The strengths of the present study are identification of resistin as a fetal factor derived from inflammatory cells that is affected by maternal diabetes and demonstration of a role for resistin in inhibiting placental mitochondrial metabolism. Limitations of the present study include the differences in baseline characteristics (including maternal age, maternal BMI, and gestational age) between the control and diabetic groups which could complicate data analysis and interpretation. However, to improve the assessment on their potential effects on resistin levels, these factors were statistically adjusted by the multiple regression analysis which suggested they were unlikely to contribute to the difference of resistin levels between control and diabetic groups. Also, the specific downstream signaling underlying resistin effects on mitochondrial biogenesis and the roles of resistin on other fetal tissues remain to be explored. Four distinct receptors have been identified to bind to resistin, including Toll-like receptor 4 (TLR4), decorin, receptor tyrosine kinase-like orphan receptor 1 (ROR1), and adenylyl cyclase-associated protein 1 (CAP1) (Zhao et al. 2019; Miao et al. 2018; Lee et al. 2014). Resistin/TLR4 has been shown to inhibit AMP activated kinase (AMPK) (Miao et al. 2018; Hardie 2007), an important regulator of mitochondrial biogenesis (Hardie 2007). TLR4 and AMPK inhibition can be the potential mechanism underlying resistin-induced decrease in placental mitochondrial metabolism. However, which of these receptors and the specific downstream pathways responsible for the effects of resistin on mitochondrial metabolism remains to be investigated. In addition, elevated fetal resistin can potentially impact energy metabolism and development of other fetal tissues, such as muscle, which remain to be studied.