This study investigated why Göttingen Minipigs, despite obesity and dyslipidemia induced by a high-fat, fructose, and cholesterol (FFC) diet, lacked key human pathological hepatic findings like hepatocellular ballooning and abundant steatosis. High-throughput expression profiling of metabolic genes in liver, subcutaneous adipose tissue (SAT), and visceral adipose tissue (VAT) was performed in minipigs fed standard chow (SD), FFC diet, and FFC diet with streptozotocin-induced diabetes (FFCDIA). While both FFC groups developed severe obesity and dyslipidemia, insulin signaling pathways remained unaffected. Key genes involved in lipid metabolism (PPARG, LPL, CD36, FABP4) were highly deregulated in the liver, but adipose tissue showed minimal inflammation. The results suggest that obese Göttingen Minipigs are protected from obesity-associated metabolic and hepatic abnormalities due to their remarkable ability to expand adipose compartments to accommodate excess calories.
