Incomplete restoration of the secretion of ghrelin and PYY compared to insulin after food ingestion following weight gain in anorexia nervosa

被引:71
作者
Nakahara, Toshihiro [1 ]
Kojima, Shinya [1 ]
Tanaka, Muneki [1 ]
Yasuhara, Daisuke [1 ]
Harada, Toshiro [1 ]
Sagiyama, Ken-ichiro [1 ]
Muranaga, Tetsuro [1 ]
Nagai, Nobuathu [1 ]
Nakazato, Masamitsu [1 ]
Nozoe, Shin-ichi [1 ]
Naruo, Tetsuro [1 ]
Inul, Akio [1 ]
机构
[1] Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Behav Med, Kagoshima 8908520, Japan
关键词
ghrelin; PYY3-36; anorexia nervosa; weight gain;
D O I
10.1016/j.jpsychires.2006.07.021
中图分类号
R749 [精神病学];
学科分类号
100205 ;
摘要
Background: In humans, ghrelin has been found to stimulate appetite while PYY3-36 to reduce it; these orexigenic and anorexigenic peptides play significant roles in appetite control. We investigated pre- and postprandial responses of ghrelin and PYY in anorexia nervosa (AN) and the influence of weight gain. Methods: Plasma ghrelin, PYY3-36, glucose and insulin responses after ingestion of a 400 kcal standard meal were measured in 14 patients with restricting type of AN and 12 controls. The AN patients were evaluated before therapy and after inpatient therapy. Psychometry was performed by the use of Eating Disorders Inventory. Results: Ghrelin was suppressed during the meal test, while PYY3-36 was increased in all of the groups. Before therapy, AN patients had significantly increased levels of ghrelin and PYY3-36 compared to the control (P < 0.01). After therapeutic intervention, as the nutritional status of AN patients improved, the secretion of these hormones were increased (P < 0.05), but not normalized as in psychological testing. In contrast, insulin and glucose responses were normalized after inpatient therapy. Conclusions: We found that both ghrelin and PYY3-36 increased in AN patients and these changes were not normalized in contrast to insulin after treatment. The increase in both orexigenic ghrelin and anorexigenic PYY3-36 may have a role in pathological eating behavior in AN. (c) 2006 Elsevier Ltd. All rights reserved.
引用
收藏
页码:814 / 820
页数:7
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