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Fructose Effects in Brain May Contribute to Overeating
Megan Brooks, Jan 02, 2013
Consuming fructose appears to cause changes in the brain that may lead to overeating, a new study suggests.
“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 Kathleen A. Page, MD, and colleagues from Yale University in New Haven, Connecticut, write.
In this study, they showed in healthy volunteers that although 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. 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 issue of the Journal of the American Medical Association.
Glucose vs Fructose
Fructose ingestion produces smaller increases in circulating satiety hormones compared with glucose ingestion, and central administration of fructose provokes feeding in rodents, whereas centrally administered glucose promotes satiety, the authors write. “Thus, fructose possibly increases food-seeking behavior and increases food intake.”
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 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 after ingestion of an equal amount of fructose. Not only did fructose fail to diminish hypothalamic activity, but it also 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,” Jonathan Q. Purnell, MD, and Damien A. Fair, PhD, from Oregon Health & Science University, Portland, write in an accompanying editorial.
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 U.S. society are indeed extending the supersizing concept to the population’s collective waistlines.”
The study was supported in part by grants from the National Institutes of Health and the Yale Center for Clinical Investigation. The authors and editorialists have disclosed no relevant financial relationships.
JAMA. 2013;309:63-70, 85-86. Abstract Editorial