Date of Award
Master of Science
Dr. Murray Huff
Increased dietary cholesterol promotes the inflammatory response in adipose tissue and liver, which may contribute to atherosclerosis. We hypothesized that the citrus flavonoid naringenin would prevent inflammation and atherosclerosis in Ldlr1' mice fed a cholesterol-enriched, high-fat or low-fat diet. The dyslipidemia and insulin resistance induced by cholesterol-feeding was markedly attenuated by naringenin. Naringenin significantly decreased hepatic steatosis, leading to reduced hepatic inflammation and macrophage infiltration. Furthermore, naringenin prevented diet-induced obesity and adipocyte hypertrophy, thereby attenuating the inflammatory response in adipose tissue. Collectively, the improvement in metabolic function by naringenin protected against the development of complex atherosclerotic lesions. Mice lacking FGF21, a recently characterized metabolic regulator, were used to determine if FGF21 was essential for the function of naringenin. Although these studies establish that naringenin does not require FGF21, they highlight the possibility that naringenin activates other FGF/FGF receptor molecules. Therefore, naringenin is a promising therapeutic candidate for the treatment of metabolic disease
Assini, Julia Marie, "PREVENTION OF METABOLIC DYSREGULATION, INFLAMMATION, AND ATHEROSCLEROSIS BY THE CITRUS FLAVONOID NARINGENIN" (2011). Digitized Theses. 3659.