Everything below concerns somatotroph cell. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2025-12-02. Where a claim depends on a specific study, the study is described rather than over-claimed.
Published work tends to frame tesamorelin as a tool for studying the GHRH axis and as a compound with measurable effects on body composition. Reports often describe visceral adipose tissue as an endpoint, assessed by imaging rather than by inference. Analytical sections commonly describe liquid chromatography with tandem mass spectrometry to confirm identity and purity, because immunoassays may cross-react with related fragments. Where results diverge between studies, differences in assay choice, sampling timing, and population are frequent explanations offered. Whether effects persist after treatment stops remains an open question.
Tesamorelin binds the growth hormone–releasing hormone receptor on pituitary somatotroph cells. The receptor signals through the Gs protein, raising intracellular cAMP and activating protein kinase A. That cascade triggers release of stored growth hormone in pulses rather than a steady stream. Because the drug acts at the receptor that normally controls this process, its effect depends on the body's own signaling architecture rather than on a synthetic pathway. The resulting hormone profile reflects the timing of each pulse, not only its size.
Clinical study of tesamorelin has centered on adults with HIV-associated lipodystrophy, a condition in which abdominal fat accumulates while peripheral fat is lost. In controlled trials, treated participants showed reductions in visceral adipose tissue measured by imaging, alongside modest shifts in some lipid values. Effects on subcutaneous fat were smaller and less consistent across studies. Whether these changes translate into fewer cardiovascular events remains an open question, because the trials were not designed or powered to answer it.
Tesamorelin is a synthetic peptide that acts as an analog of growth hormone-releasing hormone, a natural hypothalamic signal. Its sequence corresponds to the forty-four amino acid form of the human hormone, with a small acyl group attached near the amino terminus. That modification slows enzymatic breakdown and extends the time the peptide remains active in circulation. The compound was developed as a pharmacological way to raise endogenous growth hormone output rather than supplying the hormone directly.
| Property | Value | Notes |
|---|---|---|
| Primary target | GHRH receptor | Located on pituitary somatotroph cells |
| Signaling route | cAMP–protein kinase A | Gs-coupled receptor pathway |
| Downstream markers | Growth hormone and IGF-1 | Used as pharmacodynamic readouts |
| Common detection | LC-MS/MS | Separates intact peptide from fragments |
| Typical storage | 2–8 °C, protected from light | Applies to solid form before reconstitution |
Questions remain about how much of the observed fat reduction reflects direct GHRH-receptor signaling versus the downstream growth hormone and IGF-1 surge. It is also unclear whether the compound produces meaningful benefit in populations without lipodystrophy, since trials in cognitive impairment did not reach their stated goals. Long-term effects on glucose metabolism and on cardiovascular outcomes are not fully characterized. Published work generally describes effects on surrogate markers rather than on hard clinical endpoints, and independent replication of some findings is limited.
Tesamorelin acts on the growth hormone-releasing hormone receptor, a G-protein-coupled receptor found on somatotroph cells in the anterior pituitary. Binding triggers a rise in intracellular cyclic AMP, which in turn opens ion channels and raises calcium concentrations, leading to release of stored growth hormone into the bloodstream. Because the peptide works through the same receptor as the body's own GHRH, the resulting secretion follows a pulsatile pattern rather than a continuous elevation. The N-terminal modification slows enzymatic breakdown, so the signal persists longer than it would with the unmodified hormone.
Growth hormone released from the pituitary stimulates the liver and other tissues to produce insulin-like growth factor 1, a stable circulating protein that serves as a practical marker of activity. Clinical studies therefore track IGF-1 concentrations alongside the hormone itself, and they commonly measure body composition with imaging rather than relying on body weight alone. Visceral adipose tissue, the fat surrounding abdominal organs, is quantified by computed tomography in the studies that supported approval. Adverse effects reported in trials include injection-site reactions, joint pain, and increases in blood glucose, which is why monitoring accompanies use.
监管记录显示，特沙莫瑞林于 2010 年在美国首次获得批准，用于人类免疫缺陷病毒感染相关的脂肪营养不良患者。批准依据来自降低内脏脂肪的临床试验，而非体重或瘦体重的普遍改善。后续出现了不同制剂版本，但其核心适应症保持一致。关于长期心血管结局和死亡率影响，现有证据仍不充分。
在临床研究之外，特沙莫瑞林常被讨论为生长激素分泌促进剂，但这一说法需要限定。它并不等同于生长激素本身，也不属于普通减重药物。部分研究关注其减少腹部脂肪和改善脂质谱的潜力，另一些研究则关注胰岛素抵抗和 IGF-1 升高等信号。这些效应的临床意义仍在评估中，尚未形成统一结论。
特沙莫瑞林是一种合成肽，其序列与人生长激素释放激素的 44 个氨基酸形式相关。它在 N 端带有反式-3-己烯酰基修饰，这一改动可减缓二肽基肽酶 IV 的降解。该化合物属于生长激素释放激素受体激动剂，可刺激垂体释放生长激素。研究文献通常将其归入合成肽类药物，而非小分子化合物。
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.
