The downregulation of RIZ1 activates the AKT/mTOR in pregnant women with obesity

RIZ1表达下调会激活肥胖孕妇体内的AKT/mTOR通路。

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Abstract

Riz1 knockout mice demonstrated obesity with activation of the V-Akt murine thymoma viral oncogene homolog (PKB) (AKT)/mechanistic target of rapamycin (mTOR) pathway. Whether the decrease in RIZ1 and the activation of AKT/mTOR exist in pregnant women with obesity is still unknown. This study examined the association between RIZ1, AKT/mTOR, and obesity through a prospective methodological approach in pregnant women. A total of 260 pregnant women, including 71 lean, 75 normal weight, 56 overweight, and 58 obesity, were enrolled. Pregnant women with obesity had higher baby weights and cesarean section rates, exhibiting the highest rate of irregular meal habits with high-protein and low-vegetable/fruit dietary patterns. The plasma concentration of C0-C5 carnitine decreased gradually from the lean to the obesity group, while the levels of amino acids and C6-C26 carnitines accumulated in overweight individuals. The expression of RIZ1 was reduced in overweight and obesity groups accompanied by AKT/mTOR activation. In addition, RIZ1 inhibited cellular adipogenesis as well as AKT/mTOR molecules in 3T3-L1 cell. This study presented comprehensive data on maternal and fetal characteristics, inhibited RIZ1, and activated AKT/mTOR molecules in pregnant women with overweight and obesity, providing valuable insights into underlying mechanisms of gestational obesity.

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