**1. Introduction**

Pregnancy is a distinct situation marked by physiological insulin resistance that disappears after delivery. It is also marked by changes in the endocrine, metabolic, and circulatory systems, all of which are intended to supply energy and sustenance to the developing fetus [1]. Gestational diabetes (GDM) and pre-eclampsia (PE) may occur as complications during metabolic dysregulation in pregnancy. GDM is a type of glucose intolerance that develops or is first noticed during pregnancy [2]. A previous diagnosis of gestational or pre-diabetes, impaired fasting glycemia, a family history of type 2 diabetes mellitus (DM) in a first-degree relative, maternal age, ethnic background, being overweight, and a history of previous pregnancy

resulting in a child with a high birth weight (>4 kg) are all risk factors for developing GDM [3].

The major goal of this study was to look at the relationship between adipokines, lipids, and preeclampsia, as well as the efficacy and accuracy of these markers in predicting PE [4]. PE is a pregnancy-specific illness in which women who were previously normotensive develop hypertension and proteinuria after 20 weeks of pregnancy [5]. PE affects between 2 and 5% of pregnancies and contributes significantly to fetal, neonatal, and maternal morbidity and mortality. In Ghana, the incidence rate is around 7% [6, 7], however, a prevalence of 8.3% was reported in a study at the Volt Regional Hospital, Ho [8]. PE can develop anywhere from 20 weeks post-conception to 6 weeks post-delivery, and it's commonly considered early inception if it happens before 34 weeks. It shares some of the risk factors of metabolic syndrome, such as insulin resistance, subclinical inflammation, and obesity, and data suggests that women with PE are more likely to develop cardiovascular disease later in life [1].

#### **1.1 Adiponectin**

Adiponectin, also known as gelatin-binding protein of 28 kDa (GBP28), adipocyte complement-related protein of 30 kDa (ACRP30), adipoQ, adipose most abundant gene transcript 1 (apM1) is an adipocyte-specific secreted protein with roles in glucose and lipid metabolism [9]. The adiponectin gene is located on chromosome 3q27.3 and it is the most abundant protein released by adipose tissue and circulates in plasma as a low-molecular-weight trimer, a middle-molecular-weight hexamer, and a high-molecular-weight 12–18-mer [10, 11]. The biological activity of various variants varies, with HMW adiponectin being the most physiologically active [12]. The effects of adiponectin on glucose metabolism are mediated by two receptors, AdipoR1 and AdipoR2, respectively [13]. AdipoR2 is particularly abundant in the liver, whereas AdipoR1 is found in almost all bodily tissues [14]. Adiponectin activates adenosine monophosphate protein kinase (AMPK) and peroxisome proliferator-activated receptor alpha (PPAR-) by binding to its receptors AdipoR1 and AdipoR2, which leads to the activation of adenosine monophosphate protein kinase (AMPK) and peroxisome proliferator-activated receptor alpha (PPAR-α). In obesity-related insulin resistance, both adiponectin and its receptors are downregulated [13].

Adiponectin levels in the blood have a positive correlation with HDL cholesterol and a negative correlation with triglycerides [15]. Gender, age, and lifestyle all influence plasma adiponectin levels. Adiponectin gene expression is inhibited by β-adrenergic stimulation, glucocorticoids, and TNF-α [16, 17]. Type 2 diabetes, insulin resistance, obesity, hypertension, and left ventricular hypertrophy are all linked to low adiponectin levels in the blood [18].

Even in the absence of obesity, increased fat buildup in the body during pregnancy leads to a steady drop in adiponectin secretion [19]. Both adiponectin concentration and adiponectin mRNA are negatively correlated with fat mass hence with increased adipose tissue secretion during pregnancy, it's possible that signals are sent to the adipose tissue, resulting in a decrease in adiponectin production even in the absence of obesity [19]. Despite the fact that some researchers have been unable to find adiponectin mRNA expression in the placenta [20, 21], studies show that it could be a source of the hormone [22].

A counterintuitive and considerable increase in adiponectin concentration has been found in several studies during pregnancy complicated with PE [23, 24]. Other researchers, on the other hand, discovered no significant differences in adiponectin mRNA expression in adipose tissue between PE patients and healthy controls [25].
