Key result
Maternal type 1 diabetes is linked to elevated infant atherogenic markers and ~11% higher placental MTP activity.
Observational
Answers are grounded in this paper and cite their sources.
BACKGROUND: Proatherogenic stimuli during foetal life may predispose to development of atherosclerosis in adulthood. Elevated plasma low-density lipoprotein (LDL) cholesterol and C-reactive protein (CRP) expression is associated with increased risk of atherosclerosis. METHODS AND RESULTS: In this study, we examined how maternal type 1 diabetes affects foetal plasma LDL cholesterol and CRP. In comparison with healthy mothers, the plasma LDL cholesterol was not increased in the mothers with diabetes, however, the umbilical-cord plasma LDL cholesterol was increased in their infants. CRP was increased in infants of mothers with diabetes and high haemoglobin A1c (HbA1c, > or = 6.2%). Human placenta expresses microsomal triglyceride transfer protein (MTP), which facilitates secretion of apolipoprotein B-containing lipoproteins. Microsomal triglyceride transfer activity was slightly higher (11%) in placentas from mothers with diabetes and HbA1c > or = 6.2% compared with the controls. CONCLUSION: The results suggest that maternal type 1 diabetes increases the foetal plasma LDL cholesterol and CRP concentration and thus might predispose the offspring to development of atherosclerosis.
No takes yet. Share an insight, caveat, or question.
Lindegaard et al. (2008) conducted an observational in Maternal type 1 diabetes and foetal dyslipidemia/inflammation. Maternal type 1 diabetes vs. Healthy mothers without diabetes was evaluated on Umbilical-cord plasma LDL cholesterol, C-reactive protein (CRP), and placental microsomal triglyceride transfer activity. Maternal type 1 diabetes increased infant umbilical-cord plasma LDL cholesterol and CRP, with 11% higher placental MTP activity when maternal HbA1c was >=6.2%.
Synapse has enriched 10 related papers. Consider them for comparative context: