Mancini pointed to a population of cells with high lipid levels and low levels of PPAR gamma. There were cells with the opposite situation.

Hartig said reduced levels of SRC-2 and 3 resulted in more cells with low levels of lipid and increased PPAR gamma.

This is important because some drugs used to treat type 2 diabetes increase the activity of PPAR gamma. These include the thiazolidines such as Actos and Avandia, which increase the levels of genes associated with sensitivity to insulin. However, because PPAR gamma stimulates fat cell production, these drugs can also lead to increased abdominal fat and, more recently, cardiovascular complications.

"If you could find a way to increase the proportion of cells that have PPAR gamma but don't accumulate lipids, you might have a positive outcome. That would probably require a drug with a different structure," said Mancini.

The automated microscopy makes it possible to monitor the effects of drugs on different populations of a large number of cells, said Mancini.

"Had we not been able to analyze the cell-to-cell differences, we would not necessarily have understood how this favorable switch controlling PPAR gamma transcriptional activity might manifest itself. Identification of compounds that target the SRC and PPAR gamma interface might be alternatives to current therapeutic strategies for type 2 diabetes," said Hartig.

Source: Baylor College of Medicine