|Hadsell, Darryl -|
|Hadsell, Louise -|
|Olea, Walter -|
Submitted to: Endocrine Society Meeting
Publication Type: Abstract Only
Publication Acceptance Date: May 15, 2012
Publication Date: June 23, 2012
Citation: Hadsell, D.L., Hadsell, L.A., Olea, W. 2012. An obesity-dependent lactation defect in the viable yellow agouti mouse is associated with mammary inflammation [abstract]. Proceedings of the 94th Annual Meeting and Expo of the Endocrine Society, Session: Obesity Topics, June 23–26, 2012, Houston, Texas. # MON-133. Technical Abstract: Maternal obesity is known to delay lactogenesis in breast-feeding women, as well as negatively impact lactation in other species. Obesity is also understood to be associated with inflammation. Work with the viable yellow agouti (Avy) mouse in our laboratory has documented a lactation defect in obese yellow A(vy) females. The hypothesis for this study was that increased mammary infiltration of inflammatory macrophages is present with the obesity-dependent lactation defect in A(vy) mice. At weaning, female a/A(vy) mice (obese) and their a/a littermates (lean) were allowed ad-libtum access to standard chow until Obese mice reached over 40% body fat at mating. A cohort of a/A(vy) mice was diet restricted (CR) to match the weight of Lean littermates, both of which had less than 16% body fat. At day 1 or 4 postpartum, dams were killed and mammary glands (MG) were harvested. Litter gain and pup survival was lower (P<0.05) in Obese than Lean dams. This defect was rescued by preventing obesity in a/A(vy) females with food restriction. Immunostaining for the macrophage marker F4/80 demonstrated that there was both an increase in macrophages and an increase in the presence of crown-like structures in mammary glands of obese mice. Double-labeling for F4/80 and iNOS showed that the percentage of iNOS-positive macrophages was higher in mammary tissue of obese dams. Real-time PCR on total mammary tissue RNA demonstrated that the mRNA for Lalba and Csn2 were decreased in obese dams, while those for F4/80, Ccl2, and Tnfa were increased. These changes were prevented by preventing obesity through food-restriction. These results support the conclusion that the lactation defect and the presence of mammary inflammation in the A(vy) mouse are due to maternal obesity.