Abstract
Increased insulin resistance and inflammatory action are observed in pregnancy-induced hypertension (PIH), but similar insulin resistance is observed also in successful pregnancy. To estimate insulin resistance and inflammatory activity in normal pregnancy and PIH, serum concentrations of free fatty acids (FFA; corrected with albumin to estimate unbound FFA), monocyte chemoattractant protein (MCP)-1, and high-molecular weight (HMW) adiponectin were measured in severe PIH patients with a BMI less than 25 kg/m2 and were measured 3 times during the course of pregnancy in women with normal pregnancies. FFA/albumin, MCP-1, and HMW adiponectin concentrations were significantly higher in PIH patients than in women with normal pregnancies. The 3 measurements of FFA/albumin showed a significant increase through the course of uncomplicated pregnancies. In contrast, MCP-1 and HMW adiponectin were significantly decreased during the course of pregnancy. These results suggest that the reduced MCP-1 concentration in normal pregnancy may be a pathway to inhibit the induction of pathological features from physiological insulin resistance and homeostatic inflammation.
Highlights
Pregnancy-induced hypertension (PIH), a leading complication in pregnancy that affects the mother and fetus, is becoming more frequent mainly because of increasing maternal age [1]
It was recently revealed that free fatty acids (FFA) are mediators of toll-like receptor (TLR)-4 and the NF-kappaB pathway of macrophages within adipose tissue and are regarded as key molecules in systemic inflammation, which plays a role in type 2 diabetes and cardiovascular disease [10, 12, 13]
We recently reported that increased brain-type natriuretic peptide (BNP) correlated with increased adiponectin in PIH [17], similar to the findings in acute coronary syndrome [20] and cardiomyopathy [21]
Summary
Pregnancy-induced hypertension (PIH), a leading complication in pregnancy that affects the mother and fetus, is becoming more frequent mainly because of increasing maternal age [1]. On the other hand, increased insulin resistance is observed in PIH as well as in successful pregnancies [4,5,6]. In the course of a normal pregnancy, insulin resistance is correlated with increased maternal adipose tissue deposition [5] and supports placental formation and fetal growth. Increased circulating FFA have been observed in gestational diabetes mellitus, preterm delivery, or other adverse maternal outcomes in pregnant subjects [6, 9, 14, 15], increased circulating FFA have been described in normal pregnancy [16]. Different pathways which do not induce systemic inflammation observed in PIH [4] in insulin resistance remain unclear
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