PubMed · 11794598
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
Ross Bullock. 2002. Hyperventilation.. https://pubmed.ncbi.nlm.nih.gov/11794598/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
BACKGROUND: Changes in maternal bone during pregnancy may affect fetal bone mineralization. ISSUES: The biphasic changes in maternal bone histology (temporary loss of cancellous bone in early pregnancy restored by term gestation) are consistent with corresponding blood biochemistry changes; increased bone resorption markers in the first trimester, while bone formation markers increased in the last trimester. Postpartum bone mineral density (BMD) by DEXA is increased at cortical bone and decreased at trabecular bone sites compared with prepregnancy values. The mean reduction of spine BMD is 3.5% from prepregnancy to immediate postpartum. Neonatal bone mineral content (BMC) is different by season of birth, low weight relative to gestation, and having a diabetic mother. Lower total body BMC and high bone resorption marker in winter vs. summer-born newborns was related to low vitamin D, indicating alterations of fetal bone metabolism by maternal D deficiency. Lower BMC and decreased bone formation marker in infants born small for gestational age than those born appropriate for gestation may relate to reduced transplacental mineral transfer. Low BMC in infants of diabetic mother was correlated inversely with poor control of maternal diabetes during early pregnancy. CONCLUSIONS: During pregnancy, maternal bone mineral metabolism are changed, and influences on fetal bone mineralization occur in utero.
Explore the source record for details and available documents.
AIMS/HYPOTHESIS: Type 2 diabetes is not only associated with hyperglycaemia, but also with disorders of lipid metabolism. The aim of this study was to investigate the association of triglyceride and non-HDL-cholesterol concentrations with cardiovascular disease in subjects with normal and abnormal glucose metabolism. METHODS: Subjects were 869 men and 948 women aged 50 to 75 who participated in the Hoorn Study, a population-based cohort study that started in 1989. Glucose metabolism was determined by a 75 g OGTT. High fasting triglyceride and non-HDL-cholesterol concentrations were defined as above the median of the study population. RESULTS: After 10 years of follow-up, the age- and sex-adjusted hazard ratios for cardiovascular disease were 1.35 (1.11-1.64) and 1.71 (1.40-2.08) for high triglycerides and high non-HDL-cholesterol, respectively, after mutual adjustment. After stratification for glucose metabolism status, the hazard ratios for cardiovascular disease for non-HDL-cholesterol were 1.70 (1.31-2.21) in normal glucose metabolism and 1.56 (1.12-2.18) in abnormal glucose metabolism. Triglycerides were not a risk factor in subjects with normal glucose metabolism, with a hazard ratio of 0.94 (0.73-1.22), but in subjects with abnormal glucose metabolism, the hazard ratio for cardiovascular disease was 1.54 (1.07-2.22). In subjects with abnormal glucose metabolism, the hazard ratio for the combined presence of high triglycerides and non-HDL-cholesterol was 2.12 (1.35-3.34). CONCLUSION: Our data suggest that in people with abnormal glucose metabolism, but not in those with normal glucose metabolism, high triglyceride concentration could be associated with the risk of cardiovascular disease, particularly in people with high non-HDL-cholesterol.