Muhammed Maged, Burton-Murray Helen, Plessow Franziska, Becker Kendra R, Breithaupt Lauren, Lauze Meghan, Slattery Meghan, Lee Hang, Thomas Jennifer J, Eddy Kamryn T, Lawson Elizabeth A, Misra Madhusmita
Neuroendocrine Unit, Division of Endocrinology, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA; Division of Endocrinology, Diabetes and Hypertension, Brigham and Women's Hospital, Boston, MA, USA; Adult Inpatient Medicine, Department of Medicine, Newton Wellesley Hospital, Newton, MA, USA; Multidisciplinary Eating Disorders Research Collaborative, Mass General Brigham, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
Multidisciplinary Eating Disorders Research Collaborative, Mass General Brigham, Boston, MA, USA; Harvard Medical School, Boston, MA, USA; Center for Neurointestinal Health, Division of Gastroenterology, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA; Eating Disorders Clinical and Research Program, Department of Psychiatry, Massachusetts General Hospital, Boston, MA, USA.
Psychoneuroendocrinology. 2025 Feb;172:107257. doi: 10.1016/j.psyneuen.2024.107257. Epub 2024 Dec 16.
Appetite-regulating hormones are implicated in anorexia nervosa (AN) pathophysiology, however, data are limited for appetite-regulating hormones across the AN weight spectrum. We aimed to investigate fasting and post-prandial concentrations of appetite-regulating hormones - peptide YY (PYY), cholecystokinin (CCK), and ghrelin - among adolescent and young adult females across the AN weight spectrum, specifically those with AN and Atypical AN, and healthy controls (HC).
Participants (N = 95; ages 11-22 years) included 33 with AN, 25 with Atypical AN, and 37 HC. AN was differentiated from Atypical AN by BMI < 10th percentile for age and sex (if <18 years) or < 18.5 kg/m(if ≥18 years). Blood samples were collected fasting and 30, 60 and 120 minutes following a standardized meal to assess total PYY, CCK, and total ghrelin concentrations.
Median fasting and post-prandial PYY concentrations were significantly higher in AN vs. HC with medium differences (p = .001-.006, r = .34-.43). Atypical AN had significantly higher PYY concentrations compared to HC at T-0 (p = .027, r = .29) only, and did not significantly differ from concentrations in AN (p = .105-.413, r = .11-.22). Area under the curve (AUC; p = .001; r = .41) and peak PYY concentrations (p = .003; r = .41) were also significantly higher in AN vs. HC with medium differences. There were no significant differences in fasting (p = .885) or post-prandial (p = .846-.993) CCK concentrations across groups. AN and Atypical AN each had significantly higher ghrelin concentrations than HC with small to medium effect (AN vs HC p = .004-.025, r = .27-.36; Atypical AN vs HC p = .004-.033; r = .28-.28).
Higher peak postprandial concentrations of anorexigenic PYY in AN (compared to HC) may facilitate dietary restriction and contribute to maintenance of lower weight. Lack of CCK suppression in AN is maladaptive in the context of undernutrition. Despite continued restriction, ghrelin is adaptively higher in AN overall and may not be differentiated by weight status.
食欲调节激素与神经性厌食症（AN）的病理生理机制有关，然而，关于整个AN体重范围内食欲调节激素的数据有限。我们旨在研究整个AN体重范围内青少年和年轻成年女性中食欲调节激素——肽YY（PYY）、胆囊收缩素（CCK）和胃饥饿素——的空腹和餐后浓度，特别是那些患有AN和非典型AN的患者以及健康对照（HC）。
参与者（N = 95；年龄11 - 22岁）包括33例AN患者、25例非典型AN患者和37例HC。根据年龄和性别对应的BMI <第10百分位数（如果<18岁）或<18.5 kg/m²（如果≥18岁），将AN与非典型AN区分开来。在空腹时以及标准化餐后30、60和120分钟采集血样，以评估总PYY、CCK和总胃饥饿素浓度。
与HC相比，AN患者的空腹和餐后PYY浓度中位数显著更高，差异中等（p = 0.001 - 0.006，r = 0.34 - 0.43）。仅在T - 0时，非典型AN患者与HC相比，PYY浓度显著更高（p = 0.027，r = 0.29），且与AN患者的浓度无显著差异（p = 0.105 - 0.413，r = 0.11 - 0.22）。与HC相比，AN患者的曲线下面积（AUC；p = 0.001；r = 0.41）和PYY峰值浓度（p = 0.003；r = 0.41）也显著更高，差异中等。各组之间的空腹（p = 0.885）或餐后（p = 0.846 - 0.993）CCK浓度无显著差异。AN和非典型AN患者的胃饥饿素浓度均显著高于HC，效应大小为小到中等（AN与HC相比，p = 0.004 - 0.025，r = 0.27 - 0.36；非典型AN与HC相比，p = 0.004 - 0.033；r = 0.28 - 0.28）。
与HC相比，AN患者餐后厌食性PYY的峰值浓度更高，这可能有助于饮食限制并有助于维持较低体重。在营养不良的情况下，AN患者缺乏CCK抑制是适应不良的。尽管持续节食，但总体上AN患者的胃饥饿素适应性更高，且可能无法通过体重状态进行区分。
