Fructose intake may contribute to overeating

Megan Brooks

January 03, 2013

New Haven, CT - Consuming fructose appears to cause changes in the brain that may lead to overeating, a new study suggests [1].

"Increases in fructose consumption have paralleled the increasing prevalence of obesity, and high-fructose diets are thought to promote weight gain and insulin resistance," lead author Dr Kathleen A Page (University of Southern California Keck School of Medicine, Los Angeles; Yale University, New Haven, CT) and colleagues write.

In this study, they showed in healthy volunteers that glucose ingestion resulted in reduced activation of the hypothalamus, insula, and striatum on MRI—areas that regulate appetite, motivation, and reward processing—as well as increased functional connections between the hypothalamic-striatal network and increased satiety. By contrast, fructose ingestion had none of these effects.

"The disparate responses to fructose were associated with reduced systemic levels of the satiety-signaling hormone insulin and were not likely attributable to an inability of fructose to cross the blood-brain barrier into the hypothalamus or to a lack of hypothalamic expression of genes necessary for fructose metabolism," they conclude.

Their findings are published in the January 2, 2013 issue of the Journal of the American Medical Association.

In this study, the researchers used arterial spin labeling MRI to quantify regional cerebral blood flow in 20 healthy normal-weight adult volunteers before and after drinking a 75-g beverage of either pure glucose or fructose. They observed that glucose (but not fructose) ingestion reduced activation of the hypothalamus, insula, and striatum. Glucose ingestion also increased functional connections between the hypothalamic-striatal network and increased ratings of satiety and fullness.

Brain responses were markedly different following ingestion of an equal amount of fructose. Not only did fructose fail to diminish hypothalamic activity, it induced a small, transient increase in hypothalamic activity. The striatum, as with the hypothalamus, also did not deactivate with fructose ingestion, which may cause decreased inhibitory responses. Fructose ingestion was also associated with reduced systemic levels of the satiety-signaling hormone insulin.

"These findings support the conceptual framework that when the human brain is exposed to fructose, neurobiological pathways involved in appetite regulation are modulated, thereby promoting increased food intake," Drs Jonathan Q Purnell and Damien A Fair (Oregon Health & Science University, Portland) write in an accompanying editorial [2].

They say the implications of this study, coupled with mounting evidence from epidemiologic, metabolic-feeding, and animal studies, are that the "advances in food processing and economic forces leading to increased intake of added sugar and accompanying fructose in US society are indeed extending the supersizing concept to the population's collective waistlines."

The study was supported in part by g rants from the National Institutes of Health and the Yale Center for Clinical Investigation. The authors and editorialists have disclosed no relev ant financial relationships.


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