Insulin-like growth factor 1 is produced largely in the liver in response to growth hormone signaling. Its concentration shifts over days rather than minutes, which makes it practical for tracking changes across a study period. Interpretation still depends on age, nutritional status, and concurrent illness, all of which independently affect the marker. Reference ranges are therefore stratified, and comparisons are usually made within an individual over time rather than against a single population threshold.
Receptor-level activity begins when the peptide binds the GHRH receptor, a class B G-protein-coupled receptor found on pituitary somatotroph cells. Occupancy triggers Gs-mediated activation of adenylyl cyclase and a rise in intracellular cyclic AMP, which in turn promotes synthesis and pulsatile release of growth hormone. Because the compound acts upstream of the growth hormone axis rather than supplying hormone directly, its effect depends on intact pituitary function. Binding studies in cell culture and animal models have established this pathway; the detailed kinetics of receptor recycling in humans remain less well characterized.
Physicochemical behavior is dominated by the peptide backbone. The molecule is hydrophilic and carries a net positive charge near neutral pH, owing to several arginine and lysine residues. In solution it adopts a largely unstructured conformation, and aggregation is a known concern for peptide products of this size. Oxidation of methionine and deamidation of asparagine or glutamine residues are the principal chemical degradation routes. These liabilities shape how the material is formulated, handled, and analyzed, and they explain why lyophilized presentations are common in research settings.
Tesamorelin is a synthetic peptide analog of growth hormone-releasing hormone, built from 44 amino acids. Its sequence follows the natural human GHRH(1-44) backbone, with a trans-3-hexenoyl group attached to the N-terminal tyrosine. This modification blocks recognition by dipeptidyl peptidase IV, the enzyme that rapidly truncates the native hormone in circulation. The result is a molecule with a substantially longer plasma residence time than unmodified GHRH, which makes it practical for clinical and laboratory study.
=== Changes in menus === To make MREs more palatable to service members and match ever-changing trends in popular tastes, the military is constantly seeking feedback to adjust MRE menus and ingredients. In the following list, only main entrees are listed. Vegetarian menus are marked and footnoted on their first appearance.
=== Benzene toxicity === Benzene poisoning can increase risk of hematological cancers and other disorders. The mechanism of benzene metabolism and how it affects toxicity has not been completely understood. A general observation is that there is high variation in the extent of damage due to benzene poisoning. A possible explanation is the accumulation of phenols and hydroquinone in the target organ—the bone marrow—and subsequent oxidation of these metabolites to reactive quinone metabolites via a number of possible pathways. A case-control study conducted in China showed that patients with two copies of the NQO1 C609T (NQO1*2 polymorphism) mutation had a 7.6-fold increased risk of benzene poisoning compared to those who carried one or two wild-type NQO1 alleles.
== History == Since its discovery in 1967, serine protease DPP-4 has been a popular subject of research. Inhibitors of DPP-4 have long been sought as tools to elucidate the functional significance of the enzyme. The first inhibitors were characterized in the late 1980s and 1990s. Each inhibitor was important to establish an early structure activity relationship (SAR) for subsequent investigation. The inhibitors fall into two main classes, those that interact covalently with DPP-4 and those that do not. DPP-4 is a dipeptidase that selectively binds substrates that contain proline at the P1-position, thus many DPP-4 inhibitors have 5-membered heterocyclic rings that mimic proline, e.g. pyrrolidine, cyanopyrrolidine, thiazolidine and cyanothiazolidine. These compounds commonly form covalent bonds to the catalytic residue Ser630. In 1994, researchers from Zeria Pharmaceuticals unveiled cyanopyrrolidines with a nitrile function group that was assumed to form an imidate with the catalytic serine. Concurrently other DPP-4 inhibitors without a nitrile group were published but they contained other serine-interacting motifs, e.g. boronic acids, phosphonates or diacyl hydroxylamines. These compounds were not as potent because of the similarity of DPP-4 and prolyl oligopeptidase (PEP) and also suffered from chemical instability. Ferring Pharmaceuticals filed for patent on two cyanopyrrolidine DPP-4 inhibitors, which they published in 1995. These compounds had excellent potency and improved chemical stability. In 1995, Edwin B.
Viola canina – heath dog violet Viola hirta – hairy violet Viola labradorica – alpine violet Viola odorata – sweet violet Viola persicifolia – fen violet Viola riviniana – common dog violet Viola rostrata – long-spurred violet Viola sororia – common blue violet, hooded violet Section Xylinosium
Cameron McCormick (born April 2, 1998) is an American former college football player who was a tight end for the Oregon Ducks and Miami Hurricanes. He is currently a scouting assistant with the New England Patriots of the National Football League (NFL). After suffering multiple season-ending injuries requiring surgeries and 1 extra year of COVID eligibility, McCormick was granted his ninth year of NCAA eligibility extending through the 2024 NCAA Division I FBS football season in 2022. He is thought to be the first football player to have been granted such eligibility.
