title: LPS-induced inflammation downregulates mammary gland glucose, fatty acid, and L-carnitine transporter expression at different lactation stages.
abstract: Glucose, fatty acids, and L-carnitine are important substrates that support mammary epithelial cell metabolism, biosynthetic capacity, and milk yield and composition. Our study investigated the effects of LPS-induced inflammation on the expression of several glucose, fatty acid, and L-carnitine transporters in the lactating rat mammary gland at different lactation stages. Day 4, 11, and 18 lactating rats (n=3/treatment) were administered LPS (1 mg/kg) or saline by intraperitoneal (i.p.) injection. Fold differences in the mRNA expression of glucose transporters Glut1, Glut8 and Sglt1, fatty acid transporters Fatp1, Fatp4 and Fabp3, and L-carnitine transporters Octn1, Octn2, and Octn3 were determined using the Comparative C(T) method. The mRNA expression levels of all transporters evaluated, except Fatp4 and Octn2 were markedly higher in mammary gland at lactation day 11 compared to lactation day 4. LPS caused a marked decrease in transporter mRNA expression at each lactation stage except for Octn3 and Fatp1, which were markedly increased with LPS administration at lactation day 4, and Sglt1, which was slightly increased at day 11 of lactation. Our results suggest LPS-induced inflammation generally downregulates glucose, fatty acid, and L-carnitine transporter expression. Whether such changes lead to reductions in transporter substrate availability to the lactating mammary epithelial cell requires investigation since decreases in the availability of these nutrients may significantly impact mammary epithelial function and milk quality and yield.
authors.affiliation: College of Pharmacy and Nutrition, University of Saskatchewan, 110 Science Place, Saskatoon, Saskatchewan, Canada S7N5C9.
authors.forename: Binbing
authors.initials: B
authors.lastname: Ling
authors.forename: Jane
authors.initials: J
authors.lastname: Alcorn
mesh_terms: D000818:Animals; D015536:Down-Regulation; D005227:Fatty Acids / Q000378:metabolism; D005260:Female; D005786:Gene Expression Regulation / Q000502:physiology; D005947:Glucose / Q000378:metabolism; D007249:Inflammation / Q000139:chemically induced*; D007774:Lactation / Q000502:physiology*; D008070:Lipopolysaccharides / Q000633:toxicity*; D008321:Mammary Glands, Animal / Q000378:metabolism*; D008413:Mastitis / Q000139:chemically induced* / Q000378:metabolism; D027701:Organic Cation Transport Proteins / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D000074058:Solute Carrier Family 22 Member 5
chemical_list: D005227:Fatty Acids; D008070:Lipopolysaccharides; D027701:Organic Cation Transport Proteins; D012333:RNA, Messenger; C115441:Slc22a5 protein, rat; D000074058:Solute Carrier Family 22 Member 5; D005947:Glucose