Abstract
Epidemiological studies have linked intrauterine growth retardation (IUGR) to the metabolic diseases, consisting of insulin resistance, type 2 diabetes, obesity and coronary artery disease, during adult life. To determine the internal relationship between IUGR and islet β cell function and insulin sensitivity, we established the IUGR model by maternal nutrition restriction during mid- to late-gestation. Glucose tolerance test and insulin tolerance test(ITT) in vivo and glucose stimulated insulin secretion(GSIS) test in vitro were performed at different stages in IUGR and normal groups. Body weight, pancreas weight and pancreas/body weight of IUGR rats were much lower than those in normal group before 3 weeks of age. While the growth of IUGR rats accelerated after 3 weeks, pancreas weight and pancreas/body weight remained lower till 15 weeks of age. In the newborns, the fasting glucose and insulin levels of IUGR rats were both lower than those of controls, whereas glucose levels at 120 and 180 min after glucose load were significantly higher in IUGR group. Between 3 and 15 weeks of age, both the fasting glucose and insulin levels were elevated and the glucose tolerance was impaired with time in IUGR rats. At age 15 weeks, the area under curve of insulin(AUCi) after glucose load in IUGR rats elevated markedly. Meanwhile, the stimulating index of islets in IUGR group during GSIS test at age 15 weeks was significantly lower than that of controls. ITT showed no significant difference in two groups before 7 weeks of age. However, in 15-week-old IUGR rats, there was a markedly blunted glycemic response to insulin load compared with normal group. These findings demonstrate that IUGR rats had both impaired pancreatic development and deteriorated glucose tolerance and insulin sensitivity, which would be the internal causes why they were prone to develop type 2 diabetes.
Highlights
Intrauterine growth retardation (IUGR), as the most common cause of poor fetal growth, is a common complication of pregnancy with incidence of 6.39% in China
The effects exerted by suboptimal fetal environments due to inadequate nutrition, infection, gestational diabetes, smoking or hypoxia in the mother on various systems in the offspring persist into adulthood and make the individual predisposed to metabolic diseases including insulin resistance/ type 2 diabetes, hypertension, obesity, coronary artery disease, cancer and so on in the later stages of life [7,8,9,10,11,12]
While the growth of IUGR rats accelerated after 3 weeks of age and the body weight of IUGR rats even surpassed that of control at 15 weeks, pancreas weight and pancreas weight /body weight remained lower till 15 weeks of age(P,0.05)
Summary
Intrauterine growth retardation (IUGR), as the most common cause of poor fetal growth, is a common complication of pregnancy with incidence of 6.39% in China. The effects exerted by suboptimal fetal environments due to inadequate nutrition, infection, gestational diabetes, smoking or hypoxia in the mother on various systems in the offspring persist into adulthood and make the individual predisposed to metabolic diseases including insulin resistance/ type 2 diabetes, hypertension, obesity, coronary artery disease, cancer and so on in the later stages of life [7,8,9,10,11,12]. In the few cases which had been investigated morphologically there was evidence of a reduced pancreatic b cell mass [20] This suggested impaired functional development of islet b cell in growth-retarded fetuses. This study was undertaken to investigate the internal association between IUGR and type 2 diabetes
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