Conzen worked closely with colleague Martha McClintock, PhD, professor of psychology at the University of Chicago, to carefully model chronic social stress exposure in female mice. In previous joint projects they showed that a measurable chronic stress response could reliably be induced in mice by raising them in isolation after weaning, rather than housing them in small groups.
In this study, Conzen also worked with colleague, Matthew Brady, PhD, associate professor of medicine and a specialist in fat cell biology, to decipher the effect of stress on the mammary fat.
"By separating fat cells in the breast from the other cell types, we were able to measure expression of genes involved in metabolism in those fat cells and not other fat cells or different cell types from the breast tissue," Brady said.
The researchers looked for differences in gene expression in multiple tissues and circulating hormones between group-housed and isolated mice. To their surprise, there were no significant differences in circulating hormones.
They found a dramatic change, however, in fat cells located within mammary glands. Measurements of those cells taken at 15 weeks of age showed that social isolation stimulated significant increases in the expression of three genesHk2 (hexokinase), Acly (ATP citrate lyase) and Acaca (acetyl-CoA carboxykase).
All three are crucial to the uptake and metabolism of glucose, the primary source of cellular energy. Mammary fat cells in the stressed mice took up about twice as much glucose as the same fat cells from unstressed mice, indicating a significant increase in metabolic activity.
These cells use glucose to synthesize lipidsfatty substances, often used to convey biological signals. Increased fat cell metabolism was associated with increased local secretion of substances such as leptin, an important chemical messenger produced by fat cells. Leptin can stimulate pro
|Contact: John Easton|
University of Chicago Medical Center