title: Streptozotocin-induced diabetes is associated with changes in NGF levels in pancreas and brain.
abstract: Type 1 diabetes mellitus (DM), a "classical" result of a pancreatic-beta cell damage, is associated with various metabolic, neuronal, endocrine and immune alterations at cellular, tissue and organ levels. Nerve growth factor (NGF) is one of the most extensively studied neurotrophic factors, which is produced and released by numerous cells including the pancreatic beta cells. NGF plays an important role during brain development and may be able to delay or even reverse damaged forebrain cholinergic neurons that undergo degeneration in aged animals and in Alzheimer's disease (AD). Recent reports indicate that experimentally induced DM in rodents can cause brain biochemical and molecular alterations similar to those observed in sporadic AD. Given the importance of NGF in the pathophysiology of brain cholinergic neurons, we looked for NGF changes in the pancreas and brain of diabetic rats. The aim of this study was, therefore, to investigate the effect of streptozotocin-induced DM on NGF and NGF receptor expression in pancreas and brain. The results showed that DM is associated with altered NGF, NGF-receptor expression in both pancreas and brain.
authors.affiliation: Institute of Neurobiology and Molecular Medicine, NGF Section, CNR, Rome, Italy.
authors.forename: V
authors.initials: V
authors.lastname: Sposato
authors.forename: L
authors.initials: L
authors.lastname: Manni
authors.forename: G N
authors.initials: GN
authors.lastname: Chaldakov
authors.forename: L
authors.initials: L
authors.lastname: Aloe
mesh_terms: D000818:Animals; D000903:Antibiotics, Antineoplastic; D001786:Blood Glucose / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D002536:Cerebral Arteries / Q000187:drug effects / Q000378:metabolism; D019610:Cytoprotection / Q000187:drug effects; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000187:drug effects; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects / Q000378:metabolism; D007150:Immunohistochemistry; D007515:Islets of Langerhans / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D020932:Nerve Growth Factor / Q000378:metabolism*; D009419:Nerve Tissue Proteins; D010179:Pancreas / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D020917:Receptor, trkA / Q000378:metabolism; D017978:Receptors, Growth Factor; D017475:Receptors, Nerve Growth Factor / Q000378:metabolism; D013311:Streptozocin; D015854:Up-Regulation / Q000187:drug effects; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D000903:Antibiotics, Antineoplastic; D001786:Blood Glucose; D009419:Nerve Tissue Proteins; D017978:Receptors, Growth Factor; D017475:Receptors, Nerve Growth Factor; D042461:Vascular Endothelial Growth Factor A; C068313:Ngfr protein, rat; D013311:Streptozocin; D020932:Nerve Growth Factor; D020917:Receptor, trkA