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Published on: February 12, 2015
Developmental cigarette smoke exposure II: Hepatic proteome profiles in 6 month old adult offspring
Rachel E Neal1, Jing Chen2, Cindy Webb3
1Department 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.
Insights
Developmental cigarette smoke exposure (CSE) in mice led to low birth weight and impaired liver function in adulthood. This study reveals altered carbohydrate metabolism and potential insulin signaling issues in adult offspring exposed to CSE.
Area of Science:
- Toxicology
- Metabolism
- Proteomics
Background:
- Developmental exposure to cigarette smoke (CSE) can impact offspring health.
- Previous studies noted decreased gluconeogenesis and oxidative stress in weanling offspring post-CSE cessation.
Purpose of the Study:
- To investigate the long-term effects of developmental CSE on the liver proteome of adult mice.
- To determine the impact of CSE on hepatic carbohydrate metabolism and related regulatory pathways.
Main Methods:
- A mouse model of active CSE from gestational day 1 to postnatal day 21.
- Liver tissue analysis using 2D-SDS-PAGE and Partial Least Squares-Discriminant Analysis (PLS-DA).
Main Results:
- CSE offspring exhibited impaired hepatic carbohydrate metabolism and decreased serum glucose levels at 6 months of age.
- Increased abundances of gluconeogenic enzymes (PEPCK, PGC1α) and decreased SIRT1 expression were observed.
- Findings suggest inappropriately timed gluconeogenesis in adult offspring.
Conclusions:
- Developmental CSE disrupts normal liver function and carbohydrate metabolism in adult mice.
- Altered enzyme expression indicates potential disruptions in insulin signaling pathways.
- CSE exposure during development has lasting detrimental effects on metabolic health.
Abstract:
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.
