1242-P: Effect of Intensity and Duration of Lactation on Postpartum Adiponectin after Gestational Diabetes

Higher circulating adiponectin is associated with insulin sensitivity. Prior studies from pregnancy to 12 mo postpartum suggest that adiponectin is suppressed from mid pregnancy until 6-12 mo postpartum in women practicing exclusive lactation, regardless of glucose tolerance during pregnancy. A decrease in adiponectin during pregnancy and lactation is consistent with physiologic insulin resistance. Therefore, our objective was to determine the relationship between intensity and duration of lactation and the suppression of circulating adiponectin in women after GDM delivery. In this prospective study, we evaluated longitudinal blood samples collected during 2-h 75 g OGTTs at 6 wk (V1 baseline), 1 yr (V2) and 2 yr (V3) postpartum in women with recent GDM and without diabetes (DM) at V1 in the SWIFT study. The outcome variables were change in adiponectin from V1-V2 and V2-V3 stratified by incident DM (Y/N); 4 exposure categories for breastfeeding duration (BF current, BF recent, BF past, BF minimal); covariables: age, BMI, log HOMA-IR, and log HOMA-B at V1 in multivariable regression models. Compared with 6 wk postpartum, at 1 yr postpartum (1) adiponectin was lower in the 4 exposure categories, (2) the magnitude of the decrease in adiponectin was greatest in the BF past versus BF current within incident DM at follow up, (3) the magnitude of the decrease in adiponectin was greatest in the BF recent versus BF current in the group without DM at follow up. From 1 yr to 2 yr postpartum, BF past was the only group with incident DM with an increase in adiponectin.

In conclusion, lactation followed by weaning triggers an accelerated decrease in adiponectin that depends on current DM status. In addition, the 2-year visit captured the greater increases in adiponectin among women who lactated and stopped lactation within months from the assessment. We suggest that low adiponectin during lactation communicates to insulin-dependent tissues that a shift in the priority of glucose utilization has occurred.