Single Amino Acids
Luke R. Bucci in Nutrition Applied to Injury Rehabilitation and Sports Medicine, 2020
The use of large doses of single amino acids or amino acid mixtures to release somatotropin has become popular with some athletes and exercising persons. However, the available data shows that possible induction of somatotropin is only accomplished at very high doses that usually cause unwanted side effects (diarrhea or drowsiness). The chance of being a responder to oral amino acid induction of somatotropin release is up to 60%, meaning that each individual has about an even chance for high-dose single amino acids to elicit a somatotropin response. Lower doses are reproducibly useless for inducing somatotropin response, unless the findings of Isidori can be reproduced.238 Also, the long-term implications of amino acid somatotropin releasing agents is unclear. Does long-term intake of high doses of single amino acids desensitize hormone release? Does catabolism of that amino acid increase to negate the effects? Does the hormone released have physiological benefits that are maintained for long time periods? Many pertinent questions still remain to be answered before use of single amino acids as somatotropin (or other hormone)-releasing agents can be fully condoned. Therefore, at this time, the general application of single amino acids to elicit somatotropin release is impractical.
The Endocrine System and Its Disorders
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss in Understanding Medical Terms, 2020
Pituitary hypersecretion of the growth hormone somatotropin during the period of skeletal development results in giantism, an abnormal increase in the length of skeletal structures causing unusually large body size (hence the name). Acromegaly (acro = extremity, plus megaly, large), a form of gigantism that affects adults, is often caused by a pituitary tumor that produces excess growth hormone after skeletal development is normally complete. Rather than affecting skeletal length, its effects are seen as thickening of cartilage and bone with widening of the jaw, hands, feet, eyebrow ridges, and soft tissue. Conversely, hyposecretion of somatotropin results in dwarfism, the condition seen in dwarfs and midgets. Dwarfism can also result from a deficiency in thyroid hormones.
The endocrine system
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella in Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Also known as somatotropin, this is one of the few hormones that exerts its effects on organs and tissues throughout the body. Growth hormone is essential for the normal growth and development of the skeleton as well as visceral, or soft, tissues from birth until young adulthood. Growth of the skeleton involves both an increase in bone thickness and an increase in bone length. The mechanism of this growth involves the stimulation of osteoblast (bone-forming cell) activity and the proliferation of the epiphyseal cartilage in the ends of the long bones. The growth of visceral tissues occurs by hyperplasia (increasing the number of cells) and hypertrophy (increasing the size of cells). Growth hormone causes hyperplasia by stimulating cell division and by inhibiting apoptosis (programmed cell death). Growth hormone causes cellular hypertrophy by promoting protein synthesis and inhibiting protein degradation.
Octreotide and Octreotide-derived delivery systems
Published in Journal of Drug Targeting, 2023
Mingliang Fan, Yue Huang, Xinlin Zhu, Jiayu Zheng, Mingwei Du
The tetradecapeptide somatostatin is secreted by hypothalamus or delta cells in gastrointestinal tract and interacts with somatostatin receptors (SSTRs), which is a group of GPCRs (G-protein-coupled receptors) with five human receptor subtypes (SSTR 1-5). Somatostatin can inhibit the release of a series of hormones or neuropeptides in many organs, including growth hormone, insulin, glucagon, among others, thus taking important roles in many physiological functions. However, its clinical applications are remarkably restricted by poor circulation time (about 3 min) in the blood. Hence a variety of somatostatin analogs with longer circulation time have been developed for clinical use since 1970s [1]. Among them, Octreotide (SMS 201-995) is the most widely developed representative of somatostatin analog and stands the test of clinical application [2]. As a therapeutic agent and targeting ligand, Octreotide (OCT) has also been involved in the construction of many novel pharmaceutical systems for tumour targeted treatment. Given OCT-derived radionuclide therapy and radionuclide imaging were well reviewed by previous publication [3], we herein focus on the preclinical studies of some novel pharmaceutical delivery systems related to OCT, including microsphere, conjugate, liposome, polymeric nanoparticle, hydrogel and inorganic nanoparticle.
Current advances in the management of cluster headaches
Published in Expert Opinion on Pharmacotherapy, 2021
Theodoros Mavridis, Marianthi Breza, Christina Deligianni, Dimos D. Mitsikostas
Octreotide is a somatostatin analog that mimics natural somatostatin by inhibiting serotonin release, and the secretion of gastrin, VIP, insulin, glucagon, secretin, motilin, and pancreatic polypeptide. It provides more potent inhibition of growth hormone, glucagon, and insulin as compared to endogenous somatostatin. Octreotide has a level C recommendation for the acute treatment of CH [29]. Octreotide 100 mg given subcutaneously has shown effectiveness in improving headache response compared to placebo. In terms of response rate and time to initial relief, it is believed to be inferior to both subcutaneous and intranasal sumatriptan [42,43]. The adverse effects (AE) are nonserious and include injection site reactions, diarrhea, abdominal bloating, nausea, dull background headache and dizziness/somnolence [27,29].
Occurrence of Hypopituitarism in Tunisian Turner Syndrome patients: familial versus sporadic cases
Published in Gynecological Endocrinology, 2021
M. Mnif-Feki, W. Safi, N. Bougacha-Elleuch, G. Abid, M. Moalla, M. Elleuch, D. H. Ben Salah, N. Rekik, N. Belguith, F. Abdelhedi, T. Kammoun, M. Hachicha, N. Charfi, F. Mnif, H. Kammoun, H. Hadj Kacem, F. Hadj-Kacem, M. Abid
TS is known to be associated with congenital abnormalities, yet association with Hypopituitarism is an unfamiliar finding. The first case of a pituitary deficiency co-occurring with gonadal dysgenesis owing to a TS was described by Efstathiadou in 2000 [7]. At the onset, the patient was diagnosed with somatotropin, thyrotropin, and gonadotropin deficiencies. Afterward, with the ascertainment of several clinical characteristics and the absence of ovarian tissue on ultrasound, karyotype was carried out. Results revealed concrete gonadal dysgenesis secondary to TS with no evidence of mosaicism. MRI showed a hypoplastic pituitary gland and an ectopic localization of neuro-hypophysis. So far, only nine cases of TS associated with Hypopituitarism have been reported in the literature (Table 3). Three congenital cases with such an association were already reported in 2016 by our team, as described in Table 1 (cases 4, 5, and 6) [4]. Up to date, only 12 cases with Hypopituitarism associated with TS are described (half of them are reported in our series). Interestingly, the familial occurrence of this association is seen in 5 out of 12 patients.
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