The effects of myo-inositol and probiotic supplementation in a high-fat-fed preclinical model of glucose intolerance in pregnancy.

Glucose intolerance during pregnancy - a major driver of gestational diabetes mellitus (GDM) - has significant short- and long-term health consequences for both the mother and child. As GDM prevalence continues to escalate, there is growing need for preventative strategies. There is limited but suggestive evidence that myo-inositol (MI) and probiotics (PB) could improve glucose tolerance during pregnancy. The present study tested the hypothesis that MI and/or PB supplementation would reduce the risk of glucose intolerance during pregnancy. Female C57BL/6 mice were randomised to receive either no treatment, MI, PB (Lactobacillus rhamnosus and Bifidobacterium lactis) or both (MIPB) for 5 weeks. They were then provided with a high-fat diet for 1 week before mating commenced and throughout mating/gestation, while remaining on their respective treatments. An oral glucose tolerance test occurred at gestational day (GD) 16·5 and tissue collection at GD 18·5. Neither MI nor PB, separately or combined, improved glucose tolerance. However, MI and PB both independently increased adipose tissue expression of Ir, Irs1, Akt2 and Pck1, and PB also increased Pparγ. MI was associated with reduced gestational weight gain, whilst PB was associated with increased maternal fasting glucose, total cholesterol and pancreas weight. These results suggest that MI and PB may improve insulin intracellular signalling in adipose tissue but this did not translate to meaningful differences in glucose tolerance. The absence of fasting hyperglycaemia or insulin resistance suggests this is a very mild model of GDM, which may have affected our ability to assess the impact of these nutrients.

Effect of prenatal hypoxia in transgenic mouse models of preeclampsia and fetal growth restriction.

Mice lacking endothelial nitric oxide synthase (eNOS(-)(/-)) or catechol-O-methyl transferase (COMT(-/-)) exhibit a preeclampsia-like phenotype and fetal growth restriction. We hypothesized that a hypoxic insult would result in a more severe phenotype. Pregnant eNOS(-/-), COMT(-/-) and control (C57BL/6J) mice were randomized to hypoxic (10.5% O(2)) or normal conditions (20.9% O(2)) from gestational day 10.5 to 18.5. Hypoxia increased the blood pressure in all genotypes and proteinuria in C57BL/6J and eNOS(-/-) mice. Fetal survival was significantly reduced following hypoxia, particularly in eNOS(-/-) mice. Birth weight was decreased in both C57BL/6J and COMT(-/-) mice. Placentas from COMT(-/-) mice demonstrated increased peroxynitrite. Despite similar hypoxia-induced effects on maternal blood pressure and proteinuria, eNOS(-/-) embryos have a decreased tolerance to hypoxia. Compared to C57BL/6J, COMT(-/-) mice exhibited less severe changes in proteinuria and fetal growth when exposed to prenatal hypoxia. This relative resistance to prenatal hypoxia was associated with a significant increase in placental levels of peroxynitrite.

Effect of gestational diabetes on maternal artery function.

Endothelial dysfunction has been observed systemically in women with gestational diabetes (GDM). Important cardiovascular adaptations occur during pregnancy, including enhanced endothelium-dependent vasodilation in systemic and uterine arteries, which are necessary to ensure the health of both mother and fetus. The effects of GDM, however, on uterine artery function and the possible mechanisms that mediate endothelial dysfunction remain unknown. The aim of this study was to utilize a mouse model of GDM to investigate (a) effects on uteroplacental flow, (b) endothelial function of uterine and mesenteric arteries, and (c) possible mechanisms of any dysfunction observed. Pregnant mice heterozygous for a leptin receptor mutation (Lepr(db) (/+); He) spontaneously develop GDM and were compared to wild-type (WT) mice at day 18.5 of gestation. Uterine artery flow was assessed using ultrasound biomicroscopy. Uterine and mesenteric artery function was assessed using wire myography. Arterial superoxide production was measured using oxidative fluorescence microphotography. In vivo uteroplacental perfusion was impaired in mice with GDM, indicated by a significant increase in uterine artery resistance index. Maximal endothelium-dependent relaxation to methacholine was significantly impaired in mesenteric arteries from mice with GDM, while sensitivity was significantly reduced in uterine arteries. Both uterine and mesenteric arteries from mice with GDM exhibited a greater dependence on nitric oxide and increased superoxide production compared with those from mice with a healthy pregnancy. A significant source of superoxide in GDM mice was uncoupled nitric oxide synthase. These changes may contribute to the development of some of the fetal and maternal complication associated with GDM.

Satisfaction and patient outcomes of a telephone-based nurse triage service.

PURPOSE: Describe patient satisfaction and patient-reported outcomes after voluntary use of a telephone-based nurse triage service. METHODS: A random sample of symptomatic callers who contacted the triage service in 1999 was identified. A computer-assisted telephone survey was conducted, resulting in a response rate of 58.9 percent and a sample size of 35,374. SUMMARY: Overall satisfaction with the service was 90.4 percent and did not vary greatly when stratified by demographic and health status characteristics. Of all callers who reported following the triage recommendation to use self-care instructions while monitoring the condition for change (n = 12,037), 11.5 percent scheduled an office visit and 1.5 percent used hospital emergency-room (ER) services for further care. CONCLUSIONS: Overall satisfaction with telephone-based nurse triage services was high and did not vary substantially by caller characteristics.