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Review

Effects of maternal obesity on early and long-term outcomes for offspring

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Pages 43-53 | Published online: 22 Mar 2014

Figures & data

Figure 1 Placental and adipose tissue physiology in obese pregnancy.

Notes: Macrophage infiltration of the placenta is thought to contribute to increased production of pro-inflammatory cytokines (TNF-α and IL-6). These contribute to increased insulin resistance and increased lipolysis. The increase in plasma fatty acids as a result of lipolysis also increases insulin resistance. Altered transport of nutrients in obese pregnancy may include: increased glucose transport (via increased insulin resistance), increased amino acid transport (via pro-inflammatory cytokines) and increased lipid transport (via fat mobilization).
Abbreviations: IL, interleukin; TNF, tumor necrosis factor.
Figure 1 Placental and adipose tissue physiology in obese pregnancy.

Figure 2 Placental modifications in obese pregnancy.

Notes: In obese pregnancy, reduced placental cell turnover (as demonstrated by lower detected levels of apoptosis marker) (cytokeratin M30) may contribute to overall larger size of placenta. Alterations of vessel muscularity and vasodilatation properties may affect placental oxygen and nutrient transport and place the fetus at risk. A higher rate of maternal inflammatory response lesions (consistent with chorioamnionitis) has also been reported.
Figure 2 Placental modifications in obese pregnancy.

Table 1 Increased risk of congenital malformations in obese pregnancy