Abstract
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). …
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