How palatable food disrupts appetite regulation

被引:235
作者
Erlanson-Albertsson, C [1 ]
机构
[1] Lund Univ, Dept Expt Med, Sect Endocrinol & Metabol, Lund, Sweden
关键词
D O I
10.1111/j.1742-7843.2005.pto_179.x
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Appetite regulation is part of a feedback system that controls the energy balance, involving a complex interplay of hunger and satiety signals, produced in the hypothalamus as well as in peripheral organs. Hunger signals may be generated in peripheral organs (e.g. ghrelin) but most of them are expressed in the hypothalamus (neuropeptide Y, orexins, agouti-related peptide, melanin concentrating hormone, endogenous opiates and dopamine) and are expressed during situations of energy deficiency. Some satiety signals, such as cholecystokinin, glucagon-like peptide 1, peptide YY and enterostatin are released from the digestive tract in response to food intake. Others, such as leptin and insulin, are mobilized in response to perturbations in the nutritional state. Still others are generated in neurones of the hypothalamus (alpha-melanocyte-stimulating hormone and serotonin). Satiety signals act by inhibiting the expression of hunger signals and/or by blunting their effect. Palatable food, i.e. food rich in fat and sugar, up-regulates the expression of hunger signals and satiety signals, at the same time blunting the response to satiety signals and activating the reward system. Hence, palatable food offsets normal appetite regulation, which may explain the increasing problem of obesity worldwide.
引用
收藏
页码:61 / 73
页数:13
相关论文
共 155 条
[1]   Small molecule insulin mimetics reduce food intake and body weight and prevent development of obesity [J].
Air, EL ;
Strowski, MZ ;
Benoit, SC ;
Conarello, SL ;
Salituro, GM ;
Guan, XM ;
Liu, K ;
Woods, SC ;
Zhang, BB .
NATURE MEDICINE, 2002, 8 (02) :179-183
[2]   NEUROPEPTIDE-Y DISTRIBUTION IN THE RAT-BRAIN [J].
ALLEN, YS ;
ADRIAN, TE ;
ALLEN, JM ;
TATEMOTO, K ;
CROW, TJ ;
BLOOM, SR ;
POLAK, JM .
SCIENCE, 1983, 221 (4613) :877-879
[3]   NALTREXONE SUPPRESSES HYPERPHAGIA INDUCED IN THE RAT BY A HIGHLY PALATABLE DIET [J].
APFELBAUM, M ;
MANDENOFF, A .
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR, 1981, 15 (01) :89-91
[4]   A role for the endogenous opioid β-endorphin in energy homeostasis [J].
Appleyard, SM ;
Hayward, M ;
Young, JI ;
Butler, AA ;
Cone, RD ;
Rubinstein, M ;
Low, MJ .
ENDOCRINOLOGY, 2003, 144 (05) :1753-1760
[5]   Impaired transport of leptin across the blood-brain barrier in obesity is acquired and reversible [J].
Banks, WA ;
Farrell, CL .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2003, 285 (01) :E10-E15
[6]   Is obesity a disease of the blood-brain barrier? Physiological, pathological, and evolutionary considerations [J].
Banks, WA .
CURRENT PHARMACEUTICAL DESIGN, 2003, 9 (10) :801-809
[7]   Impaired transport of leptin across the blood-brain barrier in obesity [J].
Banks, WA ;
DiPalma, CR ;
Farrell, CL .
PEPTIDES, 1999, 20 (11) :1341-1345
[8]   Differential permeability of the blood-brain barrier to two pancreatic peptides: Insulin and amylin [J].
Banks, WA ;
Kastin, AJ .
PEPTIDES, 1998, 19 (05) :883-889
[9]   Behavioral characterization of neuropeptide Y knockout mice [J].
Bannon, AW ;
Seda, J ;
Carmouche, M ;
Francis, JM ;
Norman, MH ;
Karbon, B ;
McCaleb, ML .
BRAIN RESEARCH, 2000, 868 (01) :79-87
[10]   Insulin and leptin: dual adiposity signals to the brain for the regulation of food intake and body weight [J].
Baskin, DG ;
Lattemann, DF ;
Seeley, RJ ;
Woods, SC ;
Porte, D ;
Schwartz, MW .
BRAIN RESEARCH, 1999, 848 (1-2) :114-123