Nutrition and Metabolic Adaptations in Physiological and Complicated Pregnancy: Focus on Obesity and Gestational Diabetes

Abstract

Pregnancy offers a window of opportunity to program the future health of both mothers and offspring. During gestation, women experience a series of physical and metabolic modifications and adaptations, which aim to protect the fetus development and are closely related to both pre-gestational nutritional status and gestational weight gain. Moreover, pre-gestational obesity represents a challenge of treatment, and nowadays there are new evidence as regard its management, especially the adequate weight gain. Recent evidence has highlighted the determinant role of nutritional status and maternal diet on both pregnancy outcomes and long-term risk of chronic diseases, through a transgenerational flow, conceptualized by the Development Origin of Health and Diseases (Dohad) theory. In this review we will analyse the physiological and endocrine adaptation in pregnancy, and the metabolic complications, thus the focal points for nutritional and therapeutic strategies that we must early implement, virtually before conception, to safeguard the health of both mother and progeny. We will summarize the current nutritional recommendations and the use of nutraceuticals in pregnancy, with a focus on the management of pregnancy complicated by obesity and hyperglycemia, assessing the most recent evidence about the effects of ante-natal nutrition on the long-term, on either maternal health or metabolic risk of the offspring.

Keywords: body composition; diet; fetal development; gestational diabetes; obesity; pregnancy.

Figure 1

The Placenta is an endocrine organ which produces several metabolic proteins (Leptin, Adiponectin, Ghrelin), peptide hormones (hPL, PGH, CRH), steroid hormones (Progesterone, Estrogens), and cytokines (TNFα, IL-6) which have significant influence on establishing and maintaining a healthy pregnancy, regulating glucose and lipid metabolism and their adaptation throughout pregnancy. IRS-1, insulin receptor substrate 1; GDM, Gestational Diabetes; TNF-α, Tumor Necrosis Factor α; WAT, white adipose tissue.

Figure 2

Maternal obesity, excessive GWG and GDM may be associated with a state of low-grade chronic inflammation that configure a metabolic condition (Gestational Diabesity) sharing a common pathogenetic substrate: the loss of balance between the physiological pro- and anti-inflammatory responses of pregnancy and an enhanced pro-inflammatory response. Increased levels of leptin and TNF- α, a state of hypoxia, abnormal oxidative stress, vascular maladaptation and enhanced ROS generation result in insulin resistance in the feto-placental vasculature, with reduced levels of adiponectin and IL-10 and increasing NO bioavailability. At the systemic level, there is a de-regulation of the immune system, with reduction of Treg cells and their tolerogentic activity of immune-suppression. hPL, Human Placental Lactogen; TNFα, Tumor Necrosis Factor α; FFA, Free Fatty Acids; IL-6, Interleukin 6; IL-10-Interleukin-10; ROS, Reactive oxygen species.