posted on 2020-05-08, 17:23authored byAda AdminAda Admin, Maria A. Ramos-Roman, Majid M. Syed-Abdul, Beverley Adams-Huet, Brian M. Casey, Elizabeth J. Parks
Milk production may
involve a transient development of insulin resistance in non-mammary tissues to
support redistribution of maternal macronutrients to match the requirements of
the lactating mammary gland. In the
present study, adipose and liver metabolic responses were measured in the
fasting state and during a 2-step (10 and 20 mU/m2/min) hyperinsulinemic-euglycemic
clamp with stable isotopes, in 6-week postpartum women who were lactating (n=12)
or formula-feeding (n=6) their infants and who were closely matched for
baseline characteristics (e.g., parity, body composition, intrahepatic lipid). When controlling for the low insulin
concentrations of both groups, the lactating women exhibited a fasting rate of endogenous
glucose production (EGP) that was 2.6-fold greater, and a lipolysis rate that
was 2.3-fold greater than the formula-feeding group. During the clamp, the groups exhibited similar
suppression rates of EGP and lipolysis.
In the lactating women only, higher prolactin concentrations were
associated with greater suppression rates of lipolysis, lower intrahepatic
lipid and plasma triacylglycerol concentrations. These data suggest that whole-body alterations
in glucose transport may be organ specific and facilitate nutrient partitioning
during lactation. Recapitulating a shift
toward noninsulin-mediated glucose uptake could be an early postpartum strategy
to enhance lactation success in women at risk for delayed onset of milk
production.
Funding
American Diabetes Association (1-14-TS-33); National Institutes of Health (R03 DK097463)