Diabetes and Vascular Disease

SAT-546 - Cd1A-Mediated Inflammation Abrogates Resistance to Metabolic Dysfunction in Female Mice on High Fat Diet

Saturday, June 13, 2026

9:30 AM - 4:30 PM CT

Location: ENDOExpo; Poster Floor

Abstract Poster Presenter(s)

JA

Julio Ayala Angulo, Graduate Student

Graduate student
UNIVERSITY OF CA - IRVINE
Irvine, CA, United States

Co-Author(s)

KW

Kiara Dominique Wiggins, n/a

Graduate Student
UNIVERSITY OF CA - IRVINE
Irvine, California, United States
ML

Miranda Lopez, PhD Candidate

University of California, Irvine
Irvine, United States
ZD

Zena Del Mundo, PhD Candidate

University of California, Irvine
Irvine, California, United States
NU

Naveena Ujagar, n/a

University of California, Irvine
Irvine, United States

Senior Author/Primary Investigator(s)

Dequina A. Nicholas, PhD (she/her/hers)

Assistant Professor
University of California Irvine
Irvine, CA, United States

Co-Author(s)

Dequina A. Nicholas, PhD (she/her/hers)

Assistant Professor
University of California Irvine
Irvine, CA, United States

Disclosure(s):

Dequina A. Nicholas, PhD: No financial relationships to disclose

Type 2 Diabetes (T2D) is a metabolic disease closely related with obesity currently affecting hundreds of millions globally. Manifestations of T2D vary between sexes and have different hormonal co-morbidities in females. Diet Induced Obesity (DIO) mouse models have failed to faithfully model mechanistic factors and sex differences seen in humans resulting in no effective cure for T2D. Specifically, T2D-related inflammation is markedly different. Using a human CD1a, a lipid antigen presenting receptor, transgenic mouse model we sought to improve modeling of human pathogenesis in mice. We hypothesized that CD1a would increase anti-lipid inflammatory responses that in turn worsen metabolic health. As early as 6 weeks on a 45% Kcal from fat diet (HFD), CD1a female mice developed significantly elevated fasting blood glucose levels relative to WT HFD controls (p < .0001) which persisted beyond 22 weeks despite no differences in weight gain. CD1a HFD mice also developed higher fasting insulin (p <.05) and HOMA-IR (p <.01) relative to WT HFD female mice. Interestingly, CD1a HFD Female mice stall in the diestrus stage suggesting development of reproductive dysfunction. Together, these data suggest a female specific vulnerability to DIO mediated diabetes and reproductive disorder mediated through CD1a-driven inflammation in contrast to conventional C57BL/6 mice which are resistant to DIO. This model poses an improved model to investigate the underpinning mechanisms of sex-specfic metabolic dysfunction and their intersection with immunity while also highlighting a gap in our approach in addressing the T2D crisis.

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