**1. Introduction**

Preeclampsia/hypertensive disorders of pregnancy (PE/HDP) is a serious and potentially lifethreatening disease appearing as a complication in about 2–12% of all pregnancies and associated with significant perinatal and maternal mortality [1,2]. It is estimated that more than 60,000 women worldwide die of the disease each year; it is one of the main causes of maternal mortality [3]. There is considerable evidence that maternal obesity, increased insulin resistance, inflammation, and aberrant fatty acid metabolism are involved in the pathogenesis of PE/HDP [4,5]. Inflammatory reactions have recently been attracting attention as the pathophysiological characteristics of PE/HDP, including vascular endothelial dysfunction and placental abnormalities [6–14]. Shallow trophoblast invasion and inadequate artery remodeling in pregnancy may cause placental hypoperfusion, hypoxia, or ischemia, which play an important role in the pathogenesis of PE/HDP [15]. The link between adiposity, inflammation, and insulin resistance has been increasingly acknowledged since Spiegelman and

his colleagues demonstrated the relationship [16]. White adipose tissue secretes pro-inflammatory cytokines which contribute significantly to the chronic inflammatory state and metabolic complications of obesity [17]. It is plausible that similar disturbances in adipocyte function might contribute to the development of the clinical syndrome of PE/HDP, a state of inflammation and insulin resistance.

Adipose tissue, complex tissue composed of preadipocytes, adipocytes, and stromal vascular cells, is one of the representative organs to contribute to worsening insulin resistance through inflammation and subsequent dysfunction. Visceral adiposity correlates with metabolic risk factor [18] and adverse metabolic outcomes in pregnancy including gestational diabetes mellitus and PE/HDP [19–21]. Adipokines are cytokines expressed in and secreted from adipocytes in response to the systemic nutritional status, and some of them induce macrophage infiltration and inflammatory cytokine secretion [22,23]. In the present study, we analyzed expression of adipokines including inflammatory cytokines in adipocytes and found the involvement of receptor for advanced glycation endproducts (RAGE) in expression of interleukin-6 (IL-6) and C-C motif chemokine ligand 2 (CCL2) in adipocytes.
