Overweight is associated with impaired beta-cell function during pregnancy: a longitudinal study of 553 normal pregnancies.
OBJECTIVE
To monitor beta-cell function and insulin sensitivity longitudinally in a large cohort of pregnant women to elucidate mechanisms that influence glycemic control in pregnancy.


METHODS
Five hundred and fifty-three pregnant Scandinavian women underwent 75 g oral glucose tolerance test (OGTT) at weeks 14-16 and 30-32. Insulin sensitivity (Matsuda index) and beta-cell function (ratio of AUC(insulin) to AUC(glucose), AUC(ins/glc)) were calculated from 520 complete tests, and subsequently beta-cell function was adjusted for insulin sensitivity, rendering an oral disposition index (DI(o)).


RESULTS
Eleven women (2.1%) had gestational diabetes mellitus (GDM1) at weeks 14-16, and 49 (9.4%) at weeks 30-32 (GDM2), which is higher than that previously reported in this region. In the subdivision of OGTT, more overweight (body mass index>25) was found in glucose-intolerant groups (glucose-tolerant women (normal glucose tolerance, NGT) 38 versus GDM2 women 58 and GDM1 women 82%, P<0.005). In early pregnancy, insulin sensitivity was lowest in GDM1, intermediate in GDM2, and highest in NGT. In late pregnancy, insulin sensitivity decreased in all groups, most in gestational diabetes. beta-cell function demonstrated minor shifts during pregnancy, but when adjusted for decreasing insulin sensitivity, DI(o) levels fell by 40% (P<0.001). DI(o) was significantly attenuated relative to glucose intolerance (GDM1 25% and GDM2 53%) during pregnancy. In overweight women, DI(o) levels were lower throughout pregnancy (P<0.001 versus normal weight women), this reduction was significant (P<0.01) in both NGT (21-25%) and GDM2 subjects (26-49%).


CONCLUSIONS
beta-cell function adjusted for insulin sensitivity (DI(o)) deteriorated during pregnancy in both glucose-tolerant and glucose-intolerant women. The failure to compensate the decrease in insulin sensitivity was accentuated in overweight women.
Department of Endocrinology, Rikshospitalet, Oslo University Hospital, Oslo, Norway.
E
E
Qvigstad
N
N
Voldner
K
K
Godang
T
T
Henriksen
J
J
Bollerslev
D000328:Adult; D015331:Cohort Studies; D016640:Diabetes, Gestational / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D005260:Female; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D050417:Insulin-Secreting Cells / Q000473:pathology / Q000502:physiology*; D008137:Longitudinal Studies; D050177:Overweight / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D011247:Pregnancy; D011446:Prospective Studies; D055815:Young Adult