Insulin Acts As Satiety Signal in Postprandial PeriodLast Updated: February 21, 2012. Brain insulin may act as a satiety signal during the postprandial period and is associated with decreased appetite and reduced intake of highly palatable food, according to a study published online Feb. 16 in Diabetes.
TUESDAY, Feb. 21 (HealthDay News) -- Brain insulin may act as a satiety signal during the postprandial period and is associated with decreased appetite and reduced intake of highly palatable food, according to a study published online Feb. 16 in Diabetes.
Manfred Hallschmid, Ph.D., from the University of Lübeck in Germany, and colleagues investigated the role of brain insulin signaling in the control of food intake. In two groups of healthy women, 160 IU insulin or vehicle were administered after lunch, and two hours later, the consumption of cookies of varying palatability was evaluated under the pretext of a taste test. Intranasal insulin was administered to fasted females as a control study.
The researchers found that, compared with placebo, insulin administration in the postprandial state, but not in the fasted state, decreased appetite along with intake and rated palatability of the most palatable snack offered. Intranasal insulin administration was associated with a small decrease in plasma glucose, but no effect on serum insulin concentration was seen.
"Postprandially administered intranasal insulin enhances the satiating effect of meals and reduces palatable snack intake, suggesting that insulin acts as a relevant signal in the short-term regulation of satiety in humans," the authors write. "Considering that the rewarding effect of palatable food overriding the homeostatic control of energy intake may promote obesity, insulin's potential to curb the appetite for hedonically salient, calorie-rich food deserves particular attention."
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