EARLY NEONATAL EVENTS AND THE DISEASE INCIDENCE IN NONOBESE DIABETIC MICE

Citation
G. Dahlquist et B. Kallen, EARLY NEONATAL EVENTS AND THE DISEASE INCIDENCE IN NONOBESE DIABETIC MICE, Pediatric research, 42(4), 1997, pp. 489-491
Citations number
20
Categorie Soggetti
Pediatrics
Journal title
ISSN journal
00313998
Volume
42
Issue
4
Year of publication
1997
Pages
489 - 491
Database
ISI
SICI code
0031-3998(1997)42:4<489:ENEATD>2.0.ZU;2-V
Abstract
Epidemiologic studies have shown that perinatal events are associated with an increased risk for type 1 (insulin-dependent) diabetes in chil dhood. We used nonobese diabetic mice to examine whether neonatal sepa ration from the mother with or without phototherapy would affect the i ncidence of diabetes in this genetically susceptible mouse model. The newborn pups were taken from their mothers for two 4-h periods during each of five successive days. One group of animals was just taken from their mothers and were left lying in daylight in the cage, whereas an other group was exposed to identical light as used for treatment of ne onatal jaundice in infants. Treatment resulted in a 30% death rate, Fo r animals surviving more than 3 mo the incidence of diabetes was signi ficantly higher in both treatment groups compared with control animals , allowed to stay with their mother. The odds ratio for treatment vers us control, stratifying for sex, Tvas 3.42 (95% confidence interval, 1 .57-7.74). Histologic insulitis did not differ between treated and unt reated animals when examined either at clinical diabetes onset or at 8 mo of age. Blood glucose values at 8 mo of age (in animals without cl inical diabetes) did not differ between treated and untreated animals. It is concluded that neonatal separation of the nonobese diabetic mic e from their mothers will lead to a significantly increased risk for d iabetes. This increase in risk seems to be associated with the inducti on of metabolic alterations leading to increased peripheral insulin ne ed rather than with an increased rate of beta cell destruction.