Possible roles of exercise and apelin against pregnancy complications

Abstract

The prevalence of maternal obesity during pregnancy is associated with the risk of gestational diabetes, preeclampsia, and cardiomyopathy. Environmental factors such as active lifestyles and apelin may lead to beneficial changes. In rats, apelin and exercise (45 to 65% VO2max for 6 to 9 weeks) during pregnancy increase brown adipose tissue (BAT) proteins such as Cidea, Elovl3, UCP1, PRDM16, and PGC-1α in males and females fetuses, while white adipose tissue (WAT) is reduced. In humans and animals, apelin and exercise stimulate the expression of the glucose transporters (GLUT1/2/4) in the muscle and adipose tissue through the PI3K/Akt and AMPK pathways. Hence, exercise and apelin may are known as regulators of energy metabolism and be anti-obesity and anti-diabetic properties. In mice, exercise also creates a short-term hypoxic environment in the pregnant mother, activating HIF-1, VEGF, and VEGFR, and increasing angiogenesis. Exercise and apelin also increase vasodilation, angiogenesis, and suppression of inflammation through the L-arginine/eNOS/NO pathway in humans. Exercise can stimulate the ACE2-Ang-(1-7)-Mas axis in parallel with inhibiting the ACE-Ang II-AT1 pathway. Exercise and apelin seem to prevent preeclampsia through these processes. In rats, moderate-intensity exercise (60 to 70% VO2max for 8 weeks) and apelin/APJ also may prevent pathological hypertrophy in pregnancy by activating the PI3K/Akt/mTOR/p70S6K pathway, PI3k-Akt-ERK1/2-p70S6K pathway, and the anti-inflammatory cytokine IL-10. Since pre-clinical studies have been more on animal models, future research with scientific guidelines should pay more attention to human specimens. In future research, time factors such as the first, second, and third trimesters of pregnancy and the intensity and duration of exercise are important variables that should be considered to determine the optimal intensity and duration of exercise.

Non-invasive prediction of preeclampsia using the maternal plasma cell-free DNA profile and clinical risk factors

“…The cfDNA profile in C EPE model contained eight genes, of which pTSS coverages of FOSL2 , CAMKK2 , CCND1 , ITPR1 , PRKACB , WNT7B , CACNB2 and NRF1 genes were stably differential between pregnant women with early-onset PE and healthy controls. CAMKK2 , CCND1 , ITPR1 , PRKACB and WNT7B genes were enriched in more than two pathways associated with PE, including “Hedgehog signaling pathway” ( 35 ), “Hippo signaling pathway” ( 36 ), “AMPK signaling pathway” ( 37 ), “Apelin signaling pathway” ( 38 ), “Autophagy” ( 39 ), “Oxytocin signaling pathway” ( 40 ), “Wnt signaling pathway” ( 41 ) and “VEGFA-VEGFR2 signaling” ( 42 ). The AMPK signaling pathway has been repeatedly reported to be associated with PE based on omics data ( 37 , 43 ).…”

Comparative Evaluation of Adipokine Metrics for the Diagnosis of Gestational Diabetes Mellitus

“…Apelin is also involved in glucose homeostasis, and higher levels of apelin were observed in obesity and T2DM [ 91 ]. In humans and animals, apelin is a stimulant of the glucose transporters (GLUT1/2/4) expression in the muscle and adipose tissue via the PI3K/Akt and AMPK pathways [ 92 ]. It has been noticed that the placenta produces significant amounts of apelin, and apelin levels in the foetal blood are higher than in mothers [ 93 ].…”

Evaluation of changes of apelin and apelin receptor (APJ) expression in cervix-uterus and placental axis in an LPS-induced preterm labor model

“…However, they emphasized that the role of the apelin/aPJ system in placental endothelial and vascular function should be confirmed in future studies (lim et al, 2013). moreover, the necessity of examining the APLN/APJ axis, especially in the first, second, and third trimesters, with a focus on temporal change, is also emphasized in the literature (alizadeh Pahlavani, 2022). Studies in mice have shown that apelin can increase glucose utilization (Dray et al, 2008).…”