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Review
. 2023 Jan 21;13(2):301.
doi: 10.3390/life13020301.

The Role of Adiponectin during Pregnancy and Gestational Diabetes

Brittany L Moyce Gruber  1   2 , Vernon W Dolinsky  1   2
Affiliations
Review

The Role of Adiponectin during Pregnancy and Gestational Diabetes

Brittany L Moyce Gruber et al. Life (Basel). .

Abstract

Pregnancy involves a range of metabolic adaptations to supply adequate energy for fetal growth and development. Gestational diabetes (GDM) is defined as hyperglycemia with first onset during pregnancy. GDM is a recognized risk factor for both pregnancy complications and long-term maternal and offspring risk of cardiometabolic disease development. While pregnancy changes maternal metabolism, GDM can be viewed as a maladaptation by maternal systems to pregnancy, which may include mechanisms such as insufficient insulin secretion, dysregulated hepatic glucose output, mitochondrial dysfunction and lipotoxicity. Adiponectin is an adipose-tissue-derived adipokine that circulates in the body and regulates a diverse range of physiologic mechanisms including energy metabolism and insulin sensitivity. In pregnant women, circulating adiponectin levels decrease correspondingly with insulin sensitivity, and adiponectin levels are low in GDM. In this review, we summarize the current state of knowledge about metabolic adaptations to pregnancy and the role of adiponectin in these processes, with a focus on GDM. Recent studies from rodent model systems have clarified that adiponectin deficiency during pregnancy contributes to GDM development. The upregulation of adiponectin alleviates hyperglycemia in pregnant mice, although much remains to be understood for adiponectin to be utilized clinically for GDM.

Keywords: adiponectin; gestational diabetes; pregnancy.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Metabolic adaptations of late gestation and the impact of gestational diabetes. ↑ increased, ↓ decreased. Created with BioRender.com.
Figure 2
Figure 2
Impact of adiponectin signalling on metabolism and fetal growth. Adiponectin is secreted from adipocytes and exists in circulation in a variety of forms, including low-molecular-weight (LMW) trimers bound by disulphide bonds; large, high-molecular-weight (HMW) complexes; and globular adiponectin that has been proteolytically cleaved from the collagen domain. These isoforms have different tissue and receptor specificity and are postulated to have varying metabolic activity. Adiponectin receptors ADIPOR1 and ADIPOR2 are present in differing levels of abundance in insulin-sensitive tissues [112]. White adipose tissue contains both ADIPOR1 and ADIPOR2 [162], and increasing adiponectin signalling in WAT has been shown to increase insulin sensitivity, improve healthy expansion and decrease inflammation and macrophage infiltration. Adiponectin signalling in the liver occurs through ADIPOR2 and in the pancreas through ADIPOR1, and both ADIPOR1 and ADIPOR2 have been identified in the placenta [163,164,165]. Adiponectin increases AMPK signalling in the liver and skeletal muscle, leading to increased glucose uptake and increased mitochondrial biogenesis in skeletal muscle, as well as improved lipid metabolism and decreased glucose output in the liver [144]. In the pancreas, increased signalling through ERK1/2 downstream of adiponectin leads to decreased inflammation, resulting in improved β-cell survival and insulin synthesis and secretion [154,155,157]. In contrast, placental adiponectin signalling from the maternal side promotes reduced glucose transport and decreased insulin signalling and insulin-mediated amino acid transport, which is postulated to contribute to reduced fetal growth [111]. ↑ increased, ↓ decreased. Created with BioRender.com.
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