Presenting Author: Ramiah D Jacks
, Postdoctoral Research Fellow at Michigan Med., Univ. of Michigan
Abstract:
Obesity can generate a pro-inflammatory state contributing to immune dysregulation and metabolic disease. Adipose tissue is a site of obesity-induced inflammation. Adipose tissue T cells (ATTs) from mice fed a long-term high-fat diet (HFD) have an exhausted phenotype. Knowing this, we sought to determine the factors that regulate ATT function using short-term HFD models.We hypothesized that ATTs respond to early fat expansion and these responses contribute to the orchestration of adipose tissue inflammation with obesity. To test this, we placed mice on short-term HFD (up to 14 days) and assessed ATT kinetics. Mice on HFD gained significantly more total body, epidydimal white adipose tissue (eWAT), and inguinal WAT (iWAT) weight compared to controls. We observed significant proliferation of memory, but not naïve, ATTs with 7 days of HFD in the eWAT, iWAT and omental WAT. In female mice, we observed no change in fat pad weights, however, proliferation of memory ATTs was induced in the gWAT with 7 days of HFD. Adipocyte size was increased with 14 days of HFD in the gonadal WAT (gWAT) and iWAT of male and female mice. These data suggest that memory ATTs uniquely and intensely respond to signals present during HFD-induced rapid adipose tissue expansion in male and female mice. Ongoing studies seek to determine the factor(s) that drive memory ATT proliferation and their cytokine profiles to elucidate their contribution(s) to obesity-associated adipose tissue inflammation.
Rapid adipose tissue expansion induces proliferation of memory adipose tissue T cells
Category
Poster and Podium (Block Symposium)
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Date: May 4 Presentation Time: 11:30 AM to 12:45 PM Room: Exhibit Hall F1