placental insufficiency/triglyceride

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Uteroplacental insufficiency alters hepatic fatty acid-metabolizing enzymes in juvenile and adult rats.

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Multiple adult morbidities are associated with intrauterine growth retardation (IUGR) including dyslipidemia. We hypothesized that uteroplacental insufficiency and subsequent IUGR in the rat would lead to altered hepatic fatty acid metabolism. To test this hypothesis, we quantified hepatic mRNA

Cord blood triglyceridemia in cases of placental insufficiency.

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Cord blood triglyceride concentration increased in cases of placental insufficiency. The significant relationship has been found between elevated triglyceride, decreased Apgar score, and low pH values. We suggest that the measurement of cord blood triglyceridemia might be used as a valuable

Uteroplacental insufficiency and reducing litter size alters skeletal muscle mitochondrial biogenesis in a sex-specific manner in the adult rat.

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Uteroplacental insufficiency has been shown to impair insulin action and glucose homeostasis in adult offspring and may act in part via altered mitochondrial biogenesis and lipid balance in skeletal muscle. Bilateral uterine vessel ligation to induce uteroplacental insufficiency in offspring

Uteroplacental insufficiency programs regional vascular dysfunction and alters arterial stiffness in female offspring.

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Intrauterine growth restriction caused by uteroplacental insufficiency increases the risk of cardiovascular disease in adulthood. Vascular mechanisms in female offspring are poorly understood. The aim of this study was to investigate the effects of uteroplacental insufficiency on blood pressure,

[Concentrations of antiangiogenic factors, triglycerides, glucose and insulin in women with two types of preeclampsia].

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OBJECTIVE Assessment of serum concentrations of antiangiogenic factors, triglycerides, glucose, insulin and SHBG in women with two forms of preeclampsia (placental and maternal). METHODS The study was conducted among 30 patients with placental preeclampsia and 20 women with maternal form of the

Transgenerational metabolic outcomes associated with uteroplacental insufficiency.

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Intrauterine growth restriction increases adult metabolic disease risk with evidence to suggest that suboptimal conditions in utero can have transgenerational effects. We determined whether impaired glucose tolerance, reduced insulin secretion, and pancreatic deficits are evident in

Placental insufficiency contributes to fatty acid metabolism alterations in aged female mouse offspring.

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Intrauterine growth restriction (IUGR) is an accepted risk factor for metabolic disorders in later life, including obesity and type 2 diabetes. The level of metabolic dysregulation can vary between subjects and is dependent on the severity and the type of IUGR insult. Classical IUGR animal models

Uteroplacental insufficiency after bilateral uterine artery ligation in the rat: impact on postnatal glucose and lipid metabolism and evidence for metabolic programming of the offspring by sham operation.

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Ligation of the uterine arteries (LIG) in rats serves as a model of intrauterine growth restriction and subsequent developmental programming of impaired glucose tolerance, hyperinsulinemia, and adiposity in the offspring. Its impact on lipid metabolism has been less well investigated. We compared

Pregnancy in a patient with homozygous familial hypercholesterolemia treated with long-term low-density lipoprotein apheresis.

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The pregnancy and delivery of a subject with homozygous familial hypercholesterolemia (FH) and coronary artery disease (CAD) were monitored closely for signs of maternal and fetal distress. Biweekly treatment with low-density lipoprotein (LDL) apheresis using dextran-sulfate cellulose columns was

Clinical outcome, biochemical and therapeutic follow-up in 14 Austrian patients with Long-Chain 3-Hydroxy Acyl CoA Dehydrogenase Deficiency (LCHADD).

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BACKGROUND LCHADD is a long-fatty acid oxidation disorder with immediate symptoms and long-term complications. We evaluated data on clinical status, biochemical parameters, therapeutic regimens and outcome of Austrian LCHADD patients. METHODS Clinical and outcome data including history, diagnosis,

Effect of Curcumin on Growth Performance, Inflammation, Insulin level, and Lipid Metabolism in Weaned Piglets with IUGR.

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The possible causes of intrauterine growth retardation (IUGR) might stem from placental insufficiency, maternal malnutrition, inflammation in utero, and other causes. IUGR has had an adverse influence on human health and animal production. Forty weaned piglets with normal birth weights (NBWs) or

Influence of birth weight and gender on lipid status and adipose tissue gene expression in lambs.

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Intrauterine growth restriction (IUGR) is a risk factor for obesity, particularly when offspring are born into an unrestricted nutritional environment. In this study, we investigated the impact of IUGR and gender on circulating lipids and on expression of adipogenic, lipogenic and adipokine genes in

Maternal inflammation at midgestation impairs subsequent fetal myoblast function and skeletal muscle growth in rats, resulting in intrauterine growth restriction at term.

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Maternal inflammation induces intrauterine growth restriction (MI-IUGR) of the fetus, which compromises metabolic health in human offspring and reduces value in livestock. The objective of this study was to determine the effect of maternal inflammation at midgestation on fetal skeletal muscle growth

Plasma lipids and blood glucose in infants of toxemic mothers.

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Maternal and cord blood of 34 toxemic and 27 non-toxemic mothers and their infants were studied for lipids and glucose. All the lipid fractions in cord blood were significantly lower (P less than .001) than that of the mother in all groups due to relative impermeability of the placenta. AFD infants

[Effect of hormonally-induced prolongation of pregnancy in rabbits on maternal and fetal serum lipids].

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The alterations of the lipid metabolism produced by placental insufficiency were investigated in animal experiments. Pregnant rabbits received Chlormadinon-acetate by intramuscular injection. The pregnancy was prolongated for 4 days, and a placental insufficiency developed. The lipid metabolism of

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