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Mammary Inflammation and Hypoxia During Lactogenesis in the Obese Viable Yellow Agouti (Avy) Mouse
Author(s) -
Hadsell Darryl,
Tong Junfeng,
Olea Walter,
Draper Patricia,
Hadsell Louise
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.590.6
To understand how obesity impairs lactation we studied lactogenesis in the A vy mouse. 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 reach over 40% body fat at mating. A cohort of a/A vy mice was diet restricted to match the weight of Lean littermates, both of which had less than 16% body fat. At day 4 or day 10 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. The defect was rescued by preventing obesity in A vy females with food restriction. At day 4 postpartum, MG of Obese dams were heavier (P<0.05) than Lean, but total epithelial area as measured in H&E‐stained tissue sections was similar between the two groups. Mammary adipocytes of Obese dams were larger in diameter than that of Lean dams. Mammary tissue from Obese dams also exhibited increased (P<0.05) mRNA abundance for Hif1a , Hmox1, and Mcp1, and had higher (P<0.05) numbers of macrophages. Our results suggest that defective lactation in obese A vy mice is linked to mammary gland hypoxia and increased intra‐mammary residence of inflammatory cells. This project was funded by a grant from NICHD # 1 R21 HD056439‐01A2/02.