Researcher ORCID Identifier

0009-0002-2738-2021

Graduation Year

2026

Date of Submission

4-2026

Document Type

Open Access Senior Thesis

Degree Name

Bachelor of Arts

Department

Neuroscience

Reader 1

Diana Williams, PhD

Reader 2

Xiao Zhang, PhD

Terms of Use & License Information

Terms of Use for work posted in Scholarship@Claremont.

Rights Information

© 2026 Jaimie Yu

Abstract

Binge eating disorder (BED), one of the most common eating disorders in the United States (Definition & Facts for Binge Eating Disorder - NIDDK, n.d.), is characterized by recurrent episodes of consuming large quantities of food in a short period of time accompanied by a sense of loss of control. The intermittent access (INT) model reliably produces binge-like eating in adult rodents, with animals showing episodic hyperphagia upon time-limited access to a high-fat, high-sugar (HFHS) diet. In adult female rats, INT access produces elevated meal size and reduced satiety ratio relative to controls (Maske et al., 2020), and promotes microglial reactivity in the hypothalamus and nucleus of the solitary tract (NTS), brain regions critical for regulating satiation and post-meal satiety (Campanile & Eckel, 2025). However, whether adolescent animals are similarly vulnerable to these behavioral and neuroinflammatory effects remains unknown.

The present study had two aims: first, to determine whether INT access to an HFHS diet produces binge-like meal patterns in adolescent rats comparable to those observed in adults; and second, to examine whether this feeding pattern is associated with elevated microglial reactivity in the hypothalamus and NTS. Fifteen adolescent female Sprague-Dawley rats were assigned to one of three dietary conditions beginning at postnatal day 31: INT (n = 4), continuous HFHS access alongside chow (CONT, n = 5), or chow only (CHOW, n = 5). Food intake was monitored continuously using the BioDAQ automated feeding system across 31 days. Brains were processed for immunohistochemical detection of Iba-1, a marker of microglial reactivity, in the hypothalamus and NTS; quantitative analysis is ongoing.

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