抄録
Obesity has increased at an alarming rate in recent years. Evidence indicates that obese animals have blunted satiety, raising the possibility that defective satiety signaling in the brain may contribute to the etiology of obesity. Therefore, food intake suppression is considered crucial for preventing obesity. Food intake suppression via the peripheral nervous system mainly focuses on cholecystokinin and enterostatin relaying to the central nervous system (CNS). The mechanism of food intake coordination via the CNS per se is extremely complex. In this article, leptin, insulin, melanocortin receptor, dopamine, serotonin, norepinephrine, brain-derived neurotrophic factor, cannabinoid-1 receptor blocker, cytokines, tumor necrosis factor-alpha, lipopolysaccharide, interleukin, cholecystokinin, enterostatin, estrogen, testosterone and apolipoprotein E will be discussed. Most of them have definite effect on food intake, while a few of them are elusive. There is still a great challenge in obesity treatment by way of suppressing food intake. Future appetite-suppressing medications should selectively affect the desire to eat, with minimal adverse effects from these medications.
