Gastrointestinal morphology, tight junction gene expression, and microbiota of the Ossabaw obese pig model (816.1)

Abstract

Obesity is characterized by chronic low‐grade inflammation, with reduced gastrointestinal (GI) barrier function hypothesized to be a contributing factor. Animal models are invaluable for understanding disease pathophysiology, with porcine models offering several advantages over rodents, including anatomical similarities to humans. A pilot study was undertaken to characterize GI differences in obese Ossabaw pigs vs. lean controls. Ossabaw gilts (n=8) were fed a high‐fat, high‐sugar diet ad libitum until 12 months of age and compared to lean Yorkshire controls (n=9). Plasma inflammatory markers (TNF‐α, IL‐6, and LPS‐binding protein) and intestinal morphology, tight junction protein gene expression, and mucosal microbiota populations were assessed. Preliminary results indicate that LPS‐binding protein concentrations tended to be greater (P=0.08) in obese vs. lean pigs (6233 vs.3802 µg/L). Blood TNF‐α concentrations were numerically, but not significantly increased in obese vs. lean pigs (39 vs. 29 ng/L; P=0.24). Obese pigs had greater (P=0.03) cecal crypt depth (494 vs. 430 µm) and tended to have greater (P=0.09) ileal villus height (477 vs. 400 µm) compared to lean controls. Our findings suggest a correlation between GI architecture, systemic inflammation, and obesity in high‐fat, high‐sugar fed Ossabaw pigs, supporting its use as a model of human obesity and metabolic syndrome.Grant Funding Source: Supported by USDA Hatch #ILLU‐538‐384