Hi, I’m Ghrelin peptide!

My name is Ghrelin peptide. My MW is 3314.8 Da. My formula is C147H245N45O42 and I was reacting with rat. My tested applications are ESI-MS and HPLC.  So, you may feel free to use me. My purity is greater than 98% purified which is mean I’m very pure. However, I need to be stored aliquot and store at-20°C. Avoid repeated freeze/thaw cycles. To tell you a secret, my sequence is

Gly-Ser-[Ser(n-octanoyl)]-Phe-Leu-Ser-Pro-Glu-His-Gln-Lys-Ala-Gln-Gln-Arg-Lys-Glu-Ser-Lys-Lys-Pro-Pro-Ala-Lys-Leu-Gln-Pro-Arg. My target is Ghrelin who is my best partner. That’s me. I’m Ghrelin peptide!

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Do you know what is Ghrelin?

Ghrelin is a hormone produced mainly by P/D1 cells lining the fundus of the human stomach and epsilon cells of the pancreas that stimulates hunger. Ghrelin levels increase before meals and decrease after meals. It is considered the counterpart of the hormone leptin, produced by adipose tissue, which induces satiation when present at higher levels. In some bariatric procedures, the level of ghrelin is reduced in patients, thus causing satiation before it would normally occur.

Do you know how Ghrelin generated?

Ghrelin is also produced in the hypothalamic arcuate nucleus, where it stimulates the secretion of growth hormone from the anterior pituitary gland. Receptors for ghrelin are expressed by neurons in the arcuate nucleus and the lateral hypothalamus. The ghrelin receptor is a G protein-coupled receptor, formerly known as the GHS receptor (growth hormone secretagogue receptor).

Do you know what’s the function of Ghrelin?

Ghrelin plays a significant role in neurotrophy, particularly in the hippocampus, and is essential for cognitive adaptation to changing environments and the process of learning. Recently, ghrelin has been shown to activate the endothelial isoform of nitric oxide synthase in a pathway that depends on various kinases including Akt.

Do you know how the Ghrelin come into effect?

Small synthetic molecules called growth-hormone secretagogues (GHSs) stimulate the release of growth hormone (GH) from the pituitary. They act through GHS-R, a G-protein-coupled receptor for which the ligand is unknown. Recent cloning of GHS-R strongly suggests that an endogenous ligand for the receptor does exist and that there is a mechanism for regulating GH release that is distinct from its regulation by hypothalamic growth-hormone-releasing hormone (GHRH). We now report the purification and identification in rat stomach of an endogenous ligand specific for GHS-R. The purified ligand is a peptide of 28 amino acids, in which the serine 3 residue is n-octanoylated. The acylated peptide specifically releases GH both in vivoand in vitro, and O-n-octanoylation at serine 3 is essential for the activity. We designate the GH-releasing peptide ‘ghrelin’ (ghre is the Proto-Indo-European root of the word ‘grow’). Human ghrelin is homologous to rat ghrelin apart from two amino acids. The occurrence of ghrelin in both rat and human indicates that GH release from the pituitary may be regulated not only by hypothalamic GHRH, but also by ghrelin.

Ghrelin receptors and diseases

Diabetic encephalopathy (DE) is a major central nervous system complication of diabetes mellitus, manifested as acquired cognitive dysfunction and physiological changes of brain disease, resulting in the complete loss of cognitive ability and self-care ability. DE and prognosis are not only affected by the overall blood sugar level, but also closely related to the fluctuation of blood glucose. In vitro, experiments have also shown that glucose levels with fluctuations in extracellular are more harmful to cells than sustained high glucose levels. Besides, the abnormal changes of hippocampal structure and function are the direct cause of DE, and the fluctuation of blood glucose is more obvious as a kind of stimulation signal, which is an independent damage of hippocampal neurons. Studies show that persistent hyperglycemia and diabetic blood glucose fluctuations all cause cognitive dysfunction in rats, and the disorder caused by blood glucose fluctuation is more serious, which is closely related to the expression of ghrelin and GHSR1a in rat's hippocampus. Therefore, the changes of ghrelin and GHSR1a play an important role in the process of speeding up the incidence of blood glucose fluctuation.