Sex-dependent programming of glucose and fatty acid metabolism in mouse offspring by maternal protein restriction.

Background: Nutritional conditions during fetal life influence the risk of the development of metabolic syndrome and cardiovascular diseases in adult life (metabolic programming). Impaired glucose tolerance and dysregulated fatty acid metabolism are hallmarks of metabolic syndrome.

Objective: We aimed to establish a mouse model of metabolic programming focusing on the sex-specific effects of a maternal low-protein diet during gestation on glucose and lipid metabolism in the adult offspring.

VEGF-SPECT with ¹¹¹In-bevacizumab in stage III/IV melanoma patients.

Purpose: A feasibility study was performed to investigate the presence of VEGF in melanoma lesions by VEGF-SPECT with (111)In-bevacizumab. In addition the effect of a single therapeutic bevacizumab dose on (111)In-bevacizumab uptake was compared with VEGF levels in resected melanoma lesions.

Patients And Methods: Eligible were patients with stage III/IV melanoma who presented with nodal recurrent disease.

The effects of intrauterine malnutrition on maternal-fetal cholesterol transport and fetal lipid synthesis in mice.

Intrauterine malnutrition is associated with increased susceptibility to chronic diseases in adulthood. Growth-restricted infants display a less favorable lipid profile already shortly postnatal. Maternal low protein diet (LPD) during gestation is a well-defined model of fetal programming in rodents and affects lipid metabolism of the offspring.

The liver X-receptor gene promoter is hypermethylated in a mouse model of prenatal protein restriction.

Prenatal nutrition as influenced by the nutritional status of the mother has been identified as a determinant of adult disease. Feeding low-protein diets during pregnancy in rodents is a well-established model to induce programming events in offspring. We hypothesized that protein restriction would influence fetal lipid metabolism by inducing epigenetic adaptations.

Fetal liver X receptor activation acutely induces lipogenesis but does not affect plasma lipid response to a high-fat diet in adult mice.

There is increasing evidence that the metabolic state of the mother during pregnancy affects long-term glucose and lipid metabolism of the offspring. The liver X receptors (LXR)α and -β are key regulators of cholesterol, fatty acid, and glucose metabolism. LXRs are activated by oxysterols and expressed in fetal mouse liver from day 10 of gestation onward.