Sources: en.wikipedia.org
Although 'a new departure', and notably indirect in its reference to the monarchy, it was criticised by nationalists and republicans for making any reference to the Crown, the claim being that it was a direct oath to the Crown, a fact arguably incorrect by an examination of its wording, but in 1922 Ireland and beyond, many argued that the fact remained that as a dominion the king (and therefore the British) was still head of state and that was the practical reality that influenced public debate on the issue. The Free State was not a republic. The Oath became a key issue in the resulting Irish Civil War that divided the pro and anti-treaty sides in 1922–23.
== In other organisms == Many bacteria synthesize menaquinones from chorismic acid. They use it as a part of the electron transport chain, playing a similar role as other quinones such as ubiquinone. Oxygen, heme, and menaquinones are needed for many species of lactic acid bacteria to conduct respiration. Variations in biosynthetic pathways mean that bacteria also produce analogues of vitamin K2. For example, MK9(II-H), which replaces the second geranylgeranyl unit with a saturated phytyl, is produced by Mycobacterium phlei. There also exists a possibility of cis–trans isomerism due to the double bonds present. In M. phlei, the 3'-methyl-cis MK9(II-H) form seems to be more biologically active than trans MK9(II-H). However, with human enzymes, the naturally abundant trans form is more efficient. One hydrogenated MK that sees relevant amounts of human consumption is MK-9(4H), found in cheese fermented by Propionibacterium freudenreichii. This variation has the second and third units replaced with phytyl.
On 1 September 1998, 13 police forces raided alleged members of an international child pornography ring known as the Wonderland Club. The operation was code-named Operation Cathedral and resulted in the confiscation of 750,000 images and videos depicting 1,263 different children. Mendonça was among the few children (just 16 in total) that could be identified. However, his whereabouts remain unknown. Police suspect that he was murdered by his abductors after being abused on camera for other members of the child sex ring. In Switzerland, a boy was heard saying in a restaurant in 2007: "I was also kidnapped. I'm from Famalicão and for me no one is looking." Police informed the family that the lead was not consistent. It was also highlighted that the boy could have been Rui Pereira, who disappeared two days before Rui Pedro. In later years, Rui Pedro has been identified in pictures regarding the child sex ring and the worldwide Operation Cathedral movement.
Hepatitis B is endemic in China. Of the 350 million individuals worldwide infected with the hepatitis B virus (HBV), one-third reside in China. As of 2006 China has immunized 11.1 million children in its poorest provinces as part of several programs initiated by the Chinese government and as part of the Global Alliance for Vaccines and Immunization (GAVI). However, the effects of these programs have yet to reach levels of immunization that would limit the spread of hepatitis B effectively.
== History == Finasteride was the first 5-ARI to be introduced for medical use. It was marketed for the treatment of BPH in 1992 and was subsequently approved for the treatment of pattern hair loss in 1997. Epristeride was the second 5-ARI to be introduced and was marketed for the treatment of BPH in China in 2000. Dutasteride was approved for the treatment of BPH in 2001 and was subsequently approved for pattern hair loss in South Korea in 2009 and in Japan in 2015. The patent protection on finasteride and dutasteride has expired and both drugs are available as generic medications.
Sources: en.wikipedia.org
Codex Alimentarius Codex Alimentarius General Standard for Irradiated Foods (CAC/STAN 106-1983, rev.1 2003) at the Wayback Machine (archived 2007-09-26) Codex Alimentarius Recommended International Code of Practice Code for Radiation Processing of Foods (CAC/RCP 19-1979, rev.2 – 2003) Archived October 5, 2021, at the Wayback Machine General Standard for the Labelling of Prepacked Foods (CODEX STAN 1-1985) Archived April 6, 2011, at the Wayback Machine Food Irradiation Processing Alliance FIPA represents the irradiation service industry, manufacturers of food irradiators and suppliers of cobalt-60 sources. Irradiation of Food and Food Packaging at the Wayback Machine (archived 2009-03-04), Center for Food Safety and Applied Nutrition (US Government) Facts about Food Irradiation at the Wayback Machine (archived 2006-03-16), a series of 14 fact sheets, International Consultative Group on Food Irradiation, International Atomic Energy Agency, Vienna, 1991 Bibliography on Food Irradiation Archived May 3, 2006, at the Wayback Machine, Federal Research Centre for Nutrition and Food, Karlsruhe, Germany IAEA interactive map of irradiation facilities Archived April 20, 2021, at the Wayback Machine Keener, Kevin M. "Department of Food Science Food Irradiation: To Zap or not to Zap?" (PDF). North Carolina State University. Archived from the original (PDF) on September 7, 2015. Retrieved January 12, 2021.
