Intrauterine Growth Restriction: Hungry for an Answer

Abstract

Intrauterine growth restriction (IUGR) has been defined in several ways, but in general describes a condition in which the fetus exhibits poor growth in utero. This complication of pregnancy poses a significant public health burden as well as increased morbidity and mortality for the offspring. In human IUGR, alteration in fetal glucose and insulin homeostasis occurs in an effort to conserve energy and survive at the expense of fetal growth in an environment of inadequate nutrient provision. Several animal models of IUGR have been utilized to study the effects of IUGR on fetal glucose handling, as well as the postnatal reprogramming of energy metabolite handling, which may be unmasked in adulthood as a maladaptive propensity for cardiometabolic disease. This developmental programming may be mediated in part by epigenetic modification of essential regulators of glucose homeostasis. Several pharmacological therapies and nonpharmacological lifestyle modifications have shown early promise in mitigating the risk for or severity of adult metabolic phenotypes but still require further study of unanticipated and/or untoward side effects.

The impact of IUGR on pancreatic islet development and β-cell function

“…Current reviews suggest maternal or neonatal nutrient supplementation has little impact in mitigating IUGR in humans (Brown et al 2011; Devaskar and Chu 2016; Hay 2008). Furthermore, most nutritional interventions are associated with increased adiposity and not increased linear growth.…”

Placental‐Specific Overexpression of sFlt‐1 Alters Trophoblast Differentiation and Nutrient Transporter Expression in an IUGR Mouse Model

“…Intrauterine growth restriction (IUGR) is characterized by insufficient growth of the fetus during pregnancy, resulting from an adverse maternal environment, such as poor nutrition or reduced oxygen supply at the fetomaternal interface [Devaskar and Chu, ]. IUGR is associated with a high incidence of perinatal morbidity and mortality, short‐term and long‐term metabolic and cardiovascular alterations and neurological disorders [Zohdi et al, ; Cohen et al, ].…”

The Tubular Damage Markers: Neutrophil Gelatinase-Associated Lipocalin and Kidney Injury Molecule-1 in Newborns with Intrauterine Growth Restriction

“…It is characterized as a rate of fetal growth of less than normal for the gestational age-appropriate growth potential [1, 2]. The diagnosis of IUGR is usually assigned to infants with a birth weight < 10th percentile for gestational age and called small for gestational age (SGA) [3].…”

“…A number of autopsy studies have reported a significant reduction in nephron numbers as a result of IUGR [1, 10]. The linear relationship was reported between the number of glomeruli (and therefore nephrons) and birth weight in full-term neonates; neonates < 10th percentile of birth weight had 30% fewer glomeruli than those with birth weights > 10th percentile [11].…”

“…In addition, many experimental studies in various animal models demonstrated that IUGR led to a reduced nephron endowment at birth [12, 13]. In general, at the time of birth, kidney size is proportional to body size and nephron number is directly proportional to kidney size [1]; however, in the situation that the growth restriction occurs late in gestation when nephrogenesis is complete (or nearing completion), this relationship does not exist [14]. Nephrogenesis, which is the formation of new nephron units, is complete at 34 weeks of gestation, when each kidney contains its definitive complement of approximately 800,000 to 12 million nephrons [15].…”