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Basic Science

Poster Session 2

(621) CD4+T-Cells cause increased glucose, hypertension, and organ dysfunction in a rat model of gestational diabetes

Tuesday, February 13, 2024

3:30 PM – 5:00 PM

Location: Prince George's Exhibit Hall CDE, Lower Atrium Level

Primary & Presenting Author(s)

JV

Jean Vel, MD

Fellow
University of Mississippi Medical Center
Madison, MS, United States

Coauthor(s)

JW

Jan Williams, PhD

University of Mississippi Medical Center
Jackson, MS, United States
Danielle Frieson, MD, MS (she/her/hers)

Fellow
University of Mississippi Medical Center
Jackson, MS, United States
BZ

Baoying Zheng, MS

University of Mississippi Medical Center
Jackson, MS, United States
MW

Mariah Wilson, BS

University of Mississippi Medical Center
Jackson, MS, United States
NC

Nathan Campbell, BS

University of Mississippi Medical Center
Jackson, MS, United States
Babbette LaMarca, PhD

Professor, Chair
University of Mississippi Medical Center
Jackson, MS, United States
Evangeline Deer, PhD (she/her/hers)

Instructor
University of Mississippi Medical Center
Jackson, MS, United States

Objective: Gestational diabetes mellitus (GDM), impacts 10% of all pregnancies and refers to glucose intolerance, insulin sensitivity and beta islet cell dysfunction during pregnancy which is a risk factor for hypertensive disorders of pregnancy. The mechanisms of GDM are unknown and the management strategies are limited. The lack of an appropriate animal model of GDM further limits our understanding of this disease. Many studies show CD4+ T cells play a role in diabetes, therefore we hypothesize that CD4+ T cells play a role in the pathogenesis of GDM.

Study Design:

Splenic CD4+Tcells from female streptozotocin (STZ)-induced diabetic Dahl Salt Sensitive (DM-SS) rats and control nondiabetic female Dahl SS rats were injected on gestational day (GD) 12 into pregnant Sprague Dawley (SD) rats to create the DM-CD4+ T cells and nondiabetic control SS-CD4+ T cell pregnant rats. Glucose, blood pressure, renal, pancreatic and placental function were assessed on gestation day 19. Renal and pancreatic tissues were stained for Periodic acid Schiff (PAS) and hematoxylin and eosin (H&E). A one-way ANOVA was used for statistical analysis.

Results: MAP increased in DM-CD4+ T cell rats (106±2, n=11, p< 0.05) and SS-CD4+ T cell rats (109±2, n=9, p< 0.05) compared to pregnant SD controls (92±2 mmHg, n=7). Proteinuria occurred with DM CD4+ T cells (9±1 p< 0.05) and SS-CD4+ T cells (10±1 p< 0.05) compared to pregnant SD controls (4±1 ml/day). Glucose tolerance was impaired and blood glucose was elevated only in recipients of DM-CD4+ T cells (136 ± 9 mg/dl, p< 0.05). Glomerular and pancreatic damage occurred in DM-CD4+T cell recipient rats (p< 0.05). Markers of renal dysfunction KIM-1 and NGAL were increased in DM-CD4+ T cell rats (42±8; 449 ±3, p< 0.05) compared to SS-CD4+ T cell rats(36±5; 47±4 pg/mg, p< 0.05) and pregnant SD rats (11±2;19±3 pg/mg). Placental mitochondrial dysfunction was impaired with DM-CD4T cells.

Conclusion: Collectively, these data indicate that CD4+ T cells induce a GDM phenotype identifying a new animal model for studying mechanisms of the pathophysiology of GDM.