== Epidemiology == The National Eye Institute reports keratoconus is the most common corneal dystrophy in the United States, affecting about one in 2,000 Americans, but some reports place the figure as high as one in 500. In the pediatric populations, ages three to 18, the prevalence of keratoconus was found to be as high as one in 334 children. The inconsistency may be due to variations in diagnostic criteria, with some cases of severe astigmatism interpreted as those of keratoconus, and vice versa. A long-term study found a mean incidence rate of 2.0 new cases per 100,000 population per year. Some studies have suggested a higher prevalence amongst females, or that people of South Asian ethnicity are 4.4 times as likely to develop keratoconus as Caucasians, and are also more likely to be affected with the condition earlier. Keratoconus is normally bilateral (affecting both eyes) although the distortion is usually asymmetric and is rarely completely identical in both corneas. Unilateral cases tend to be uncommon, and may in fact be very rare if a very mild condition in the better eye is simply below the limit of clinical detection. It is common for keratoconus to be diagnosed first in one eye and not until later in the other. As the condition then progresses in both eyes, the vision in the earlier-diagnosed eye will often remain poorer than that in its fellow.
===== MeSH D08.811.913.696 – phosphotransferases (EC 2.7) ===== MeSH D08.811.913.696.175 – diphosphotransferases MeSH D08.811.913.696.175.300 – gtp pyrophosphokinase MeSH D08.811.913.696.175.650 – ribose-phosphate pyrophosphokinase MeSH D08.811.913.696.175.825 – thiamin pyrophosphokinase MeSH D08.811.913.696.310 – myosin type iii MeSH D08.811.913.696.445 – nucleotidyltransferases MeSH D08.811.913.696.445.035 – n-acylneuraminate cytidylyltransferase MeSH D08.811.913.696.445.184 – choline-phosphate cytidylyltransferase MeSH D08.811.913.696.445.308 – dna nucleotidyltransferases MeSH D08.811.913.696.445.308.300 – dna-directed dna polymerase MeSH D08.811.913.696.445.308.300.112 – dna polymerase beta MeSH D08.811.913.696.445.308.300.225 – dna polymerase i MeSH D08.811.913.696.445.308.300.230 – dna polymerase ii MeSH D08.811.913.696.445.308.300.235 – dna polymerase iii MeSH D08.811.913.696.445.308.300.750 – RNA-directed dna polymerase MeSH D08.811.913.696.445.308.300.750.375 – hiv-1 reverse transcriptase MeSH D08.811.913.696.445.308.300.750.750 – telomerase MeSH D08.811.913.696.445.308.300.875 – taq polymerase MeSH D08.811.913.696.445.308.325 – dna nucleotidylexotransferase MeSH D08.811.913.696.445.400 – glucose-1-phosphate adenylyltransferase MeSH D08.811.913.696.445.600 – nicotinamide-nucleotide adenylyltransferase MeSH D08.811.913.696.445.625 – 2',5'-oligoadenylate synthetase MeSH D08.811.913.696.445.650 – polynucleotide adenylyltransferase MeSH D08.811.913.696.445.692 – rec a recombinases MeSH D08.811.913.696.445.735 – rna nucleotidyltransferases MeSH D08.811.913.696.445.735.265 – dna, catalytic MeSH D08.811.913.696.445.735.270 – dna-directed rna polymerases MeSH D08.811.913.696.445.735.270.375 – dna primase MeSH D08.811.913.696.445.735.270.750 – rna polymerase i MeSH D08.811.913.696.445.735.270.762 – rna polymerase ii MeSH D08.811.913.696.445.735.270.775 – rna polymerase iii MeSH D08.811.913.696.445.735.270.887 – rna polymerase sigma 54 MeSH D08.811.913.696.445.735.532 – polyribonucleotide nucleotidyltransferase MeSH D08.811.913.696.445.735.630 – q beta replicase MeSH D08.811.913.696.445.735.720 – rna helicases MeSH D08.811.913.696.445.735.720.500 – eukaryotic initiation factor-4a MeSH D08.811.913.696.445.735.780 – rna replicase MeSH D08.811.913.696.445.735.917 – rna, ribosomal, self-splicing MeSH D08.811.913.696.445.800 – sulfate adenylyltransferase MeSH D08.811.913.696.445.825 – transposases MeSH D08.811.913.696.445.825.500 – hiv integrase MeSH D08.811.913.696.445.837 – transposon resolvases MeSH D08.811.913.696.445.850 – UDP-glucose—hexose-1-phosphate uridylyltransferase MeSH D08.811.913.696.445.875 – UTP—glucose-1-phosphate uridylyltransferase MeSH D08.811.913.696.445.900 – UTP—hexose-1-phosphate uridylyltransferase MeSH D08.811.913.696.445.950 – vdj recombinases MeSH D08.811.913.696.620 – phosphotransferases (alcohol group acceptor) MeSH D08.811.913.696.620.010 – adenosine kinase MeSH D08.811.913.696.620.155 – choline kinase MeSH D08.811.913.696.620.175 – deoxycytidine kinase MeSH D08.811.913.696.620.200 – diacylglycerol kinase MeSH D08.811.913.696.620.225 – fructokinases MeSH D08.811.913.696.620.225.850 – phosphofructokinases MeSH D08.811.913.696.620.225.850.500 – phosphofructokinase-1 MeSH D08.811.913.696.620.225.850.500.249 – phosphofructokinase-1, liver type MeSH D08.811.913.696.620.225.850.500.500 – phosphofructokinase-1, muscle type MeSH D08.811.913.696.620.225.850.500.750 – phosphofructokinase-1, type c MeSH D08.811.913.696.620.225.850.750 – phosphofructokinase-2 MeSH D08.811.913.696.620.240 – galactokinase MeSH D08.811.913.696.620.250 – glucokinase MeSH D08.811.913.696.620.275 – glycerol kinase MeSH D08.811.913.696.620.300 – hexokinase MeSH D08.811.913.696.620.475 – kanamycin kinase MeSH D08.811.913.696.620.525 – 1-phosphatidylinositol 3-kinase MeSH D08.811.913.696.620.550 – 1-phosphatidylinositol 4-kinase MeSH D08.811.913.696.620.650 – phosphoenolpyruvate sugar phosphotransferase system MeSH D08.811.913.696.620.680 – polynucleotide 5'-hydroxyl-kinase MeSH D08.811.913.696.620.682 – protein kinases MeSH D08.811.913.696.620.682.650 – phosphorylase kinase MeSH D08.811.913.696.620.682.700 – protein-serine-threonine kinases MeSH D08.811.913.696.620.682.700.062 – activin receptors MeSH D08.811.913.696.620.682.700.062.500 – activin receptors, type i MeSH D08.811.913.696.620.682.700.062.750 – activin receptors, type ii MeSH D08.811.913.696.620.682.700.109 – bone morphogenetic protein receptors MeSH D08.811.913.696.620.682.700.109.500 – bone morphogenetic protein receptors, type i MeSH D08.811.913.696.620.682.700.109.750 – bone morphogenetic protein receptors, type ii MeSH D08.811.913.696.620.682.700.125 – ca(2+)-calmodulin dependent protein kinase MeSH D08.811.913.696.620.682.700.125.500 – myosin-light-chain kinase MeSH D08.811.913.696.620.682.700.140 – casein kinases MeSH D08.811.913.696.620.682.700.140.300 – casein kinase i MeSH D08.811.913.696.620.682.700.140.300.100 – casein kinase ialpha MeSH D08.811.913.696.620.682.700.140.300.200 – casein kinase idelta MeSH D08.811.913.696.620.682.700.140.300.300 – casein kinase iepsilon MeSH D08.811.913.696.620.682.700.140.600 – casein kinase ii MeSH D08.811.913.696.620.682.700.150 – cyclic nucleotide-regulated protein kinases MeSH D08.811.913.696.620.682.700.150.125 – cyclic amp-dependent protein kinases MeSH D08.811.913.696.620.682.700.150.125.500 – beta-adrenergic-receptor kinase MeSH D08.811.913.696.620.682.700.150.150 – cyclic gmp-dependent protein kinases MeSH D08.811.913.696.620.682.700.150.575 – protamine kinase MeSH D08.811.913.696.620.682.700.200 – cyclin-dependent kinases MeSH D08.811.913.696.620.682.700.200.067 – cdc2-cdc28 kinases MeSH D08.811.913.696.620.682.700.200.067.249 – cdc2 protein kinase MeSH D08.811.913.696.620.682.700.200.067.500 – cdc28 protein kinase, s cerevisiae MeSH D08.811.913.696.620.682.700.200.067.875 – cyclin-dependent kinase 5 MeSH D08.811.913.696.620.682.700.200.067.900 – cyclin-dependent kinase 9 MeSH D08.811.913.696.620.682.700.200.323 – cyclin-dependent kinase 2 MeSH D08.811.913.696.620.682.700.200.451 – cyclin-dependent kinase 4 MeSH D08.811.913.696.620.682.700.200.515 – cyclin-dependent kinase 6 MeSH D08.811.913.696.620.682.700.200.580 – maturation-promoting factor MeSH D08.811.913.696.620.682.700.200.580.500 – cdc2 protein kinase MeSH D08.811.913.696.620.682.700.250 – dna-activated protein kinase MeSH D08.811.913.696.620.682.700.300 – eif-2 kinase MeSH D08.811.913.696.620.682.700.429 – glycogen synthase kinases MeSH D08.811.913.696.620.682.700.429.500 – glycogen synthase kinase 3 MeSH D08.811.913.696.620.682.700.494 – i-kappa B kinase MeSH D08.811.913.696.620.682.700.559 – map kinase kinase kinases MeSH D08.811.913.696.620.682.700.559.100 – map kinase kinase kinase 1 MeSH D08.811.913.696.620.682.700.559.200 – map kinase kinase kinase 2 