It was hypothesized that maternal GDM increases cord blood concentrations of glucose, insulin and leptin, but decreases concentrations of adiponectin; and that treatment of GDM with maternal dietary advice, blood glucose monitoring and insulin therapy if required, would partially prevent these consequences for the newborn baby.
Babies of women with mild GDM in both Treatment and the Routine Care group exhibited reduced cord blood concentrations of adiponectin compared with those in the Control Group, when the analysis was adjusted for parity, smoking, gestational age at birth, fetal sex, birth weight, and maternal body mass, as previously described in babies born to diabetic women [27]. This has not been examined previously in GDM. Increased adiposity in these babies reduces circulating adiponectin as in the adult [10, 15], possibly as a result of increasing adipocyte size, maturation and aging [28, 29]. Stress-related hormones and cytokines, such as glucocorticoids, catecholamines and TNF-α can inhibit adiponectin production however [30], and could be increased if these babies have a higher metabolic rate and oxygen deficit chronically in utero or during labor.
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Adaptations to an altered environment during intrauterine development such as that induced by gestational diabetes during pregnancy, may lead to permanent changes in the makeup of the human body [35]. Previous studies [3, 6, 36] have shown that infants of women with GDM have an increased risk of adolescent obesity and glucose intolerance. A recent study reported that fasting plasma adiponectin concentrations in adults could predict subsequent changes in insulin sensitivity over several years [37]. A recent study reported lower concentrations of adiponectin in young adults who had been born small for gestational age [38]. Since low and high birth weight are factors predisposing to gestational diabetes and type 2 diabetes in adult life [39], it will be important to determine if the partially normalized adiponectin-leptin ratio in cord blood is associated with improved insulin sensitivity or glucose tolerance later in life in these children. The decreased cord blood adiponectin may be predictive of insulin resistance in infancy and possibly childhood, increasing the risk of developing related disorders.
The high prevalence of 15% for GDM in this study is consistent with previous reports from Saudi Arabia [8, 9] and is not surprising considering the high prevalence of obesity among the obstetric population reported in this study. Our results pointed to modest effect of GDM on macrosomia compared to maternal obesity, these findings are consistent with the findings of Ricard et al. [18]. The pathophysiology of macrosomia in women with GDM is based on Pedersen hypothesis [26] of maternal hyperglycemia leading to fetal hyperinsulinemia and increased utilization of glucose and hence increased fetal adipose tissue. The hypothesis was further supported by the finding of high insulin levels in the cord blood of babies born to diabetic mothers [27]; however good control of blood glucose did not completely prevent the increase in macrosomia noticed in women with diabetes [28], which suggests a role for other mediators that might share a common pathway with obesity .
Low birth weight is associated with increased rates of obesity, insulin resistance and type 2 diabetes [1], which are components of the metabolic syndrome [2]. Albeit the precise mechanisms for this association remain unclear, metabolic changes that could be related to alterations in body composition can be found already in childhood [3]. For instance, people with low birth weight present with higher plasma leptin concentrations than would be expected from their degree of obesity [4, 5]. In children born with a low birth weight, leptin levels are increased after catch-up growth during childhood [6], but it is unclear what happens during later life. Further, it has been suggested that blood cord adiponectin levels are positively related with birth weight and BMI in newborns [7], with a subsequent increase in the risk of type 2 diabetes [8]; still, this statement has also been challenged [9]. Overall, whether leptin and adiponectin mediate the effects of low birth weight on obesity, insulin resistance and type 2 diabetes is unclear. 2ff7e9595c
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