Altered plasma levels of nerve growth factor and transforming growth factor-beta 2 in type-1 diabetes mellitus

Citation
St. Azar et al., Altered plasma levels of nerve growth factor and transforming growth factor-beta 2 in type-1 diabetes mellitus, BRAIN BEH, 13(4), 1999, pp. 361-366
Citations number
27
Categorie Soggetti
Neurosciences & Behavoir
Journal title
BRAIN BEHAVIOR AND IMMUNITY
ISSN journal
08891591 → ACNP
Volume
13
Issue
4
Year of publication
1999
Pages
361 - 366
Database
ISI
SICI code
0889-1591(199912)13:4<361:APLONG>2.0.ZU;2-P
Abstract
Nerve growth factor (NGF) and transforming growth factor-beta 2 (TGF-beta 2 ) are cytokines which have known immunological effects. An elevated level o f NGF has been repel-red in certain autoimmune diseases, whereas TGF-beta 2 is an immunosuppressor which is known to play a role in regulating cell pr oliferation. A role of this cytokine has been proposed in the pathogenesis of type-1 diabetes mellitus (IDDM), but no clinical studies have yet measur ed its serum level in this disease. In this study we measured the levels of NGF and TGF-beta 2 in the sera of patients with IDDM (n = 26) and values w ere compared:to those of age-matched normal subjects (n = 27) and also to p atients with type-2 diabetes mellitus (NIDDM) (n = 26) with similar HbA1c l evels and an equal duration of diabetes. Serum NGF levels were significantl y elevated in IDDM patients compared to those of age-matched controls (p <. 001) and NIDDM controls (p <.01). TGF-beta 2 levels were lower in IDDM pati ents when compared with the healthy control (p < .001) and the NIDDM contro l (p <.05), Then was no correlation between the levels of NGF and TGF-beta 2. Thc;duration of diabetes and the level of HbA1c did net affect the NGF a nd TGF-beta 2 levels in the IDDM patients. We conclude that an increase in NGF and a suppression in TGF-beta 2 levels are present in patients with typ e-1 diabetes mellitus and that both cytokines may play independent roles in the pathogenesis of this disease. (C) 1999 Academic Press.