January 2, 2013
Fructose Consumption Promotes Weight Gain And Insulin Resistance
April Flowers for redOrbit.com - Your Universe Onlinemagnetic resonance imaging, which indicated that ingestion of glucose but not fructose reduces cerebral blood flow. Activity in brain regions that regulate appetite was also reduced. The participants reported an increase in feeling sated and full from the ingestion of glucose but not fructose.
"Increases in fructose consumption have paralleled the increasing prevalence of obesity, and high-fructose diets are thought to promote weight gain and insulin resistance. 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," according to the authors. "Thus, fructose possibly increases food-seeking behavior and increases food intake."
Scientists do not fully understand how brain regions associated with fructose- and glucose-mediated changes in animal feeding behaviors translates to humans.
The research team, led by Kathleen A. Page, M.D. of Yale Medical School, studied neurophysiological factors that might underlie the associations between weight gain and fructose consumption. Participants included 20 healthy adults who ingested either a fructose or glucose drink while undergoing two magnetic imaging sessions. The researchers were primarily looking at the relative changes in hypothalamic regional cerebral blood flow (CBF) after consumption of fructose or glucose.
The study found that after glucose, but not fructose, ingestion there was a significantly greater reduction in hypothalamic CBF.
"Glucose but not fructose ingestion reduced the activation of the hypothalamus, insula, and striatum–brain regions that regulate appetite, motivation, and reward processing; glucose ingestion also increased functional connections between the hypothalamic-striatal network and increased satiety."
"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."
The findings of this study were recently published in The Journal of the American Medical Association (JAMA).