Obesity Pathway Not Linked to Insulin

Researchers have identified a molecular pathway activated by entry of nutrients into cells that is independent of the insulin pathway and that can lead to obesity even when the insulin pathway has been shut down.

Investigators at the University of Cincinnati (OH, USA) focused their attention on a molecule called hVPs34. When triggered by nutrients in the form of amino acids, hVPs34 activated the S6K1 (S6 kinase-1) enzyme. This kinase contains two non-identical kinase catalytic domains and phosphorylates several residues of the S6 ribosomal protein. The kinase activity of this protein leads to an increase in protein synthesis and cell proliferation. Amplification of the region of DNA encoding this gene and overexpression of this kinase are seen in some breast cancer cell lines. Details of these findings were published in the September 21, 2005, online edition of The Proceedings of the [U.S.] National Academy of Sciences.

"Insulin and amino acids both play a critical role in growth and development,” said Dr. George Thomas, professor of genome science at the University of Cincinnati. "Both are responsible for ‘driving' all growth. Now we have found that they actually work through independent pathways to trigger a molecule that turns on S6K1. Since we know that S6K1 is linked to obesity and insulin resistance, learning that it can actually be turned on by more than one pathway is important because it represents a potential target to regulate obesity.”




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