4.7 Article

Structurally Different Flavonoid Subclasses Attenuate High-Fat and High-Fructose Diet Induced Metabolic Syndrome in Rats

Journal

JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
Volume 66, Issue 46, Pages 12412-12420

Publisher

AMER CHEMICAL SOC
DOI: 10.1021/acs.jafc.8b03574

Keywords

apigenin; quercetin; genistein; naringenin; EGCG; metabolic syndrome

Funding

  1. National Natural Science Foundation of China [31571831]
  2. Beijing Engineering and Technology Research Center of Food Additives, Beijing Technology & Business University (BTBU)

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Metabolic syndrome is a serious health problem worldwide. Increasing evidence indicates that flavonoid-rich foods exert beneficial effects. However, the function of flavonoids in metabolic syndrome is controversial. Here, we focus on the structural effects of flavonoids by comparing the effect of five purified subclasses of flavonoids on high-fat and high-fructose diet (HFFD) induced metabolic syndrome in vivo. Sprague-Dawley (SD) rats were fed with (i) basal diet (3.21 kcal/g) (ii) HFFD (25% lard and 25% fructose, 4.70 kcal/g), and (iii) HFFD with flavonoids representing different subclasses (2.6 mmol/kg diet): apigenin (flavones), quercetin (flavonols), genistein (isoflavones), naringenin (flavanones), and epigallocatechin gallate (flavanols) for 13 weeks. Our results showed that structurally different flavonoid subclasses prevented the HFFD-induced metabolic syndrome. Apigenin significantly decreased adipose fat and leptin levels and increased adiponectin levels. Epigallocatechin gallate and naringenin were both effective on dyslipidemia and hepatic lipid accumulations. The proinflammatory cytokines TNF-alpha and IL-6 were alleviated by quercetin, genistein, and naringenin. All the flavonoids exerted significant functions on improving insulin resistance and fasting glucose. In conclusion, flavonoid subclasses structurally exert antihyperlipidemic, antidiabetic, and anti-inflammatory functions by attenuating the lipid metabolism, glucose metabolism, and inflammation of metabolic syndrome.

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