Cortical Thickness and Appetite Hormones in Adolescent Obesity and Binge Eating Disorder: A Comparative Study
INTERNATIONAL JOURNAL OF EATING DISORDERS, 2026 (SCI-Expanded, SSCI, Scopus)
- Yayın Türü: Makale / Tam Makale
- Basım Tarihi: 2026
- Doi Numarası: 10.1002/eat.70161
- Dergi Adı: INTERNATIONAL JOURNAL OF EATING DISORDERS
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Social Sciences Citation Index (SSCI), Scopus, BIOSIS, CINAHL, EMBASE, MEDLINE, Psycinfo, Social Sciences Abstracts, Academic Search Ultimate (EBSCO), Biomedical Reference Collection: Corporate Edition (EBSCO), Health Research Premium Collection (ProQuest), Psychology & Behavioral Sciences Collection (EBSCO), Sociology Source Ultimate (EBSCO)
- Dokuz Eylül Üniversitesi Adresli: Evet
Özet
Objective This study examined cortical thickness and appetite-regulating hormones-neuropeptide Y (NPY) and ghrelin-to better understand the neurobiological mechanisms underlying binge eating disorder (BED) and obesity in adolescence. We compared adolescents with BED and obesity, adolescents with obesity without BED, and healthy controls (HCs), and explored the relationships among these measures, BMI, and psychological symptoms. Method Seventy adolescents (aged 12-18 years) were included: 24 adolescents with BED and obesity, 24 adolescents with obesity without BED, and 22 HC. Cortical thickness was measured using 3.0 T structural MRI with FreeSurfer-based analysis, and fasting serum levels of NPY and ghrelin were quantified by ELISA. Participants also completed the Eating Attitudes Test-40 (EAT-40), the Eating Disorder Examination Questionnaire (EDE-Q), the Children's Depression Inventory (CDI), and the State-Trait Anxiety Inventory for Children (STAI-C). Results Both groups with obesity showed significantly elevated NPY levels compared to HCs (p < 0.001), with no difference between adolescents with and without BED; fasting total ghrelin levels did not differ across groups. Adolescents with BED exhibited reduced cortical thickness in the right posterior cingulate cortex relative to both comparison groups (p = 0.002), while left posterior cingulate thinning was observed in both groups with obesity versus HCs (p = 0.004). No significant group differences were found in insular or anterior cingulate thickness. Both groups with obesity showed greater depressive symptoms, disordered eating attitudes, and eating-related psychopathology than HCs. In multiple regression analyses adjusted for diagnostic group membership, higher BMI (beta = 0.47, p < 0.001) and lower left insular cortical thickness (beta = -0.45, p = 0.031) were independently associated with elevated NPY levels. Conclusion Findings suggest that elevated NPY levels may represent a shared neurobiological feature of adolescent obesity, whereas reduced right posterior cingulate cortical thickness may be more specifically associated with the diagnosis of BED. These findings contribute to understanding the neurobiological correlates of disordered eating behaviors during adolescence.