MeSH D08.811.913.696.620.682.700.559.300 – map kinase kinase kinase 3 MeSH D08.811.913.696.620.682.700.559.400 – map kinase kinase kinase 4 MeSH D08.811.913.696.620.682.700.559.500 – map kinase kinase kinase 5 MeSH D08.811.913.696.620.682.700.559.800 – proto-oncogene proteins c-mos MeSH D08.811.913.696.620.682.700.559.842 – raf kinases MeSH D08.811.913.696.620.682.700.559.842.249 – oncogene proteins v-raf MeSH D08.811.913.696.620.682.700.559.842.374 – proto-oncogene proteins b-raf MeSH D08.811.913.696.620.682.700.559.842.500 – proto-oncogene proteins c-raf MeSH D08.811.913.696.620.682.700.565 – mitogen-activated protein kinase kinases MeSH D08.811.913.696.620.682.700.565.100 – map kinase kinase 1 MeSH D08.811.913.696.620.682.700.565.200 – map kinase kinase 2 MeSH D08.811.913.696.620.682.700.565.300 – map kinase kinase 3 MeSH D08.811.913.696.620.682.700.565.400 – map kinase kinase 4 MeSH D08.811.913.696.620.682.700.565.500 – map kinase kinase 5 MeSH D08.811.913.696.620.682.700.565.600 – map kinase kinase 6 MeSH D08.811.913.696.620.682.700.565.700 – map kinase kinase 7 MeSH D08.811.913.696.620.682.700.567 – mitogen-activated protein kinases MeSH D08.811.913.696.620.682.700.567.342 – extracellular signal-regulated map kinases MeSH D08.811.913.696.620.682.700.567.342.500 – mitogen-activated protein kinase 1 MeSH D08.811.913.696.620.682.700.567.342.750 – mitogen-activated protein kinase 3 MeSH D08.811.913.696.620.682.700.567.342.875 – mitogen-activated protein kinase 6 MeSH D08.811.913.696.620.682.700.567.342.937 – mitogen-activated protein kinase 7 MeSH D08.811.913.696.620.682.700.567.513 – jnk mitogen-activated protein kinases MeSH D08.811.913.696.620.682.700.567.513.500 – mitogen-activated protein kinase 8 MeSH D08.811.913.696.620.682.700.567.513.750 – mitogen-activated protein kinase 9 MeSH D08.811.913.696.620.682.700.567.513.800 – mitogen-activated protein kinase 10 MeSH D08.811.913.696.620.682.700.567.878 – p38 mitogen-activated protein kinases MeSH D08.811.913.696.620.682.700.586 – oncogene protein v-akt MeSH D08.811.913.696.620.682.700.606 – phytochrome a MeSH D08.811.913.696.620.682.700.646 – proline-directed protein kinases MeSH D08.811.913.696.620.682.700.646.500 – cyclin-dependent kinases MeSH D08.811.913.696.620.682.700.646.500.500 – cdc2-cdc28 kinases MeSH D08.811.913.696.620.682.700.646.500.500.500 – cyclin-dependent kinase 5 MeSH D08.811.913.696.620.682.700.646.500.750 – cyclin-dependent kinase 2 MeSH D08.811.913.696.620.682.700.646.500.875 – cyclin-dependent kinase 4 MeSH D08.811.913.696.620.682.700.646.500.937 – cyclin-dependent kinase 6 MeSH D08.811.913.696.620.682.700.646.625 – glycogen synthase kinase 3 MeSH D08.811.913.696.620.682.700.646.750 – mitogen-activated protein kinases MeSH D08.811.913.696.620.682.700.646.750.249 – extracellular signal-regulated map kinases MeSH D08.811.913.696.620.682.700.646.750.249.500 – mitogen-activated protein kinase 1 MeSH D08.811.913.696.620.682.700.646.750.249.750 – mitogen-activated protein kinase 3 MeSH D08.811.913.696.620.682.700.646.750.249.875 – mitogen-activated protein kinase 6 MeSH D08.811.913.696.620.682.700.646.750.249.937 – mitogen-activated protein kinase 7 MeSH D08.811.913.696.620.682.700.646.750.374 – jnk mitogen-activated protein kinases MeSH D08.811.913.696.620.682.700.646.750.374.500 – mitogen-activated protein kinase 8 MeSH D08.811.913.696.620.682.700.646.750.374.750 – mitogen-activated protein kinase 9 MeSH D08.811.913.696.620.682.700.646.750.374.800 – mitogen-activated protein kinase 10 MeSH D08.811.913.696.620.682.700.646.750.843 – p38 mitogen-activated protein kinases MeSH D08.811.913.696.620.682.700.725 – protein kinase C MeSH D08.811.913.696.620.682.700.725.100 – protein kinase C-alpha MeSH D08.811.913.696.620.682.700.725.400 – protein kinase C-delta MeSH D08.811.913.696.620.682.700.725.750 – protein kinase C-epsilon MeSH D08.811.913.696.620.682.700.755 – proto-oncogene proteins C-akt MeSH D08.811.913.696.620.682.700.759 – proto-oncogene proteins C-bcr MeSH D08.811.913.696.620.682.700.776 – proto-oncogene proteins C-pim-1 MeSH D08.811.913.696.620.682.700.827 – rhodopsin