Fig. 1

Effects of apelin (as an exerkine and placentokine) on gestational diabetes in muscles and adipocytes. Apelin couples to the apelin receptor (APJ) and via Gαq activates CaMKK2 to stimulate thermogenesis. In myocytes, SERCA in the sarcoplasmic reticulum (SR) membrane transports calcium from the cytosol to the SR using ATP hydrolysis. Under hyperthermia conditions, SERCA activity is inhibited by phospholamban (PLP) or sarcolipin (SLN), but its ATPase activity remains. Therefore, to transport Ca2 + into the SR, mitochondrial ATP synthesis is increased and heat is generated. Apelin significantly activates AMPK via Gαq, then increases glucose transport by stimulating GLUT4 and GLUT1 in the heart and skeletal muscle. By activating PGC-1, exercise training stimulates mitochondrial biogenesis, increases slow-twitch fibers, and increases glucose uptake through GLUT4. Maternal exercise activates AMPK and PGC-1α in fetal muscle and then increases the expression of UCP3 and sarcolipin. This process inhibits the uptake of calcium ions into the sarcoplasmic reticulum, thereby activating CaMKK2 to generate heat through muscle contraction. After exercise, increased PI3k and AKT1 also increase GLUT4 stimulation. In addition, exercise-induced hypoxia may cause glucose transport through GLUT1. Apelin and exercise during pregnancy increase BAT markers, including UCP1, PRDM16, and PGC-1α, and increase the mRNA expression of Ucp1, Ppargc1a, Prdm16, cidea, Elovl3, and Cox7a1. This process increases body metabolism. In rodents, sympathetic stimulation by exercise activates β-adrenergic receptor 3 (β3-AR) and then stimulates BAT activity and WAT browning