Plasma Glucose, Insulin, Glucagon and Prolactin during Long Lasting Lactation

Hennart, P; Leclercq, Valérie; Delogne-Desnoeck, J.; Robyn, Claude

doi:10.1055/s-2007-1014929

Cited by 3 publications

(1 citation statement)

References 7 publications

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“…Prolactin is critical for the initiation of lactation, and its concentrations will decrease with time postpartum in all lactating women regardless of lactation intensity (48). Higher prolactin concentrations have been associated with lower adiponectin and insulin concentrations as well as lower insulin secretion rates during the postpartum period (5,13,49,50). The low adiponectin levels observed here further support the concept of peripheral insulin resistance, as has been shown in the general population (51).…”

Section: Postpartum Hormonessupporting

confidence: 77%

Lactation Versus Formula Feeding: Insulin, Glucose, and Fatty Acid Metabolism During the Postpartum Period

et al. 2020

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Milk production may involve a transient development of insulin resistance in nonmammary tissues to support redistribution of maternal macronutrients to match the requirements of the lactating mammary gland. In the current study, adipose and liver metabolic responses were measured in the fasting state and during a two-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, and 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 and 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.

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