Adiponectin in Pregnancy: Implications for Health and Disease

Abstract

Pregnancy is a unique physiologic state that is associated with profound alterations in maternal metabolic, endocrine, and vascular function, designed to ensure the delivery of appropriate energy and nutrition to the developing fetus. In this context, the role of the fat-derived hormone adiponectin is of interest, particularly in light of emerging recognition of the broad array of physiologic processes upon which this adipokine impacts. Indeed, adiponectin has pleiotropic effects on the regulation of energy homeostasis, systemic inflammation, vascular function, cell growth, and even bone metabolism. Thus, in this review, we consider existing evidence for the physiologic role of adiponectin in human gestation and how this protein may be relevant to two major medical disorders of pregnancy: gestational diabetes mellitus and preeclampsia. While studies to date have yielded many conflicting findings pertaining to adiponectin in pregnancy, further investigation in this area is essential. Ultimately, elucidation of adiponectin physiology in the setting of both normal pregnancy and its pathologic conditions may provide unique insight into fundamental processes that are relevant to health and disease in mother and child.

Relationship between vitamin D and gestational diabetes in overweight or obese pregnant women may be mediated by adiponectin

“…Similarly, one previous study examined relationships between 25(OH)D and HMWadiponectin in pregnancy and reported no association [26]. Disagreement with our finding of a positive association may be due to the smaller sample size [26] (n = 36-37 compared to n = 102 in our study); the sampling time point of 31 wk gestation (since maternal adiponectin levels decline progressively with advancing gestation [48]); and/or the lack of adjustment for ethnicity (since lower total [49] and HMW-adiponectin [50] have been reported in certain ethnic groups, such as South Asian women [49,50]). The mechanism by which vitamin D may increase adiponectin is thought to be via suppression of the TNF-␣ gene and the adipose tissue renin-angiotensin system, both of which regulate adiponectin production [51,52].…”

Longitudinal association of 25-hydroxyvitamin D with adipokines and markers of glucose metabolism among Brazilian pregnant women

“…In total, 149 women completed the study, and 32 were lost to follow-up. There were no significant differences between women who completed the study compared to those who were lost during follow-up (online Supplementary Table S1 16•0 % (n 29/181) according the cut-offs proposed by the ESPG and the IOM, repectively. Women who began the study in the winter, compared to those who began in summer, were more likely to be vitamin D insufficient (ESPG: 33•6 v. 15•6 %, respectively, P < 0•001; IOM: 51•7 v. 3•5 %, respectively, P < 0•001) ( Table 1).…”

“…Adiponectin also protects β-cells from immune attack and reduces insulin resistance through immunoregulatory and anti-inflammatory effects (11)(12)(13)(14) . In pregnant women, concentrations of adiponectin have been inversely associated with adverse maternal outcomes, such as GDM (15,16) , overweight and obesity (17) . During pregnancy, a reduction in maternal plasma adiponectin concentrations is expected (18,19) .…”

Adiponectin and β-Cell Adaptation in Pregnancy

“…Adiponectin is an adipocyte-derived hormone with pleiotropic effects on a broad array of physiological processes including energy homeostasis, vascular function, systemic inflammation, and cell growth (4,5). Most notably, it has emerged as an antidiabetic adipokine, with low serum adiponectin shown to predict incident type 2 diabetes in several populations (6).…”

“…These antidiabetic associations have been generally attributed to the well-established insulinsensitizing effects of adiponectin. However, there have also been studies linking hypoadiponectinemia to b-cell dysfunction, particularly in pregnancy (8,9), thereby raising the intriguing question of whether adiponectin could be relevant to the pathophysiology of GDM (5).…”