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ARS Home » Southeast Area » Little Rock, Arkansas » Microbiome and Metabolism Research Unit » Research » Publications at this Location » Publication #288934
Title: Maternal obesity leads to an inflammatory response and insulin resistance in ovarian tissue

Author
item RUEBEL, MEGHAN - Arkansas Children'S Nutrition Research Center (ACNC)
item SHANKAR, KARTIK - Arkansas Children'S Nutrition Research Center (ACNC)
item Badger, Thomas
item ANDRES, ALINE - Arkansas Children'S Nutrition Research Center (ACNC)

Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: 2/13/2013
Publication Date: 4/15/2013
Citation: Ruebel, M.L., Shankar, K., Badger, T.M., Andres, A. 2013. Maternal obesity leads to an inflammatory response and insulin resistance in ovarian tissue [abstract]. FASEB Journal. 27(Meeting Abstracts):109.5.

Interpretive Summary:

Technical Abstract: Maternal obesity during the pre-conception period may influence ovarian functions and affect embryo development. Lean and obese (OB) Sprague-Dawley dams were examined during the preimplantation period at dpc 4.5. Obesity was induced by controlled overfeeding (40% excess calories for 28 d) via total enteral nutrition. Hormonal and metabolic parameters and ovarian gene expression were assessed. OB dams (n=7) had significantly higher body weight, greater fat mass and lesser lean mass compared to lean dams (n=10). OB dams also displayed elevated serum concentrations of triglycerides, total cholesterol, NEFA, insulin, leptin, and CCL2 (p<0.05) compared to lean dams. Microarray analysis of ovaries showed that obesity led to a down regulation of 226 genes and an up regulation of 58 genes, with an increase of several pro-inflammatory chemokines and cytokines and down-regulation of insulin-regulated pathways. Confirmation by real-time qPCR indicated elevated ovarian expression of CCL2, CXCL10, and CXCL11 (p<0.05) and decreased expression of GLUT4 (p<0.05) in OB dams compared to lean dams. In conclusion, increased maternal adiposity was associated with inflammation and reduced glucose transport in the ovaries, which may lead to dysfunction of the follicular environment and possibly impact oocyte and embryo development.