Lower vitamin D status in obese compared with normal-weight women despite higher vitamin D intake in early pregnancy.

Background: Obesity is associated with lower vitamin D concentrations than normal-weight. Pregnancy may affect vitamin D status, especially in obese subjects.

Aims: The purpose of this study was to compare vitamin D status and intake between obese and normal-weight women during pregnancy.

Increased vitamin D-binding protein and decreased free 25(OH)D in obese women of reproductive age.

Purpose: Obese subjects have lower circulating 25-hydroxyvitamin D (25(OH)D) than normal-weight subjects. Knowledge is scarce regarding differences in vitamin D-binding protein (DBP), free 25(OH)D, and intake of vitamin D between normal-weight and obese subjects. The purpose of this study was to examine intake and vitamin D status in obese compared with normal-weight women.

Activation of placental mTOR signaling and amino acid transporters in obese women giving birth to large babies.

Context: Babies of obese women are often large at birth, which is associated with perinatal complications and metabolic syndrome later in life. The mechanisms linking maternal obesity to fetal overgrowth are largely unknown.

Objective: We tested the hypothesis that placental insulin/IGF-I and mammalian target of rapamycin (mTOR) signaling is activated and amino acid transporter activity is increased in large babies of obese women.

Dietary herring improves plasma lipid profiles and reduces atherosclerosis in obese low-density lipoprotein receptor-deficient mice.

Diet is a significant modifiable risk factor for cardiovascular disease and high fish intake has been associated with vascular health in population studies. However, intervention studies have been inconclusive. In this study, male low-density lipoprotein receptor-deficient mice were given 16-week high fat/high sucrose diets, supplemented with either minced herring fillets or minced beef.

Maternal protein restriction in the rat inhibits placental insulin, mTOR, and STAT3 signaling and down-regulates placental amino acid transporters.

The mechanisms underlying reduced fetal growth in response to maternal protein restriction are not well established. Maternal levels of insulin, IGF-I, and leptin are decreased in rats fed a low protein (LP) diet. Because these hormones stimulate placental amino acid transporters in vitro, we hypothesized that maternal protein restriction inhibits placental leptin, insulin/IGF-I, and mammalian target of rapamycin signaling and down-regulates the expression and activity of placental amino acid transporters.

Perinatal lack of maternal IL-6 promotes increased adiposity during adulthood in mice.

The perinatal environment appears important in establishing metabolic phenotypes in adulthood. Mice deficient in IL-6 (IL-6(-/-)) tend to develop mature-onset obesity, but it is unknown whether perinatal exposure to IL-6 produced by the dam influences the metabolism of adult offspring. To address this issue, we monitored IL-6(-/-) offspring of IL-6(-/-) or IL-6(+/-) dams, as well as wild-type (WT) mice.

Maternal hormones linking maternal body mass index and dietary intake to birth weight.

Background: Obese women often give birth to large-for-gestational age infants (typically defined as a birth weight greater than the 90th percentile), who are at risk of birth injuries and of developing metabolic syndrome later in life. The mechanisms underlying increased fetal growth remain to be established.

Objective: We aimed to identify maternal hormones that can explain the link between dietary intake, body mass index (BMI), and birth weight.

Mammalian target of rapamycin in the human placenta regulates leucine transport and is down-regulated in restricted fetal growth.

Pathological fetal growth is associated with perinatal morbidity and the development of diabetes and cardiovascular disease later in life. Placental nutrient transport is a primary determinant of fetal growth. In human intrauterine growth restriction (IUGR) the activity of key placental amino acid transporters, such as systems A and L, is decreased.

Brief hyperglycaemia in the early pregnant rat increases fetal weight at term by stimulating placental growth and affecting placental nutrient transport.

In pregnant women with type 1 diabetes, suboptimal glucose control in the first trimester is a strong predictor for giving birth to a large fetus. However, the mechanisms underlying this association are unknown. We hypothesized that transient hyperglycaemia in early pregnancy results in (1) increased placental growth and (2) an up-regulation of placental nutrient transport capacity, which leads to fetal overgrowth at term.

Down-regulation of placental transport of amino acids precedes the development of intrauterine growth restriction in rats fed a low protein diet.

Intrauterine growth restriction (IUGR) represents an important risk factor for perinatal complications and for adult disease. IUGR is associated with a down-regulation of placental amino acid transporters; however, whether these changes are primary events directly contributing to IUGR or a secondary consequence is unknown. We investigated the time course of changes in placental and fetal growth, placental nutrient transport in vivo and the expression of placental nutrient transporters in pregnant rats subjected to protein malnutrition, a model for IUGR.

Hormonal regulation of glucose and system A amino acid transport in first trimester placental villous fragments.

Alterations in placental nutrient transfer have been implicated in fetal growth abnormalities. In pregnancies complicated by diabetes and accelerated fetal growth, upregulations of glucose transporter 1 (GLUT1) and amino acid transporter system A have been shown in the syncytiotrophoblast of term placenta. In contrast, intrauterine growth restriction is associated with a downregulation of placental system A transporters.