January 02, 2013
Fructose Versus Glucose, The Brain, Obesity

The scientific debate continues to rage about whether a sharp rise in fructose consumption is responsible for the obesity epidemic. The latest round: glucose but not fructose causes a change in the area of the brain that regulates appetite.

CHICAGO – In a study examining possible factors regarding the associations between fructose consumption and weight gain, brain magnetic resonance imaging of study participants indicated that ingestion of glucose but not fructose reduced cerebral blood flow and activity in brain regions that regulate appetite, and ingestion of glucose but not fructose produced increased ratings of satiety and fullness, according to a preliminary study published in the January 2 issue of JAMA.

"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 background information in the article.

After drinking a soda or something else with high fructose corn syrup do you find yourself engaging in food-seeking behavior? Homo Americanus was characterized by fanatical food-seeking behavior and left behind recently discovered food preparation structures known as "fast food restaurants". Anthropologists hypothesize these structures were the cause of species extinction.

"Thus, fructose possibly increases food-seeking behavior and increases food intake." How brain regions associated with fructose- and glucose-mediated changes in animal feeding behaviors translates to humans is not completely understood.

I can see it now: Chocolates marketed with pure glucose sweetener for appetite control. Free of sucrose and corn syrup. I'm up for experimentation. How about you?

Kathleen A. Page, M.D., of Yale University School of Medicine, New Haven, Conn., and colleagues conducted a study to examine neurophysiological factors that might underlie associations between fructose consumption and weight gain. The study included 20 healthy adult volunteers who underwent two magnetic resonance imaging sessions in conjunction with fructose or glucose drink ingestion. The primary outcome measure for the study was the relative changes in hypothalamic (a region of the brain) regional cerebral blood flow (CBF) after glucose or fructose ingestion.

The researchers found that there was a significantly greater reduction in hypothalamic CBF after glucose vs. fructose ingestion. "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."

It'll take too long to genetically reengineer our hypothalamus genes to use fructose as an appetite suppression signal. We need pure glucose sweets.

Share |      Randall Parker, 2013 January 02 08:27 PM 

Nanonymous said at January 2, 2013 11:27 PM:

We need pure glucose sweets

I wonder if it's possible. Glucose is reducing sugar and will react readily with just about any food at high temperatures. And those Maillard reaction products can be quite a thing on their own (mutagens, carcinogens, etc.) In particular, I think that the amount of acrylamide generated from such cooking is bound to be much higher that with sucrose.

bbartlog said at January 4, 2013 1:08 PM:

Nice find. I've thought for a while that the leading hypothesis for explaining US overweight was that HFCS doesn't trigger a satiation response. This fits in with that (I think).

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