title: [Receptor dysfunction as a pathogenetic principle in hormone resistance and metabolic diseases].
abstract: The characterisation of receptor sites of hormones to various tissues in vivo and in vitro have introduced new insights for the evaluation of pathogenic mechanisms involved in endocrine and metabolic human diseases. Disorders at the receptor level are characterized by changes in the number of receptor sites, the affinity of the hormone to its specific receptors or by generation of anti-receptor antibodies, which impair hormone binding procedures or post-receptor metabolism. Altered receptor physiology may be of an important value as well for diagnosis and treatment of endocrine, metabolic and neoplastic diseases as for the understanding of their pathogenetic mechanisms.
mesh_terms: D000052:Acanthosis Nigricans / Q000150:complications; D000255:Adenosine Triphosphate / Q000378:metabolism; D000262:Adenylyl Cyclases / Q000378:metabolism; D000906:Antibodies; D001667:Binding, Competitive; D000242:Cyclic AMP / Q000096:biosynthesis; D048909:Diabetes Complications; D004700:Endocrine System Diseases / Q000209:etiology*; D004789:Enzyme Activation; D006111:Graves Disease / Q000276:immunology; D006160:Guanosine Triphosphate / Q000378:metabolism; D006801:Humans; D006937:Hypercholesterolemia; D007328:Insulin / Q000032:analysis; D007333:Insulin Resistance; D008077:Lipoproteins, LDL / Q000378:metabolism; D008659:Metabolic Diseases / Q000209:etiology*; D009157:Myasthenia Gravis / Q000276:immunology; D009765:Obesity / Q000503:physiopathology; D011944:Receptors, Androgen / Q000502:physiology; D011956:Receptors, Cell Surface / Q000502:physiology*; D017981:Receptors, Neurotransmitter / Q000276:immunology
chemical_list: D000906:Antibodies; D007328:Insulin; D008077:Lipoproteins, LDL; D011944:Receptors, Androgen; D011956:Receptors, Cell Surface; D017981:Receptors, Neurotransmitter; D006160:Guanosine Triphosphate; D000255:Adenosine Triphosphate; D000242:Cyclic AMP; D000262:Adenylyl Cyclases
vernacular_title: Rezeptordysfunktion als pathogenetisches Prinzip bei Hormonresistenz und Stoffwechselerkrankungen.