Aye et al. recently proposed a C57BL/6J mouse model of maternal diet-induced obesity, which was associated with maternal glucose intolerance, decreased circulating levels of high molecular weight adiponectine (ADN), and fetal overgrowth, and considered it was clinically relevant in testing the hypothesis that ADN supplementation prevents the changes in placental function and fetal overgrowth associated with maternal obesity (1).
The authors compared three groups of pregnant animals: lean mice on a control diet infused with vehicle (C/PBS), obese mice infused with vehicle (OB/PBS), and obese mice with infusion of ADN (OB/ADN), and they indeed observed that ADN supplementation completely reversed or normalized excessive fetal growth, placental glucose and amino acid transport, and insulin/mechanistic target of rapamycin complex1 signaling (1).
However, the changes in fetal weight and placental function were not associated with differences in placental weight or fetal/placental weight ratio, which is usually considered as a proxy for placental efficiency. Fetal/placental weight ratio was even slightly increased in the OB/PBS group, although the difference was not significant, in contrast with the findings of Lager et al. (2), who demonstrated in the same model that fetal/placental weight ratio was lower in obese dams (P < 0.01), in accordance with similar findings in overweight, obese, and morbidly obese pregnant women (3).
Because lower values of fetal/placental weight ratio in pregnant women are associated with a higher rate of placental lesions (4), and with both maternal prepregnancy body mass index (3, 4) and adverse obstetric outcomes (3–5), the absence of differences in fetal/placental weight ratio between OB and control groups of Aye et al.’s (1) study could raise a serious issue about the validity of this mouse model.
Footnotes
The author declares no conflict of interest.
References
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