FETAL GROWTH AND DEVELOPMENT
IN LATE PREGNANCY
The enhanced insulin resistance observed in obese pregnant women increases fetal
exposure to all major fuel sources—glucose, FFAs, ketones, and amino acids. Thus,
it is not surprising that obese mothers deliver LGA infants 1.4 to 1.8 times more
frequently than do lean mothers (37). It is striking that prepregnancy obesity is
independently and strongly associated with LGA, whereas net weight gain during
pregnancy has only a modest effect (72). As described above, maternal obesity is
associated with hyperglycemia and hyperlipidemia during gestation. A large body
of evidence indicates that substrate delivery to the placenta is the primary maternal
factor regulating fetal growth (28).Arise in the flowand/or availability of maternal
substrate levels is thought to decrease the placental release of growth-suppressive
peptides, which enhances fetal growth rates by increasing the expression of insulinlike
growth factors and decreasing their binding proteins (28). Thus, the association
between maternal adiposity and fetal size probably reflects the metabolic shifts in
fuel metabolism in obese compared with nonobese women. This is verified by
that fact that late in the third trimester, when insulin resistance reaches its peak
and circulating glucose levels are the highest, maternal glycemia is more strongly
associated with LGA than is maternal BMI (78). Also, addition of hyperlipidemia
to the presence of hyperglycemia improves the ability to predict the risk of LGA
babies (9), which implies that fetal macrosomia likely results from an increased
supply of lipids as well as glucose.
Exposure to maternal diabetes not only affects fetal size, but also alters fetal
body composition (24, 54). Asymmetric macrosomia (high fetal fat relative to fetal
length) is commonly reported in type 1, type 2, and gestational diabetes and even
with modest elevations of maternal glucose levels (24, 62). This increase in fetal
fatness appears to be specific for women with some degree of glucose intolerance,
as LGA infants born to women with normal glucose tolerance do not seem to have
increased amounts of fetal fat (24). The increase in fetal fat among infants exposed
to maternal diabetes is thought to reflect an increase in fetal glucose supply, which
in turn induces fetal insulin secretion and storage of excess glucose as fat.
A recent study shows that maternal diabetes also alters fetal growth patterns
by reducing chondrogenesis and increasing adipogenesis in specific organs or
tissues (54). In a study of 37 fetuses of diabetic mothers, exposure to diabetes
altered growth patterns of the head, limbs, and abdomen in the second and third
trimesters compared with that of 29 unexposed fetuses. Although a greater abdominal
circumference is well known among macrosomic infants (8), the effect
of diabetes on head and limb proportions has not been observed previously (54).
The occipito-frontal diameter was decreased, the upper limbs were relatively long
compared with lower limbs, and the limb length to limb circumference (volume)
was reduced in the exposed fetuses. It appeared that adipogenesis was given preference
over chondrogenesis in certain tissues among women with elevated levels
of hemoglobin A1c. The authors hypothesize that these unique shifts in the fetal
Annu. Rev. Nutr. 2006.26:271-291. Downloaded from www.annualreviews.org
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MATERNAL OBESITY 283
growth pattern reflect a hyperglycemic/hypoxemic situation. They speculate that
hypoxia results from glycosylated hemoglobin’s increased oxygen affinity making
it less available for maternal-fetal transfer and fetal cellular respiration and that
this hypoxemia in the presence of excess energy from glucose leads to alterations
in fetal growth.
These effects of fetal exposure to hyperglycemia on body size, composition, and
organ/tissue structure help explain why in utero development influences long-term
physiological function and health. Data showing a link between the fetal experience
and subsequent risk for disease have been reviewed extensively elsewhere (4–7, 39,
41); only the impact of maternal obesity or diabetes is mentioned here. Studies have
found that children born to diabetic mothers are at greater risk for becoming obese
(31, 83), developing type 2 diabetes (31, 83), and having the metabolic syndrome
(11). Also, children exposed to maternal obesity withoutGDMare at increased risk
of becoming obese (93) and developing the metabolic syndrome (11). Although
most of the studies to date have focused on the effects of exposure to maternal
diabetes and fetal growth, it appears that maternal obesity per se without diabetes
also alters the metabolic environment and places the child’s postnatal health at risk.
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