Fructose metabolism by the brain increases food intake and obesity

Amsterdam, 25 March 2009 – The journal Biochemical and Biophysical Research Communications (http://www.elsevier.com/locate/ybbrc) (BBRC), published by Elsevier, will publish an important review this week online, by M. Daniel Lane and colleagues at Johns Hopkins, building on the suggested link between the consumption of fructose and increased food intake, which may contribute to a high incidence of obesity and Type 2 diabetes.

Over the past four decades life-styles have gravitated toward the excessive consumption of ‘high energy’ foods and sedentary behavior that has resulted in a high incidence of obesity and its pathological consequences. This scenario has led to the increased occurrence of insulin resistance and Type 2 diabetes. At present, approximately thirty percent of adult Americans can be classified as obese. Moreover, these changes now extend into the younger age group.

M. Daniel Lane and co-workers at The Johns Hopkins University School of Medicine in Baltimore have now pulled together work, largely in their laboratory (many papers beginning in 2000), dealing with the role of malonyl-CoA in the signaling system in the brain (specifically the hypothalamus) that has inputs into the higher brain centers that determine feeding behavior, most notably appetite. Two papers in the journal PNAS in 2007 and 2008 showed that glucose and fructose act quite differently in the brain (hypothalamus) – glucose decreasing food intake and fructose increasing food intake. Both of these sugars signal in the brain through the malonyl-CoA signaling pathway and have inverse effects on food intake.

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