resolved. Studies have generally examined defined groups over finite periods, so long-term outcomes are less well characterized. Findings have not been uniform across all trials.
Tesamorelin is a synthetic peptide analog of growth hormone-releasing hormone (GHRH). Its sequence corresponds to the 44-amino-acid form of human GHRH with a trans-3-hexenoyl group attached to the N-terminal tyrosine. This modification slows enzymatic cleavage and extends the peptide's activity relative to the native hormone. The compound is produced by solid-phase peptide synthesis and supplied as a lyophilized powder. Researchers classify it as a GHRH receptor agonist. Its structure places it in the same family as other growth hormone secretagogues that act on the pituitary.
Binding of tesamorelin to GHRH receptors on pituitary somatotroph cells triggers cyclic AMP signaling and the release of growth hormone into circulation. Because the peptide acts upstream of the growth hormone axis, its effects are partly mediated by hepatic insulin-like growth factor 1 (IGF-1) production. The pulsatile character of endogenous growth hormone secretion is preserved rather than replaced. Whether amplified signaling produces effects beyond those of native GHRH remains an area of ongoing investigation.
Measuring the effect of a growth hormone-releasing hormone analogue requires markers that reflect pituitary output rather than the peptide itself. The two most frequently used are growth hormone and insulin-like growth factor 1. Growth hormone fluctuates sharply across the day and responds to sleep, stress, and meals, so isolated readings can be difficult to interpret. Insulin-like growth factor 1 changes more slowly and is often treated as the more stable integrated marker of axis activity.
Because growth hormone is released in pulses, single measurements can misrepresent overall secretion. Investigators sometimes use repeated sampling or overnight profiles to capture the pattern rather than a single value. Provocative testing, in which a stimulus is given and the response is tracked over time, offers another way to characterize the axis. Each approach carries trade-offs between sensitivity, burden on the participant, and the influence of non-target variables.
== Treatment devices used == The insulin pump is one device used in intensive insulinotherapy. The insulin pump is about the size of a beeper. It can be programmed to send a steady stream of insulin as basal insulin. It contains a reservoir or cartridge holding several days' worth of insulin, the tiny battery-operated pump, and the computer chip that regulates how much insulin is pumped. The infusion set is a thin plastic tube with a fine needle at the end. There are also newer "pods" which do not require tubing. It carries the insulin from the pump to the infusion site beneath the skin. It sends a larger amount before eating meals as "bolus" doses. The insulin pump replaces insulin injections. This device is useful for people who regularly forget to inject themselves or for people who don't like injections. This machine does the injecting by replacing the slow-acting insulin for basal needs with an ongoing infusion of rapid-acting insulin. Basal insulin: the insulin that controls blood glucose levels between meals and overnight. It controls glucose in the fasting state. Boluses: the insulin that is released when food is eaten or to correct a high reading. Another device used in intensive insulinotherapy is the injection port. An injection port is a small disposable device, similar to the infusion set used with an insulin pump, configured to accept a syringe. Standard insulin injections are administered through the injection port.
An isothermal titration calorimeter is composed of two identical cells made of a highly efficient thermally conducting and chemically inert material such as Hastelloy alloy or gold, surrounded by an adiabatic jacket. In this setup, one of the cells, the sample cell, holds the solution of one reactant, and the other cell, the reference cell, is filled with either a buffer or water. The second reactant, which has a higher concentration than the first, is placed in a syringe and gradually injected into the sample cell in small aliquots throughout the titration process. This process is semi-automated and the sensitive thermopile/thermocouple circuits are used to detect temperature differences between the reference cell (filled with buffer or water) and the sample cell containing the macromolecule. Prior to addition of ligand, a constant power (<1 mW) is applied to the reference cell. This directs a feedback circuit, activating a heater located on the sample cell. During the experiment, ligand is titrated into the sample cell in precisely known aliquots, causing heat to be either taken up or evolved (depending on the nature of the reaction). Measurements consist of the time-dependent input of power required to maintain equal temperatures between the sample and reference cells.
== Sources of PhIP == PhIP has been found in cooked beef, pork, chicken, and fish products. Exposure to PhIP depends on the eating habits of the individual and can vary up to 5000-fold. Exposure is also related to the type of meat, doneness, cooking method, and quantity consumed. Individual exposures can differ due to various anti-carcinogens in the diet. Different cooking methods for meat (broiling, grilling, frying, roasting, pan drippings) all contribute to formation of PhIP.
