Leptin participates in regulating energy metabolism during pregnancy. Interestingly, despite the rise in leptin concentrations during pregnancy, reduced leptin sensitivity to food intake during pregnancy has been described (Chehab, 2014; Vazquez, 2015). This "leptin resistance" may serve to promote energy storage during pregnancy and for later lactation.
Higher leptin levels during pregnancy may be disadvantageous under certain situations, such as in maternal obesity. Leptin functions as a proinflammatory cytokine in white adipose tissue, which may dysregulate the inlammatory cascade and lead to placental dysfunction in obese women (Vazquez, 2015). In addition, abnormally elevated leptin levels have been associated with preeclampsia and gestational diabetes (Bao, 2015; Taylor, 2015).
Fetal leptin is important for the development of several organs that include the pancreas, kidney, heart, and brain. Fetal levels correlate with maternal body mass index (BMI) and birthweight. Lower levels are linked to fetal-growth restriction (Brifa, 2015; Tsai, 2015).
Dozens of hormones with metabolic and/or inflammatory functions are produced by adipose tissue. Adiponectin is a peptide produced primarily in maternal fat but not in the placenta (Haghiac, 2014). Adiponectin levels inversely correlate with adiposity, and it acts as a potent insulin sensitizer. Despite reduced adiponectin levels in women with gestational diabetes, directed assays are not useful for predicting diabetes development (Hauguel-de Mouzon, 2013).
Ghrelin is a peptide secreted principally by the stomach in response to hunger. It cooperates with other neuroendocrine factors, such as leptin, in energy homeostasis modulation.
Ghrelin is also expressed in the placenta and likely has a role in fetal growth and cell proliferation (Gonzalez-Dominguez, 2016). Angelidis and associates (2012) have reviewed the many functions of ghrelin in the regulation of reproductive function.
Viatin is a peptide that was first identified as a growth fac tor for B lymphocytes, but it is mainly produced within adipose tissue. Mumtaz and colleagues (2015) propose that elevated levels of visfatin and leptin impair uterine contractility. Such findings may provide a physiological basis for the observation that maternal obesity raises the risk for dysfunctional labor.
During normal pregnancy, nearly 1000 mEq of sodium and 300 mEq of potassium are retained (Lindheimer, 1987). Although the glomerular filtration rate of sodium and potassium is increased, the excretion of these electrolytes is unchanged during pregnancy as a result of enhanced tubular resorption (Brown, 1986, 1988). Although total accumulations of sodium and potassium are elevated, their serum concentrations are diminished slightly (Appendix, p. 1257). Several mechanisms may explain these lower levels (Odutayo, 2012). In the case of potassium, it possibly involves the expanded plasma volume of pregnancy. With respect to sodium, osmoregulation is altered and the threshold for arginine vasopressin release is lowered. his promotes free water retention and diminished sodium levels.
Total serum calcium levels, which include both ionized and nonionized calcium, decrease during pregnancy. his reduction consequent decline in the amount of circulating protein-bound nonionized calcium. Serum ionized calcium levels, however, remain unchanged (Olausson, 2012).