PubMed · 11679469
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American Diabetes Association.. 2001. Insulin administration.. https://doi.org/10.2337/diacare.24.11.1984
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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.
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It is well established that strict glycemic control (hemoglobin A1c <7.0%) can prevent the microvascular complications of diabetes mellitus. Recent studies indicate that elevated plasma glucose concentrations are an independent and clinically significant risk factor for cardiovascular disease in nondiabetic and diabetic individuals. Thus, isolated postprandial hyperglycemia (2-hour postprandial glucose level >140 mg/dL [>7.8 mmol/L]) in the face of normal fasting plasma glucose (<110 mg/dL [<6.1 mmol/L]) and normal hemoglobin A1c (<6.1%) values is associated with a 2-fold increased risk of death from cardiovascular disease. These observations imply that more strict glycemic control is required to prevent macrovascular disease than microvascular disease. This review summarizes epidemiologic and experimental studies linking postprandial hyperglycemia to cardiovascular disease and therapeutic approaches available and in development to treat this disorder.