Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Somatomedins are polypeptide hormones (MW: 7500 Daltons) whose plasma concentrations are largely governed by growth hormone secretion. Somatomedins stimulate cartilage growth and mitosis and growth of several extraskeletal cell types. Somatomedins also display insulin-like activity in adipose tissue. Presently four different human somatomedins are known. Somatomedin C (SmC) and insulin like growth factor I (IGF I) turned out to be identical peptides. TO a large extent they are regulated by growth hormone. Thus they mediate growth hormone action at the tissue level. Insulin-like growth factor II (IGF II) is only minimally dependent on growth hormone secretion. Its definite biological role for growth remains to be established. The somatomedins are bound to larger carrier proteins in the circulation. Somatomedins are synthesized in mesenchymal cells of multiple organs, especially in the liver and kidneys. Somatomedins are of clinical relevance for the diagnosis of growth disturbances due to pituitary disorders. In pituitary dwarfism radioimmunological SmC/IGF plasma levels are decreased whereas in acromegaly they are increased. In a small percentage of patients both with pituitary dwarfism and acromegaly normal SmC/IGF I concentrations are encountered. These facts demonstrate that SmC/IGF I determinations cannot replace common diagnostic procedures in the analysis of growth disorders. The reliability of low SmC/IGF I concentrations is limited in conditions like low-calorie malnutrition, malabsorption, various storage diseases, hypothyroidism, chronic liver and kidney diseases, because in these disorders low SmC/IGF I plasma concentrations occur despite high growth hormone levels.
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PMID:[Somatomedins and their significance in pediatrics]. 390 54

Insulin-like growth factors [IGF I and II or somatomedins (SMS)] are polypeptides chemically and biologically correlated with insulin. The main source of synthetic activity and secretion is the liver, although many other tissues have been demonstrated to synthesize SMS. In the circulation, they are not present in a free form, but are mostly bound to a specific carrier protein independently synthesized in the liver. Hepatic or extrahepatic storage organs have not been demonstrated; the half life of the SMS-binding protein complex is between 3 and 4. Synthesis of SMS is regulated by GH, insulin, thyroxine and nutrition (caloric and protein intake, and nitrogen balance). The role of corticosteroids is still a matter of debate: in patients treated with steroids SMS blood levels have been shown to be within normal limits, while biological activity has been demonstrated to be significantly reduced by SMS inhibitors, probably induced by corticosteroid therapy. The biological properties of SMS are related to their structural homology with insulin, and can be summarized as follows: A. Insulin-like activity (glucose oxidation, lipogenesis, glycogen synthesis, inhibition of lipolysis and glycogenolysis); B. Sulphation activity (incorporation of sulphate and leucine into glycosaminglycans of the cartilage); C. Stimulation of fibroblast multiplication; D. Amplification of other hormone activities (GH); E. Complementary anabolic activity with insulin. Low levels of SMS have been demonstrated in hypopituitarism (secondary) or in other diseases independent of GH reduced secretion (primary) such as malnutrition, malabsorption, acute or chronic liver failure and uraemia. Negative nitrogen balance, hypocaloric and/or low protein diets are usually correlated with low levels of SMS. Recently, Schalch et al. reported on the role of orthotopic liver transplantation (OLT) in normalizing SMS blood levels in a group of end-stage liver diseased patients. This preliminary paper deals with changes in IGF-I plasma levels (somatomedin C) in a group of patients affected by end-stage liver cirrhosis before and after OLT.
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PMID:Somatomedin C (IGF I) plasma levels after orthotopic liver transplantation (OLT) in end-stage cirrhotic patients. 1462 70