Ever since the discovery of insulin, it has been considered the primary means of treating diabetes. A recent study by scientists from the Salk Institute discovered a second molecule, fibroblast growth factor 1 (FGF1) which is produced in the fat tissue and shares a similarity in its function with insulin in regulating blood glucose.

The study got published in ‘Cell Metabolism’ and explains the anti-diabetic property of fibroblast growth factor 1 (FGF1) mediated by the adipose FGF receptor (FGFR) 1. The hormone FGF1 regulates blood glucose by inhibiting fat breakdown (lipolysis). Like insulin, FGF1 controls blood glucose by inhibiting lipolysis. FGF1 also regulates the production of glucose in the liver, as insulin does. These similarities led the group to wonder if FGF1 and insulin use the same signaling (communication) pathways to regulate blood glucose. It is well documented that insulin suppresses lipolysis through PDE3B, an enzyme that initiates a signaling pathway, so the team tested a full array of similar enzymes, with PDE3B at the top of their list. But the study results showed that FGF1 uses a different pathway, the PDE4.

"This mechanism is basically a second loop, with all the advantages of a parallel pathway. In insulin resistance, insulin signaling is impaired. However, with a different signaling cascade, if one is not working, the other can. That way you still have the control of lipolysis and blood glucose regulation," says first author Gencer Sancar.

Identifying the PDE4 pathway creates new opportunities for drug discovery and basic research focused on high blood glucose (hyperglycemia) and insulin resistance.

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