Aims/hypothesis: Insulin resistance and type 2 diabetes risk in human subjects who were small-for-gestationalage (SGA) at birth may be a consequence of rapid early
postnatal weight gain. Materials and methods: We prospectively studied early changes in fasting insulin sensitivity
and insulin secretion, assessed by a short intravenous glucose tolerance test that was conducted several times from
birth to 3 years of age in 55 SGA (birthweight below fifth
percentile) newborns and in 13 newborns with a birthweight appropriate for gestational age (AGA). Results:
Most SGA infants showed postnatal upward weight centile
crossing and by 3 years were similar in size to AGA infants.
SGA infants had lower pre-feed insulin levels at postnatal
age 48 h than AGA infants (median 34.4 vs 59.7 pmol/l,
p<0.05), but by the age of 3 years they had higher fasting
insulin levels (median 38.9 vs 23.8 pmol/l, p<0.005),
which were related to rate of weight gain between 0 and 3
years (r=0.47, p=0.0003). First-phase insulin secretion did
not differ between SGA and AGA infants, but SGA infants
had a lower glucose disposition index (beta cell compensation) (median 235 vs 501 min mmol−1 l
−1
, p=0.02), which
persisted after allowing for postnatal weight gain (p=0.009).
Conclusions/interpretation: SGA infants showed a marked transition from lower pre-feed insulin and increased insulin
sensitivity at birth to insulin resistance over the first 3 years of
life. This transition was related to rapid postnatal weight gain,
which could indicate a propensity to central fat deposition.
The additional observation of reduced compensatory beta
cell secretion underlines the need for long-term surveillance
of glucose homeostasis in all SGA subjects, whether or not
they show postnatal catch-up growth.