Molecular evidence of RNA editing in Bombyx chemosensory protein family. PLoS ONE 2014; 9: e86932. 10. Xuan N, Rajashekar B, Kasvandik S, Picimbon JF. Structural components of chemosensory protein mutations in the silkworm moth, Bombyx mori. Agri Gene 2016; 2: 53-58. 11. Xuan N, Rajashekar B, Picimbon JF. DNA and RNA-dependent polymerization in editing of Bombyx chemosensory protein (CSP) gene family. Agri Gene 2019; 12: 100087. 12. Picimbon JF. Mutations in the insect transcriptome. J Clin Exp Pathol. 2016; 6: 3. 13. Picimbon JF. A new view of genetic mutations. Australas Med J. 2017; 10: 701-715. 14. Picimbon JF. Evolution of protein physical structures in insect chemosensory systems. In: Picimbon JF (Ed.), Olfactory Concepts of Insect Control-Alternative to Insecticides. vol. 2 Springer Nature, Switzerland, 2019, pp. 231–263. 15. Campanacci V, Lartigue A, Hällberg BM, Jones TA, Giuici-Orticoni MT, Tegoni M, et al. Moth chemosensory protein exhibits drastic conformational changes and cooperativity on ligand binding. Proc Natl Acad Sci. USA 2003; 100: 5069-5074. 16. Picimbon JF, Dietrich K, Angeli S, Scaloni A, Krieger J, Breer H et al. Purification and molecular cloning of chemosensory proteins from Bombyx mori. Arch Insect Biochem Physiol. 2000b; 44: 120-129. 17. Picimbon JF, Dietrich K, Krieger J, Breer H. Identity and expression pattern of chemosensory proteins in Heliothis virescens (Lepidoptera, Noctuidae). Insect Biochem Mol Biol. 2001; 31: 1173-1181. 18. Wanner KW, Isman MB, Feng Q, Plettner E, Theilmann DA.
Sources: en.wikipedia.org
== Academic career == In 1974, Candace Pert earned a Ph.D. in pharmacology from Johns Hopkins University School of Medicine, where she worked in the laboratory of Solomon Snyder and discovered the brain's opiate receptor. Pert conducted a National Institutes of Health Postdoctoral Fellowship with the Department of Pharmacology at the Johns Hopkins University School of Medicine from 1974 to 1975. She conducted research at the National Institute of Mental Health from 1975 to 1987. In 1983, she became the Chief of the Section on Brain Biochemistry of the Clinical Neuroscience Branch, the only female chief at NIMH. She left to found and direct a private biotech laboratory in 1987. Pert was a research professor in the department of physiology and biophysics at Georgetown University School of Medicine in Washington, D.C. In her latter years, she was with RAPID Pharmaceuticals. In 1997 she published her book Molecules of Emotion. She appeared as one of the experts in Bill Moyers 1993 PBS video production, "Healing and the Mind", and in the 2004 film What the #$*! Do We Know!?. She died on September 12, 2013, in Potomac, Maryland.
== Prognosis == As of 2012, the five-year survival rate for systemic scleroderma was about 85%, whereas the 10-year survival rate was just under 70%. This varies according to the subtype; while localized scleroderma rarely results in death, the systemic form can, and the diffuse systemic form carries a worse prognosis than the limited form. The major scleroderma-related causes of death are: pulmonary hypertension, pulmonary fibrosis, and scleroderma renal crisis. People with scleroderma are also at a heightened risk for developing osteoporosis and for contracting cancer (especially liver, lung, haematologic, and bladder cancers). Scleroderma is also associated with an increased risk of cardiovascular disease. According to a study of an Australian cohort, between 1985 and 2015, the average life expectancy of a person with scleroderma increased from 66 years to 74 years (the average Australian life expectancy increased from 76 to 82 years in the same period).
A sarcomere (Greek σάρξ sarx "flesh", μέρος meros "part") is the smallest functional unit of striated muscle tissue. It is the repeating unit between two Z-lines. Skeletal muscles are composed of tubular muscle cells (called muscle fibers or myofibers) which are formed during embryonic myogenesis. Muscle fibers contain numerous tubular myofibrils. Myofibrils are composed of repeating sections of sarcomeres, which appear under the microscope as alternating dark and light bands. Sarcomeres are composed of long, fibrous proteins as filaments that slide past each other when a muscle contracts or relaxes. The costamere is a different component that connects the sarcomere to the sarcolemma. Two of the important proteins are myosin, which forms the thick filament, and actin, which forms the thin filament. Myosin has a long fibrous tail and a globular head that binds to actin. The myosin head also binds to ATP, which is the source of energy for muscle movement. Myosin can only bind to actin when the binding sites on actin are exposed by calcium ions. Actin molecules are bound to the Z-line, which forms the borders of the sarcomere. Other bands appear when the sarcomere is relaxed. The myofibrils of smooth muscle cells are not arranged into sarcomeres.
