The Effects of Leptin on Placental Development and Function, and Off05 Behavior in Mice

Pollock, Kelly E.

doi:10.32469/10355/44194

Cited by 1 publication

(2 citation statements)

References 175 publications

(340 reference statements)

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“…The early pregnancy leptin levels were not associated with PW at term in either BMI group, despite that leptin is regarded as an essential hormonal signal during the early stages of pregnancy [ 43 – 49 ]. However, in line with the previous reports [ 50 , 51 ], we observed an inverse association between late-pregnancy leptin and PW in both BMI groups.…”

Section: Discussionmentioning

confidence: 99%

“…This could occur via combined effects on the vascular system and maternal metabolism [ 46 – 48 , 52 , 53 ]. The effects of leptin could differentiate depending on the adipose tissue size and distribution, similar to insulin sensitivity [ 10 , 17 , 43 , 54 – 57 ]. Alternatively, the association could reflect the effects of placental hormones [ 9 – 11 ], which facilitate maternal adipose tissue mobilization towards the term [ 10 , 58 ] and thereby impact maternal leptin levels [ 59 ].…”

Section: Discussionmentioning

confidence: 99%

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Maternal body mass index and placental weight: a role for fetal insulin, maternal insulin and leptin

Kristiansen

Roland

Zucknick

et al. 2022

J Endocrinol Invest

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Purpose Placental weight (PW) has been found to mediate the main effect of maternal BMI on fetal size. Still, the BMI–PW association is poorly understood. Therefore, we aimed to explore potential explanatory variables, including gestational weight gain (GWG), early- and late-pregnancy circulating levels of maternal glucose, insulin, leptin, adiponectin, triglycerides, LDL-C, and HDL-C, and fetal insulin. Methods We included two studies of pregnant women from Oslo University Hospital, Norway: the prospective STORK (n = 263) and the cross-sectional 4-vessel method study (4-vessel; n = 165). We used multiple linear regression for data analyses. A non-linear BMI-PW association was observed, which leveled off from BMI25. Therefore, BMI <25 and ≥25 were analyzed separately (n = 170/122 and 93/43 for STORK/4-vessel). Confounding variables included maternal age, parity, and gestational age. Results PW increased significantly per kg m−2 only among BMI <25 (univariate model’s std.β[p] = 0.233 [0.002] vs. 0.074[0.48]/0.296[0.001] vs. −0.030[0.85] for BMI <25 vs. ≥25 in STORK/4-vessel). Maternal early- but not late-pregnancy insulin and term fetal insulin were associated with PW. The estimated effect of early pregnancy insulin was similar between the BMI groups but statistically significant only among BMI <25 (std.β[p] = 0.182[0.016] vs. 0.203[0.07] for BMI <25 vs. ≥25). Late pregnancy leptin was inversely associated with PW with a 1.3/1.7-fold greater effect among BMI ≥25 than BMI <25 in the STORK/4-vessel. Conclusions The BMI–PW association was non-linear: an association was observed for BMI <25 but not for BMI ≥25. Leptin may be involved in the non-linear association through a placental–adipose tissue interplay. Maternal early pregnancy insulin and fetal insulin at term were associated with PW.

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