August 2020 

The prevalence of obesity continues to increase worldwide due to changes in dietary composition including the addition of sweetners to many food products  and evolving patterns of eating behaviors. In particular, excessive consumption of sugars has been linked to metabolic diseases such as diabetes, insulin resistance and type 2 diabetes. Fibroblast growth factor 21 (FGF21) is a liver-derived hormone that signals to the brain to reduce sugar intake, but the mechanism for this effect was unknown. This new study by Ph.D. student Sharon Jensen-Cody and other colleagues in the laboratory of Matt Potthoff, Associate Professor in the Fraternal Order of Eagles Diabetes Center and Department of Pharmacology and Neuroscience discovered that FGF21 signals to specific nerve cells  called glutamatergic neurons in the brain to lower sugar intake and sweet-taste preference. Interestingly, the researchers demonstrate that FGF21 signals to specific neurons in a small part of the brain called the hypothalamus to lower sugar intake by enhancing their sensitivity to glucose. These findings provide important new insights into how FGF21 functions to regulate dietary preferences and treat metabolic disease.

Importantly, from a therapeutic perspective, this breakthrough by the Potthoff laboratory raises the interesting possibility that molecular therapies could be developed to treat obesity and type 2 diabetes by improving dietary choices. Specifically, their work provides a potential approach to decrease appetite for sweets (desserts)...basically the CHANTIX for sweets...