1.
Adipokines underlie the early origins of obesity and associated metabolic comorbidities in the offspring of women with pregestational obesity.
Arroyo-Jousse, V, Jaramillo, A, Castaño-Moreno, E, Lépez, M, Carrasco-Negüe, K, Casanello, P
Biochimica et biophysica acta. Molecular basis of disease. 2020;(2):165558
Abstract
Maternal pregestational obesity is a well-known risk factor for offspring obesity, metabolic syndrome, cardiovascular disease and type 2 diabetes. The mechanisms by which maternal obesity can induce alterations in fetal and later neonatal metabolism are not fully elucidated due to its complexity and multifactorial causes. Two adipokines, leptin and adiponectin, are involved in fetal and postnatal growth trajectories, and both are altered in women with pregestational obesity. The placenta synthesizes leptin, which goes mainly to the maternal circulation and in lesser amount to the developing fetus. Maternal pregestational obesity and hyperleptinemia are associated with placental dysfunction and changes in nutrient transporters which directly affect fetal growth and development. By the other side, the embryo can produce its own leptin from early in development, which is associated to fetal weight and adiposity. Adiponectin, an insulin-sensitizing adipokine, is downregulated in maternal obesity. High molecular weight (HMW) adiponectin is the most abundant form and with most biological actions. In maternal obesity lower total and HMW adiponectin levels have been described in the mother, paralleled with high levels in the umbilical cord. Several studies have found that cord blood adiponectin levels are related with postnatal growth trajectories, and it has been suggested that low adiponectin levels in women with pregestational obesity enhance placental insulin sensitivity and activation of placental amino acid transport systems, supporting fetal overgrowth. The possible mechanisms by which maternal pregestational obesity, focusing in the actions of leptin and adiponectin, affects the fetal development and postnatal growth trajectories in their offspring are discussed.
2.
Glycemic profile assessment during betamethasone administration in women with gestational diabetes mellitus.
Kakoulidis, I, Ilias, I, Linardi, A, Milionis, C, Michou, A, Koukkou, E
Diabetes & metabolic syndrome. 2019;(1):214-215
Abstract
AIM: Betamethasone's effect on glucose homeostasis in the presence of gestational diabetes has not been adequately investigated. MATERIALS-METHODS We assessed the glycemic profile of 99 women with gestational diabetes (52 on insulin, 47 on medical nutrition therapy) who were given betamethasone during hospitalization for at risk pregnancies. RESULTS In insulin-treated women the increase in total daily insulin dose significantly linked to betamethasone dose (p = 0.014). In women on diet, the need for insulin was positively related to betamethasone dose, age and gestational age >34th week (all p < 0.05). CONCLUSION Parsimonious betamethasone use might still be beneficial with a milder effect on glycemia.
3.
High risk of metabolic syndrome after delivery in pregnancies complicated by gestational diabetes.
Shen, Y, Li, W, Leng, J, Zhang, S, Liu, H, Li, W, Wang, L, Tian, H, Chen, J, Qi, L, et al
Diabetes research and clinical practice. 2019;:219-226
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Abstract
AIMS: To investigate the risk of postpartum metabolic syndrome in women with GDM compared with those without GDM in a Chinese population. METHODS Tianjin GDM observational study included 1263 women with a history of GDM and 705 women without GDM. Multivariate logistic regression was used to assess risks of postpartum metabolic syndrome between women with and without GDM. Postpartum metabolic syndrome was diagnosed by two commonly used criteria. RESULTS During a mean 3.53 years of follow up, 256 cases of metabolic syndrome were identified by using the NCEP ATPIII criteria and 244 cases by using the IDF criteria. Multivariable-adjusted odds ratios of metabolic syndrome in women with GDM compared with those without GDM were 3.66 (95% confidence interval [CI] 2.02-6.63) for NCEP ATPIII criteria and 3.90 (95% CI 2.13-7.14) for IDF criteria. Women with GDM had higher multivariable-adjusted odds ratios of central obesity, hypertriglyceridemia, and high blood pressure than women without GDM. The multivariable-adjusted odds ratios of low HDL cholesterol and hyperglycemia were not significant between women with and without GDM, however, the multivariable-adjusted odds ratio of hyperglycemia became significant when we used the modified criteria. CONCLUSIONS The present study indicated that women with prior GDM had significantly higher risks for postpartum metabolic syndrome, as well as its individual components.