title: [Streptozotocin-induced maternal intrauterine hyperglycemia environment and its influence on development and metabolic in adult offspring with high birth weight in rats].
abstract: OBJECTIVE
  To establish and assess the high-birth-weight offspring model of the diabetic rat induced by stueptozotocin, and the long-term metabolic impact of maternal hyperglycemia of those offsprings.
  
  
  METHODS
  Streptozotocin (STZ, 25 mg/kg) was given to Wistar rats (G group, n = 14) once intraperitoneally to induce maternal hyperglycemia model (blood glucose between 10 - 20 mmol/L), and there still had a number of rats defined as severe hyperglycemia model group (SG group, n = 5). The Control group (C group, n = 7) were given the same volume citrate buffer solution. The body weight and blood glucose were recorded, and the lavaging glucose tolerance test (LGTT) was performed by a glucose meter in the gestation. The offsprings were corresponding allocated into 2 groups, and the birth weight were recorded. All the offsprings were observated body weight, blood glucose blood pressure (male rats only), and so on.
  
  
  RESULTS
  (1) The blood glucose of G group (16.8 ± 5.4 mmol/L) and SG group (20.5 ± 5.6 mmol/L) were increased significantly as compared with C group (7.0 ± 1.4 mmol/L) 5 days after the model was established (P < 0.01); and the average blood glucose of G group (16.6 ± 3.4 mmol/L) and SG group (23.8 ± 1.5 mmol/L) increased too as comparede with C group (5.8 ± 1.1 mmol/L), the difference was significance according to statistics (P < 0.01). (2) According to the LGTT result, which operationed on generation day 4 and day 10, the blood glucose of every time point of G group were increased significantly as compared with C group (P < 0.01). (3) The male and female birth weight of G group was remarkably higher than the C group and the SG group (P < 0.05), and the blood glucose of SG/G/C group was (6.5 ± 1.2) mmol/L, (4.1 ± 0.8) mmol/L, (4.1 ± 0.8) mmol/L respectively, according to the statistics results, the difference between SG group and G/C group respectively both remarkable (P < 0.05). (4) The body weight, Lee's index, fat weight, and the fat weight of mass ratio in C group mother rats after lactation presented dressed compared with the SG group (P < 0.05), and so as to the G group compared with the SG group (P < 0.05). (5) In the female offsprings of G group, the birth weight was remarkably increased compared with the C group (P < 0.05); the body weight of the female offsprings presented an increased trend compared with the C group since the 12 weeks, but had no statistical significance; there were significant differences of body weight between G group and C group since 15 weeks (P < 0.05), and the trend kept up until 26 weeks; in the male offsprings of G group, the body weight on birth day and 4 weeks had a marked rise compared with the C group (P < 0.05); and from then on, the body weight of the male offsprings presented an increased trend compared with the C group, but had no statistical significance until 26 weeks (P > 0.05). (6) In G group, the blood glucose on 30 min and 60 min of LGTT in female offsprings were increased than the C group since 20 weeks (P < 0.05); the blood glucose of LGTT (30 min) still had a marked rise until 24 weeks (P < 0.05); in G group, the blood glucose on 30 min of LGTT in male offsprings was remarkably increased than the C group since 16 weeks (P < 0.05) ; the blood glucose of LGTT (30 min) still had a marked rise until 24 weeks (P < 0.05). (7) The blood pressure of male offsprings in G group had a marked rise on 12 weeks compared with the C group (P < 0.05); from then on the blood pressure of G group kept up a rise trend until 26 weeks, but had no statistical significance (P > 0.05).
  
  
  CONCLUSIONS
  The diabetic high-birth-weight rat model could be duplicated with STZ (25 mg/kg) once intrapertoneally on the first day of gestation, which were observed some evidently metabolic changes in weight, glucose tolerance and blood pressure. These results could represent an forward step in the clinical study of human gestational diabetes mellitus and their macrosomia babies, which may suffer some metabolic disease in their later life.
authors.affiliation: Department of Obstetries and Gynecology, Peking University First Hospital, Beijing 100034, China.
authors.forename: Xin
authors.initials: X
authors.lastname: Li
authors.forename: Shu-jing
authors.initials: SJ
authors.lastname: Luo
authors.forename: Kai
authors.initials: K
authors.lastname: Zhang
authors.forename: Hui-xia
authors.initials: HX
authors.lastname: Yang
mesh_terms: D000818:Animals; D000831:Animals, Newborn / Q000254:growth & development; D001724:Birth Weight; D001786:Blood Glucose / Q000378:metabolism*; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000503:physiopathology*; D016640:Diabetes, Gestational / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology*; D004195:Disease Models, Animal; D005260:Female; D005951:Glucose Tolerance Test; D006943:Hyperglycemia / Q000139:chemically induced / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D013311:Streptozocin
chemical_list: D001786:Blood Glucose; D013311:Streptozocin