Melanocyte stimulating hormone releasing factor

The C-terminal tripeptide tail of oxytocin H-L-Pro-Leu-Gly-NH2 (melanocyte-stimulating hormone release inhibiting factor, MIF or melanostatin) is implicated as having a direct effect on the central nervous system. The ALeu analogue of melanostatin, [ALeu2-MIF] was prepared in view of the earlier work on the active conformation of melanostatin in which a (3-turn was implicated.11771 ALeu was prepared by the N-chlorination/dehydrochlorination reaction and then coupled with Boc-Pro-OH. 

A large number of 13C NMR studies on proline derivatives and proline peptides have appeared in the literature [815-830]. As the electron charge density of cis-proline carbons is different from that of franx-prolinc carbons, these isomers can be differentiated by nCNMR spectroscopy [826, 830]. On the basis of calculations Tonelli [831] predicted four conformations for the dipeptide Boc-Pro-Pro-OBzl, three of which could be detected by 13C NMR spectroscopy [826, 830], In proline-containing peptides the stereochemistry of the proline residue plays an important role for the conformation of these oligomers. The 13C chemical shift data of cis and trans proline derivatives, collected in Table 5.29, are useful to determine the stereochemistry of the amino acid-proline bond, e.g. in cyclo-(Pro-Gly)3, melanocyte-stimulating hormone release-inhibiting factor or thyrotropin-releasing hormone. 

A. Hyperpigmentation is a feature of Addison disease, the diagnosis in this case. Decreased plasma cortisol because of adrenal insufficiency releases feedback inhibition of ACTH secretion by the pituitary, resulting in elevation of ACTH biosynthesis. The ACTH precursor peptide is cleaved to also yield melanocyte-stimulating hormone, the factor responsible for hyperpigmentation even in areas not exposed to sunlight. 

The effects of melanocyte-stimulating hormone release inhibiting factor and synthetic analogs on tolerance to and physical dependence on morphine... 

Nemifitide is a peptide analogue of melanocyte-stimulating hormone release-inhibiting factor currently in clinical development for the potential treatment of moderate to severely depressed patients (93). It is rapidly absorbed, with a peak plasma concentration of 10 min and an elimination half-life of 15 to 30 minutes in most subjects. The pharmacokinetic results indicate that the dose is proportional in the dose range investigated. 

Melanocyte-stimulating-hormone release-inhibiting factor (MSH-RIF) and relea g factor (MSH-RF) 195... 

MELANOCYTE-STIMULATING-HORMONE RELEASE-INHIBITING FACTOR (MSH-RIF) AND RELEASING FACTOR (MSH-RF)... 

Karanath S, Lyson K, Aguila MC, McCann SM. Effects of lutenizing-hormone-releasing hormone, alpha-melanocyte-stimulating hormone, naloxon, dexamethasone and indomethacin on interleukin-2-induced corticotropin-releasing factor release. Neuroimmunomodulation 1995 2(3) 166-173. 

Studies have shown that, in addition to the conventional peptide hormones of pancreatic islets (insulin, glucagon, somatostatin, and pancreatic polypeptide), these tumors can also secrete (and express) ectopic peptides, in particular gastrin and VIP (vasoactive intestinal peptide),but on occasion also ACTH (adrenal corticotropic hormone),antidiuretic hormone (ADH), MSH (melanocyte-stimulating hormone), calcitonin, neurotensin, secretoneurin, 754-356 PTH (parathyroid hormone-like peptide),growth hormone and growth hormone releasing factor, secretogranin inhibin/activin, i prohormone... 

Melanocyte inhibitory factor (MIF) which inhibits melanocyte stimulating hormone (MSH) release. 

Otfier fiormones accelerate tfie release of free fatty acids from adipose tissue and raise tfie plasma free fatty acid concentration by increasing the rate of lipolysis of the triacylglycerol stores (Figure 25—8). These include epinephrine, norepinephrine, glucagon, adrenocorticotropic hormone (ACTH), a- and P-melanocyte-stimulat-ing hormones (MSH), thyroid-stimulating hormone (TSH), growth hormone (GH), and vasopressin. Many of these activate the hormone-sensitive hpase. For an optimal effect, most of these lipolytic processes require the presence of glucocorticoids and thyroid hormones. These hormones act in a facilitatory or permissive capacity with respect to other lipolytic endocrine factors. 

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