SUN-719 - Phase-Specific Associations between Splenic Adiposity, IL-6, and Oxidized LDL during Lifestyle-Induced Weight Loss in Women with Type 2 Diabetes

Background:
The spleen is increasingly recognized as a player in metabolic regulation and inflammatory signaling. While hepatic and visceral fat are established markers of cardiometabolic risk, the role of splenic adiposity—quantified via computed tomography (CT) Hounsfield Units (HU)—remains poorly understood. This study investigated the relationship between splenic adiposity, systemic inflammation, and lipid peroxidation during metabolic steady-state and active lipolysis.

Methods:
We evaluated 179 overweight Korean women with type 2 diabetes (T2DM) (mean age 54.4±6.6 years; BMI 27.3±2.8 kg/m²). Baseline measurements were taken during a metabolic steady-state. Participants then underwent a 12-week lifestyle intervention. We measured regional abdominal fat, hepatic and splenic attenuation (HU), and circulating markers: interleukin-6 (IL-6), oxidized LDL (oxLDL), and high-sensitivity C-reactive protein (hsCRP).

Results:
Steady-State (Baseline): Lower spleen HU (indicating higher adiposity) significantly correlated with higher IL-6 (r=0.242, p=0.007) and higher oxLDL (r=0.254, p=0.004). Notably, spleen HU correlated with liver HU (r=0.326, p< 0.001) but not with total, visceral, or subcutaneous abdominal fat. Active Lipolysis (Post-Intervention): Following weight loss, spleen HU increased (48.5 to 51.0 HU) and liver HU increased (54.7 to 58.1 HU), reflecting reduced organ adiposity alongside improved insulin sensitivity (K_ITT). During this phase, spleen HU maintained a strong correlation with liver HU (r=0.776, p< 0.001) and a modest correlation with oxLDL (r=0.212, p=0.005$). However, longitudinal changes in organ attenuation were not directly coupled with changes in IL-6 or oxLDL.

Conclusion:
Splenic adiposity is uniquely associated with IL-6 during metabolic steady-state and with oxLDL during active lipolysis. These findings suggest that the spleen may serve as a state-dependent marker of inflammation and lipid handling in T2DM, independent of traditional visceral fat depots.

*Unless otherwise noted, all abstracts presented at ENDO must not be released to the press or the public until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.*