=== Adherence === It has been repeatedly found that in the long-term, all diets with the same calorific value perform the same for weight loss, except for the one differentiating factor of how well people can faithfully follow the dietary programme. A study comparing groups taking low-fat, low-carbohydrate and Mediterranean diets found at six months the low-carbohydrate diet still had most people adhering to it, but thereafter the situation reversed: at two years the low-carbohydrate group had the highest incidence of lapses and dropouts. This may be due to the comparatively limited food choice of low-carbohydrate diets.
=== Prostate surgery === The preservation of both neurovascular bundles during nerve-sparing (NS) radical prostatectomy improves urinary continence and erectile function. Consequently, NS is recommended in elderly men and those with pre-existing erectile dysfunction, whom many surgeons would previously have only offered non-NS surgery. It was also found that during surgeries in which neurovascular bundles are preserved, the frequency of positive margins were only 5.8 percent.
Sources: en.wikipedia.org
However a 2020 review concluded that while PCSK9 inhibitor treatment provides additional benefits beyond maximally tolerated statin therapy in high-risk individuals, PCSK9 inhibitor use probably produces little or no difference in mortality. Regeneron Pharmaceuticals (in collaboration with Sanofi) became the first to market a PCSK9 inhibitor, with a competitor Amgen reaching market slightly later. Prices were very high, inhibiting adoption. The drugs are approved by the FDA for treatment of hypercholesterolemia, notably the genetic condition heterozygous familial hypercholesterolemia which causes high cholesterol levels and heart attacks at a young age. These drugs were later approved by the FDA for the reduction of cardiovascular events including a reduction in all-cause mortality. In recent meta-analyses, early initiation of PCSK9 inhibitors within 48 to 72 hours following acute coronary syndrome (ACS) in addition to high dose statin therapy was associated with rapid reduction in LDL-C level, and potentially other lipid profiles such as triglycerides and total cholesterol level at 4 to 12 weeks after the cardiac event. This translates into a significant reduction in ACS-related hospital readmission and the need for coronary revascularization in short-term follow-up at 1 to 18 months. Two monoclonal antibodies that bind to and inhibit PCSK9 near the catalytic domain have since been approved to lower LDL cholesterol: alirocumab (Praluent, Sanofi/Regeneron), approved by the U.S.
In the first half of the 16th century Paracelsus proposed a theory of mineral formation as an analogy to fruit-bearing plants. In 1550 Gerolamo Cardano made an early attempt to explain the shape of crystals as the result of a close packing of spheres. In 1591 Thomas Harriot studied the close packing of cannonballs (spheres). In 1597 Andreas Libavius recognized the geometrical characteristics of crystals and identified salts from their crystal shape.
=== 24 March === A representative of the Indian Air Force told the Indian parliament that a "major delivery" from Russia was not going to proceed due to the war with Ukraine. This was the first time that a government officially acknowledged shortcomings by Russia to supply weapons or components due to the ongoing war in Ukraine.
Heparin is given parenterally because it is not absorbed from the gut, due to its high negative charge and large size. It can be injected intravenously or subcutaneously (under the skin); intramuscular injections (into muscle) are avoided because of the potential for forming hematomas. Because of its short biologic half-life of about one hour, heparin must be given frequently or as a continuous infusion. Unfractionated heparin has a half-life of about one to two hours after infusion, whereas LMWH has a half-life of four to five hours. The use of LMWH has allowed once-daily dosing, thus not requiring a continuous infusion of the drug. If long-term anticoagulation is required, heparin is often used only to commence anticoagulation therapy until an oral anticoagulant e.g. warfarin takes effect. The American College of Chest Physicians publishes clinical guidelines on heparin dosing.
Sources: en.wikipedia.org
It is a laboratory-made peptide of forty-four amino acids whose sequence matches human growth hormone-releasing hormone, with a modified amino terminus. The modification is a short unsaturated fatty acid chain attached to the first residue. This change slows enzymatic breakdown and lengthens the time the peptide stays active in circulation.
The clinical program was designed around HIV-associated lipodystrophy, a condition in which fat accumulates abnormally around the internal organs. Trials enrolled that specific population, so the evidence base covers it rather than the general population. Regulators approved the drug for the studied indication only, and promotion outside it is not permitted.
Growth hormone therapy supplies the finished hormone directly, while this peptide acts upstream and asks the pituitary to secrete its own. That difference means the response depends on a functioning pituitary and on the body's normal feedback loops. It also means the circulating hormone profile is pulsatile rather than a flat, injected level.
It targets the growth hormone-releasing hormone receptor on pituitary somatotroph cells. Binding stimulates cyclic AMP signaling and growth hormone secretion. This is the same receptor used by endogenous GHRH.