kinase MeSH D08.811.913.696.620.682.700.862 – ribosomal protein s6 kinases MeSH D08.811.913.696.620.682.700.862.249 – ribosomal protein s6 kinases, 70-kda MeSH D08.811.913.696.620.682.700.862.500 – ribosomal protein s6 kinases, 90-kda MeSH D08.811.913.696.620.682.725 – protein-tyrosine kinase MeSH D08.811.913.696.620.682.725.049 – focal adhesion protein-tyrosine kinases MeSH D08.811.913.696.620.682.725.049.500 – focal adhesion kinase 1 MeSH D08.811.913.696.620.682.725.049.750 – focal adhesion kinase 2 MeSH D08.811.913.696.620.682.725.200 – mitogen-activated protein kinase kinases MeSH D08.811.913.696.620.682.725.200.100 – map kinase kinase 1 MeSH D08.811.913.696.620.682.725.200.200 – map kinase kinase 2 MeSH D08.811.913.696.620.682.725.200.300 – map kinase kinase 3 MeSH D08.811.913.696.620.682.725.200.400 – map kinase kinase 4 MeSH D08.811.913.696.620.682.725.200.500 – map kinase kinase 5 MeSH D08.811.913.696.620.682.725.200.600 – map kinase kinase 6 MeSH D08.811.913.696.620.682.725.200.700 – map kinase kinase 7 MeSH D08.811.913.696.620.682.725.300 – proto-oncogene proteins c-fes MeSH D08.811.913.696.620.682.725.400 – receptor protein-tyrosine kinases MeSH D08.811.913.696.620.682.725.400.020 – fms-like tyrosine kinase 3 MeSH D08.811.913.696.620.682.725.400.024 – receptor, fibroblast growth factor, type 1 MeSH D08.811.913.696.620.682.725.400.037 – receptor, fibroblast growth factor, type 2 MeSH D08.811.913.696.620.682.725.400.043 – receptor, fibroblast growth factor, type 3 MeSH D08.811.913.696.620.682.725.400.046 – receptor, fibroblast growth factor, type 4 MeSH D08.811.913.696.620.682.725.400.050 – proto-oncogene proteins c-kit MeSH D08.811.913.696.620.682.725.400.075 – proto-oncogene proteins c-met MeSH D08.811.913.696.620.682.725.400.087 – proto-oncogene proteins c-ret MeSH D08.811.913.696.620.682.725.400.100 – receptor, epidermal growth factor MeSH D08.811.913.696.620.682.725.400.150 – receptor, erbb-2 MeSH D08.811.913.696.620.682.725.400.175 – receptor, erbb-3 MeSH D08.811.913.696.620.682.725.400.185 – receptor, igf type 1 MeSH D08.811.913.696.620.682.725.400.200 – receptor, insulin MeSH D08.811.913.696.620.682.725.400.500 – receptor, macrophage colony-stimulating factor MeSH D08.811.913.696.620.682.725.400.660 – receptor, trka MeSH D08.811.913.696.620.682.725.400.700 – receptor, trkb MeSH D08.811.913.696.620.682.725.400.800 – receptor, trkc MeSH D08.811.913.696.620.682.725.400.850 – receptors, eph family MeSH D08.811.913.696.620.682.725.400.850.050 – receptor, epha1 MeSH D08.811.913.696.620.682.725.400.850.100 – receptor, epha2 MeSH D08.811.913.696.620.682.725.400.850.150 – receptor, epha3 MeSH D08.811.913.696.620.682.725.400.850.200 – receptor, epha4 MeSH D08.811.913.696.620.682.725.400.850.250 – receptor, epha5 MeSH D08.811.913.696.620.682.725.400.850.300 – receptor, epha6 MeSH D08.811.913.696.620.682.725.400.850.400 – receptor, epha7 MeSH D08.811.913.696.620.682.725.400.850.500 – receptor, epha8 MeSH D08.811.913.696.620.682.725.400.850.600 – receptor, ephb1 MeSH D08.811.913.696.620.682.725.400.850.650 – receptor, ephb2 MeSH D08.811.913.696.620.682.725.400.850.700 – receptor, ephb3 MeSH D08.811.913.696.620.682.725.400.850.750 – receptor, ephb4 MeSH D08.811.913.696.620.682.725.400.850.800 – receptor, ephb5 MeSH D08.811.913.696.620.682.725.400.900 – receptors, platelet-derived growth factor MeSH D08.811.913.696.620.682.725.400.900.500 – receptor, platelet-derived growth factor alpha MeSH D08.811.913.696.620.682.725.400.900.750 – receptor, platelet-derived growth factor beta MeSH D08.811.913.696.620.682.725.400.925 – receptors, tie MeSH D08.811.913.696.620.682.725.400.925.249 – receptor, tie-1 MeSH D08.811.913.696.620.682.725.400.925.500 – receptor, tie-2 MeSH D08.811.913.696.620.682.725.400.950 – receptors, vascular endothelial growth factor MeSH D08.811.913.696.620.682.725.400.950.100 – vascular endothelial growth factor receptor-1 MeSH D08.811.913.696.620.682.725.400.950.200 – vascular endothelial growth factor receptor 2 MeSH D08.811.913.696.620.682.725.400.950.300 – vascular endothelial growth factor receptor-3 MeSH