Developmental cigarette smoke exposure II: Hepatic proteome profiles in 6 month old adult offspring.
Utilizing a mouse model of 'active' developmental cigarette smoke exposure (CSE) [gestational day (GD) 1 through postnatal day (PD) 21] characterized by offspring low birth weight, the impact of developmental CSE on liver proteome profiles of adult offspring at 6 months of age was determined. Liver tissue was collected from Sham- and CSE-offspring for 2D-SDS-PAGE based proteome analysis with Partial Least Squares-Discriminant Analysis (PLS-DA). A similar study conducted at the cessation of exposure to cigarette smoke documented decreased gluconeogenesis coupled to oxidative stress in weanling offspring. In the current study, exposure throughout development to cigarette smoke resulted in impaired hepatic carbohydrate metabolism, decreased serum glucose levels, and increased gluconeogenic regulatory enzyme abundances during the fed-state coupled to decreased expression of SIRT1 as well as increased PEPCK and PGC1α expression. Together these findings indicate inappropriately timed gluconeogenesis that may reflect impaired insulin signaling in mature offspring exposed to 'active' developmental CSE.
Department of Environmental and Occupational Health Sciences, School of Public Health and Information Sciences, University of Louisville, Louisville, KY, United States; Birth Defects Center, University of Louisville, Louisville, KY, United States. Electronic address: rachel.neal@louisville.edu.
Rachel E
RE
Neal
Department of Environmental and Occupational Health Sciences, School of Public Health and Information Sciences, University of Louisville, Louisville, KY, United States.
Jing
J
Chen
Department of Molecular, Cellular, and Craniofacial Biology, ULSD, University of Louisville, Louisville, KY, United States.
Cindy
C
Webb
Department of Environmental and Occupational Health Sciences, School of Public Health and Information Sciences, University of Louisville, Louisville, KY, United States.
Kendall
K
Stocke
Department of Environmental and Occupational Health Sciences, School of Public Health and Information Sciences, University of Louisville, Louisville, KY, United States.
Caitlin
C
Gambrell
Department of Molecular, Cellular, and Craniofacial Biology, ULSD, University of Louisville, Louisville, KY, United States; Birth Defects Center, University of Louisville, Louisville, KY, United States.
Robert M
RM
Greene
Department of Molecular, Cellular, and Craniofacial Biology, ULSD, University of Louisville, Louisville, KY, United States; Birth Defects Center, University of Louisville, Louisville, KY, United States.
M Michele
MM
Pisano
D000450:Aldosterone / Q000378:metabolism; D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D050260:Carbohydrate Metabolism; D003598:Cytoskeletal Proteins / Q000378:metabolism; D005260:Female; D005978:Glutathione / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D050356:Lipid Metabolism; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D018811:Maternal Exposure / Q000009:adverse effects; D008431:Maternal-Fetal Exchange; D008810:Mice, Inbred C57BL; D018384:Oxidative Stress; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced*; D020543:Proteome / Q000187:drug effects*; D012906:Smoke / Q000009:adverse effects*; D062789:Tobacco Products; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*
D000596:Amino Acids; D001786:Blood Glucose; D003598:Cytoskeletal Proteins; D020543:Proteome; D012906:Smoke; D014028:Tobacco Smoke Pollution; D000450:Aldosterone; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D005978:Glutathione
Cigarette smoke; Developmental; Liver; Murine; Proteome; Tobacco