Intestinal Pdx1 mediates nutrient metabolism gene networks and maternal expression is essential for perinatal growth
Chin Chen1, Tripp Leavitt, Eric Sibley
1Division of Pediatric Gastroenterology, Stanford University School of Medicine, Stanford, CA 94305-5208, USA.
Insights
The homeodomain transcription factor Pdx1 plays a crucial role in intestinal lipid metabolism. Maternal Pdx1 expression is vital for proper perinatal growth in mice, impacting nutrient metabolism.
Area of Science:
- Molecular Biology
- Developmental Biology
- Metabolism
Background:
- The homeodomain transcription factor Pdx1 is critical for pancreas development and glucose homeostasis.
- Its role in intestinal cells and nutrient metabolism is less understood.
Purpose of the Study:
- To investigate the function and gene networks of Pdx1 in intestinal cells.
- To determine the impact of Pdx1 on nutrient metabolism and perinatal growth.
Main Methods:
- Overexpression of Pdx1 in human Caco-2 intestinal cells.
- Analysis of differentially expressed genes and their functional and network associations.
- Investigation of Pdx1 inactivation effects on maternal and pup growth in mice.
Main Results:
- Pdx1 overexpression in Caco-2 cells led to differential gene expression associated with nutrient metabolism.
- Network analysis identified lipid metabolism gene networks regulated by Pdx1.
- Maternal intestine-specific Pdx1 inactivation resulted in underweight, failing-to-thrive pups.
Conclusions:
- Pdx1 mediates lipid metabolism gene networks within intestinal cells.
- Maternal Pdx1 expression is essential for successful perinatal growth in mice.
Abstract:
The homeodomain transcription factor Pdx1 is essential for pancreas formation and functions in pancreatic islets cells to regulate genes involved in maintenance of glucose homeostasis. In order to investigate a role for Pdx1 in intestinal cells, we analyzed the functions and networks associated with genes differentially expressed by Pdx1 overexpression in human Caco-2 cells. In agreement with previous results for intestine isolated from mice with Pdx1 inactivation, functional analysis of genes differentially expressed with Pdx1 overexpression revealed functions significantly associated with nutrient metabolism. Similarly, network analysis examining the interactions among the differentially expressed genes revealed gene networks involved in lipid metabolism. Consistent with defects in maternal nutrient metabolism, mouse pups born to dams with intestine-specific Pdx1 inactivation are underweight and fail to thrive in the neonatal period compared to pups born to control dams. We conclude that Pdx1 mediates lipid metabolism gene networks in intestinal cells and that maternal expression is essential for perinatal growth in mice.
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