D08.811.913.696.620.682.725.500 – proto-oncogene proteins c-abl MeSH D08.811.913.696.620.682.725.800 – src-family kinases MeSH D08.811.913.696.620.682.725.800.315 – lymphocyte specific protein tyrosine kinase p56(lck) MeSH D08.811.913.696.620.682.725.800.472 – oncogene protein pp60(v-src) MeSH D08.811.913.696.620.682.725.800.551 – proto-oncogene proteins c-fyn MeSH D08.811.913.696.620.682.725.800.590 – proto-oncogene proteins c-hck MeSH D08.811.913.696.620.682.725.800.610 – proto-oncogene proteins c-yes MeSH D08.811.913.696.620.682.725.800.630 – proto-oncogene proteins pp60(c-src) MeSH D08.811.913.696.620.682.725.900 – zap-70 protein-tyrosine kinase MeSH D08.811.913.696.620.685 – pyridoxal kinase MeSH D08.811.913.696.620.695 – pyruvate kinase MeSH D08.811.913.696.620.750 – thymidine kinase MeSH D08.811.913.696.620.800 – uridine kinase MeSH D08.811.913.696.630 – phosphotransferases (carboxyl group acceptor) MeSH D08.811.913.696.630.025 – acetate kinase MeSH D08.811.913.696.630.050 – aspartate kinase MeSH D08.811.913.696.630.050.050 – aspartokinase homoserine dehydrogenase MeSH D08.811.913.696.630.700 – phosphoglycerate kinase MeSH D08.811.913.696.640 – phosphotransferases (nitrogenous group acceptor) MeSH D08.811.913.696.640.025 – arginine kinase MeSH D08.811.913.696.640.150 – creatine kinase MeSH D08.811.913.696.640.150.500 – creatine kinase, bb form MeSH D08.811.913.696.640.150.625 – creatine kinase, mb form MeSH D08.811.913.696.640.150.750 – creatine kinase, mitochondrial form MeSH D08.811.913.696.640.150.875 – creatine kinase, mm form MeSH D08.811.913.696.645 – phosphotransferases (paired acceptors) MeSH D08.811.913.696.645.700 – pyruvate, orthophosphate dikinase MeSH D08.811.913.696.650 – phosphotransferases (phosphate group acceptor) MeSH D08.811.913.696.650.025 – adenylate kinase MeSH D08.811.913.696.650.150 – atp synthetase complexes MeSH D08.811.913.696.650.150.500 – proton-translocating atpases MeSH D08.811.913.696.650.150.500.249 – bacterial proton-translocating atpases MeSH D08.811.913.696.650.150.500.500 – chloroplast proton-translocating atpases MeSH D08.811.913.696.650.150.500.750 – mitochondrial proton-translocating atpases MeSH D08.811.913.696.650.150.500.875 – vacuolar proton-translocating atpases MeSH D08.811.913.696.650.450 – guanylate kinase MeSH D08.811.913.696.650.550 – nucleoside-diphosphate kinase MeSH D08.811.913.696.650.575 – nucleoside-phosphate kinase MeSH D08.811.913.696.900 – transferases (other substituted phosphate groups) MeSH D08.811.913.696.900.074 – CDP-diacylglycerol—inositol 3-phosphatidyltransferase MeSH D08.811.913.696.900.150 – CDP-diacylglycerol—serine O-phosphatidyltransferase MeSH D08.811.913.696.900.200 – diacylglycerol cholinephosphotransferase MeSH D08.811.913.696.900.250 – ethanolaminephosphotransferase
Stoolmiller AC, Horwitz AL, Dorfman A (1972). "Biosynthesis of the chondroitin sulfate proteoglycan. Purification and properties of xylosyltransferase". J. Biol. Chem. 247 (11): 3525–32. doi:10.1016/S0021-9258(19)45172-7. PMID 5030630. Gotting C, Kuhn J, Zahn R, Brinkmann T, Kleesiek K (2000). "Molecular cloning and expression of human UDP-d-Xylose:proteoglycan core protein beta-d-xylosyltransferase and its first isoform XT-II". J. Mol. Biol. 304 (4): 517–28. doi:10.1006/jmbi.2000.4261. PMID 11099377.
Sources: en.wikipedia.org
It acts on the growth hormone–releasing hormone receptor, a Gs-coupled receptor found on pituitary somatotroph cells. Activation raises cAMP and prompts pulsatile hormone release.
IGF-1 reflects growth hormone activity but changes slowly and can be measured from one sample. Growth hormone itself is pulsatile, which makes single measurements hard to interpret.
The receptor pathway is well described, but how individual responses vary and what governs long-term outcomes remain open questions. Reported differences across studies are often attributed to assay and population factors.
It is a laboratory-made peptide that mimics growth hormone-releasing hormone. It prompts the pituitary gland to release growth hormone and has been studied mainly in adults with HIV-associated lipodystrophy.