Food and Behaviour Research

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Liver glycogen reduces food intake and attenuates obesity in a high-fat diet-fed mouse model.

López-Soldado I, Zafra D, Duran J, Adrover A, Calbó J, Guinovart JJ (2014) Diabetes    pii: DB_140728. [Epub ahead of print] 

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We generated mice that overexpress protein targeting to glycogen (PTG) in the liver (PTGOE), which results in an increase in liver glycogen. When fed a high-fat diet (HFD), these animals reduced their food intake. The resulting effect was a lower body weight, decreased fat mass and reduced leptin levels. Furthermore, PTG overexpression reversed the glucose intolerance and hyperinsulinemia caused by the HFD and protected against HFD-induced hepatic steatosis. Remarkably, when fed a HFD, PTGOE mice did not show the decrease in hepatic ATP content observed in control animals and had lower expression of neuropeptide Y (NPY) and higher expression of propiomelanocortin (POMC) in the hypothalamus. Additionally, after an overnight fast, PTGOE animals presented high liver glycogen content, lower liver triacylglycerol content, and lower serum concentrations of fatty acids and β-hydroxybutyrate compared to control mice, regardless whether they received a HFD or a standard diet (SD). In conclusion, liver glycogen accumulation caused a reduced food intake, protected against the deleterious effects of a HFD and diminished the metabolic impact of fasting.

Therefore, we propose that hepatic glycogen content be considered a potential target for the pharmacological manipulation of diabetes and obesity.


Please see the related news item here:

13 November 2014 - Science Daily - Liver, brain communicate in order to regulate appetite