**1.3 Resistin**

Resistin is a 12.5 kDa dimeric protein that circulates in human blood as two 92-amino-acid polypeptides connected by disulfide bridges at Cys-26 [42]. The signaling molecule resistin is found in monocytes, macrophages, and adipocytes [1]. The resistin gene is located on chromosome 19p13.3 and although the exact physiological role in humans is unknown, available evidence suggests that its presence in the blood is linked to a number of inflammatory indicators, including C-reactive protein, soluble TNF-receptor-2, IL-6, and lipoprotein-associated phospholipase A2 [43]. Coronary artery disease has been linked to high levels of resistin in the blood [43], and to severity of disease in sepsis and septic shock [44] and may be involved in the pathogenesis of rheumatoid arthritis [45].

Resistin concentration in PE has been reported by various researchers to remain unchanged [23] decreased [46] or increased [25]. The increased circulating resistin levels in PE could be related to the fact that its concentration in plasma is dependent on glomerular filtration, therefore as renal impairment progresses, resistin levels in plasma may rise [47].

#### **1.4 Visfatin**

Visfatin is a 52-kDa protein and is extensively produced in both human and mouse adipose tissue, and its plasma levels rise as obesity progresses [1]. Visfatin gene is located on chromosome 7q22.2 and is widely expressed in adipose tissue but can also be found in the placenta and fetal membranes [48] and myometrium [17]. It is also expressed in bone marrow, liver, muscle, heart, lung, and kidney [49] as well as by the lymphocyte. It is referred to as a pre-B cell colony enhancing factor because it enhances the maturation of B cell precursors [49]. Visfatin is released by amniotic epithelial cells during pregnancy [50] and has nicotinamide phosphoribosyltransferase activity [51].

Some contradictory results have been published on visfatin levels during pregnancy affected by preeclampsia. Some authors published increased visfatin levels in PE [52] while other investigators reported decreased levels [53] or values similar to normal pregnancy [54].

In a normal pregnancy, lipid profile changes are characterized by increases in total plasma cholesterol and triglyceride (TG) levels as a result of increased TG synthesis by the liver and very low-density lipoprotein-cholesterol (VLDL-C) synthesis in response to elevated estrogen levels [55]. The clearance of VLDL-C is reduced when the activity of lipoprotein lipase (LPL) is reduced due to estrogen-induced downregulation of LPL gene expression during pregnancy [56]. Women with PE had higher TG, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and very low-density lipoprotein cholesterol (VLDL-C), according to a study conducted in the Cape Coast metropolis in Ghana [57].

The differences in lipid profiles and abnormalities in certain adipokine metabolism described by different researchers warrant a closer look at their implications in the pathophysiology of PE. The main goal of this study was to see if the metabolism of adiponectin, leptin resistin, and visfatin are affected in the first trimester of pregnancy in pregnancies that go on to develop PE, and if these changes are significant enough in the prediction of PE to prompt interventions early enough to save the mother and baby.
