Sugar cravings may be common, but the physiological mechanisms that trigger a “sweet tooth” are not well understood.
A University of Iowa-led study in mice shows that a hormone produced by the liver, fibroblast growth factor 21 (FGF21), suppresses the consumption of simple sugars. The study, published Dec. 24, 2015, in Cell Metabolism, found that FGF21 is produced in the liver in response to high carbohydrate levels. FGF21 then enters the bloodstream, where it sends a signal to the brain to suppress the preference for sweets.
When normal mice are injected with FGF21 and given the choice between a normal diet and a sugar-enriched diet, they don’t completely stop eating sugar, but they eat seven times less than usual.
Additionally, genetically modified mice that don’t produce any FGF21 eat more sugar than normal mice, while modified mice that produce an excess of FGF21 (over 500 times more than normal mice) eat less sugar.
The research could lead to molecular therapies to improve diets and help patients who are obese or have diabetes.
. . . and another boosts physical endurance
It’s well known that exercise improves muscle performance, but the molecular underpinnings of this relationship are only partly understood.
Working with mice, University of Iowa researchers have found that exercise prompts muscles to release a peptide, which then acts to increase the muscle’s exercise tolerance. These findings establish the peptide, called musclin, as an “exercise factor”—a hormone-like substance made by skeletal muscle in response to exercise and released into the bloodstream. Increased levels of circulating musclin trigger a signaling cascade that improves muscle performance by promoting the production of mitochondria in muscle cells. The study was published online the week of Dec. 14, 2015, in the Proceedings of the National Academy of Sciences Early Edition.