标题：d-Allulose Inhibits Ghrelin-Responsive, Glucose-Sensitive and Neuropeptide Y Neurons in the Arcuate Nucleus and Central Injection Suppresses Appetite-Associated Food Intake in Mice
摘要：d-allulose, a rare sugar, has sweetness with few calories.
d-allulose regulates feeding and glycemia, and ameliorates hyperphagia, obesity and diabetes. All these functions involve the central nervous system. However, central mechanisms underlying these effects of
d-allulose remain unknown. We recently reported that
d-allulose activates the anorexigenic neurons in the hypothalamic arcuate nucleus (ARC), the neurons that respond to glucagon-like peptide-1 and that express proopiomelanocortin. However, its action on the orexigenic neurons remains unknown. This study investigated the effects of
d-allulose on the ARC neurons implicated in hunger, by measuring cytosolic Ca
2+ concentration ([Ca
2+]
i) in single neurons.
d-allulose depressed the increases in [Ca
2+]
i induced by ghrelin and by low glucose in ARC neurons and inhibited spontaneous oscillatory [Ca
2+]
i increases in neuropeptide Y (NPY) neurons.
d-allulose inhibited 10 of 35 (28%) ghrelin-responsive, 18 of 60 (30%) glucose-sensitive and 3 of 8 (37.5%) NPY neurons in ARC. Intracerebroventricular injection of
d-allulose inhibited food intake at 20:00 and 22:00, the early dark phase when hunger is promoted. These results indicate that
d-allulose suppresses hunger-associated feeding and inhibits hunger-promoting neurons in ARC. These central actions of
d-allulose represent the potential of
d-allulose to inhibit the hyperphagia with excessive appetite, thereby counteracting obesity and diabetes.
