Associations between GDF15 expression and beta cell function
during and after pregnancy
Associations between GDF15 and pregnancy induced increases in insulin
resistance and beta cell function from T1-T3 are shown in Table 2. In
this model (adjusted for BMI, age and gestational age), absolute levels
of GDF15 at T2 and T3 and increases in GDF15 between trimesters
associated with the increase in HOMA-B (Table 2). For unadjusted
correlations within groups, there were also significant associations
between increases in HOMA-B and GDF15, although the timing differed
slightly between groups. In NW, HOMA-B increase associated with GDF15 at
T2 (R= 0.467, p = 0.016) and with GDF15 change T2 to T3 (R=
0.394, p = 0.046). In OB, HOMA-B increase associated with GDF15
change T1 to T2 (R= 0.664, p < 0.001) and with change
in GDF15 T1 toT3 (R= 0.388, p = 0.046).
Fasting blood glucose decreased significantly late in pregnancy
(p = 0.008). This decrease between T2 and T3 was inversely
associated with changes in GDF15 from T1 to T2 and from T2 to T3 (Fig.
2).
Since GDF15 levels did not change significantly between time points
after pregnancy (Fig. 1A), associations between measures of glucose
metabolism and changes in GDF15 after pregnancy were not deemed
relevant. Only associations for absolute values at 6, 12, and 18 months
were investigated. GDF15 did not correlate with HOMA-IR or HOMA-B at 6
or 12 months. At 18 months, however, GDF15 was significantly associated
with HOMA-B (beta= 0.301, p = 0.039) and HOMA-IR (beta= 0.304,p = 0.009) among all women after adjustment for maternal age and
BMI. In subgroup analyses, GDF15 associated significantly with HOMA-B in
NW (beta= 0.424 ,p = 0.031) and with HOMA-IR in OB (beta= 0.587,p = 0.048).