Using normal human lung cells and precancerous human lung cells at the beginning stages of cancer, researchers fed the cells either normal or reduced level s of glucose (sugar).   They found the normal cells lived longer and the precancerous cells died when given less glucose.
The scientists also measure gene activity under these same conditions and found the normal cells that received reduced glucose had higher activity of the gene that dictates the level of telomerase.  Telomerase extends the cells lifespan by lowering the activity of the gene p16 that slows their growth.
Gerald Weissmann, M.D. Editor in Chief of the FASEB Journal said “This study confirms that we are on the path to persuading human cells to let us to live longer, and perhaps cancer free, lives.”
http://www.sciencedaily.com/releases/2009/12/091222105219.htm 

Researchers have already treated cancer and cardiovascular disease by developing drugs that increase or decrease growth factors.  Growth factors are proteins that stimulate growth and typically act as signaling molecules between cells.

Abnormalities in the number and shape of dendritic spines, the protrusions that allow communication between brain neurons have been implicated in some developmental disorders.  Previous studies have found that the growth factor, BDNF (brain derived neurotrophic factor) regulates the number and shape of dendritic spines required for spatial learning and memory.

When researchers from Georgetown University Medical Centre halted the transport of BDNF to dendritic spines, it caused dendritic spine abnormalities in mice that resembled those in humans with certain developmental disorders, they also had impaired learning and memory.

BDNF plays a key role in the regulation, survival, growth and maintenance of neurons.  A study in 2006 found that BDNF is released from the brain and is inhibited by high blood glucose levels, but interestingly not by high insulin levels.

We know that brain function is better when blood glucose is stable and can argue that this relationship of regulation between blood glucose and BDNF could be one of the reasons.  It also strengthens the case for maintaining stable blood glucose during pregnancy whether you have gestational diabetes or not.

Researchers hope to develop drugs that will increase the transport of BDNF to treat developmental disorders.

http://www.sciencedaily.com/releases/2009/10/091020161950.htm

http://docs.google.com/gview?a=v&q=cache:4oMaH5CK75IJ:inflammation-metabolism.dk/misc/download.php%3Furl%3D../files/reprints/PMID%252017151862.pdf%26type%3Dtxt+BDNF+insulin&hl=en&gl=au&pid=bl&srcid=ADGEESgn8a2FCxdG11aifqoZC6gU-Gwh4G8sLvmP8oLjCwCZJrJTHamb3tCI2dlfLmUnQ6r5pLR30wIw_wOl4nm7f8MD0fbmmXtw80iaIWgwd8ksCLWURg0GvTV0inU2-iae-wmEM2y0&sig=AFQjCNEVSfHhXbKHY0k6LbMKHN-nZRWs8w