Increased plasma leptin in gestational diabetes

Aims/hypothesis. Insulin resistance as well as marked changes in body weigh t and energy metabolism are associated with pregnancy. Its impact on plasma leptin is not known and was determined in this longitudinal study in both diabetic and normal pregnancy. Methods. At 28 gestational weeks plasma concentrations of leptin and B-cell hormones were measured at fasting and after an oral glucose load (OGTT:75 g) in women with gestational diabetes and pregnant women with normal glucos e tolerance and compared with women who were not pregnant (C). Results. Plasma leptin (ng/ml) was higher (p < 0.001) in women with gestati onal diabetes (24.9 +/- 1.6) than in women with normal glucose tolerance (1 8.2 +/- 1.5) and increased in both groups when compared with the non-pregna nt women (8.2 +/- 1,3; p < 0.0005). No change in plasma leptin concentratio ns was induced by OGTT in any group. Basal insulin release was higher (p < 0.05) in women with gestational diabetes compared with the pregnant women w ith normal glucose tolerance. Marked insulin resistance was confirmed by a 20% lower (p < 0.05) insulin sensitivity in subgroup analysis and a decreas e of almost 40% in fasting glucose/insulin ratio (p < 0.005) in women with gestational diabetes. Leptin correlated in women with gestational diabetes with basal plasma concentrations of glucose (p < 0.02), insulin (p < 0.004) and proinsulin (p<0.01) as well as with BMI (p < 0.001) and overall pregna ncy induced maternal weight gain (p < 0.009). With normalisation of blood g lucose 8 weeks after delivery in women with gestational diabetes their plas ma leptin decreased (p < 0.0005) to 17.3 =/- 1.9 ng/ml but did not complete ly normalize (p < 0.05 vs non-pregnant women). Conclusion/interpretation. Our data show that women with gestational diabet es without any change in plasma leptin upon oral glucose loading have incre ased plasma leptin concentrations during and after pregnancy, a clear assoc iation of plasma leptin with the respective concentration of glucose and in sulin resistance as well as with changes in body weight, and a failure to n ormalize spontaneously BMI to the same extent as pregnant women with normal glucose tolerance when compared with matched control subjects.