Protection from Metabolic Dysregulation, Obesity, and Atherosclerosis by Citrus Flavonoids: Activation of Hepatic PGC1<i>α</i>-Mediated Fatty Acid Oxidation

<table>Potential mechanisms for the reduction in risk factors for atherosclerosis by flavonoids. Both <i>in vitro</i> and <i>in vivo </i>data suggest that citrus flavonoids decrease macrophage uptake of oxidized LDL and macrophage CE accumulation and improve dyslipidemia. While the complete mechanisms have not been fully defined, the nuclear hormone receptors PPAR<i>α</i> and PGC1<i>α</i> represent important molecular targets. The improvement in dyslipidemia can be linked to decreased VLDL secretion as hepatic lipid availability for storage or VLDL secretion is decreased as a consequence of PPAR-stimulated fatty acid oxidation. The oxidation of fatty acids by liver prevents ectopic lipid accumulation and improves both insulin sensitivity and glucose tolerance. Arrows indicate change in response to flavonoid treatment.</table>

PPAR Research

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Figure 2: Protection from Metabolic Dysregulation, Obesity, and Atherosclerosis by Citrus Flavonoids: Activation of Hepatic PGC1<i>α</i>-Mediated Fatty Acid Oxidation 

Figure 2 | Protection from Metabolic Dysregulation, Obesity, and Atherosclerosis by Citrus Flavonoids: Activation of Hepatic PGC1α-Mediated Fatty Acid Oxidation 