Abstract |
A high-fat diet (HFD) promotes tissue inflammation, oxidative stress and insulin resistance (IR), thereby contributing to the development of obesity and diabetes. Anthocyanins from Lycium ruthenicum (AC) have demonstrated anti- obesity effects and modulated IR. To investigate the mechanism by which AC attenuates the adverse effects of consuming a HFD, C57BL/6J mice were fed a HFD supplemented with AC or a control diet without AC for 12 weeks. AC supplementation decreased the amount of weight gain, hepatic lipid, and sequentially improved dyslipidemia, inflammation, oxidative stress, and IR in HFD-fed mice. Molecular data revealed that AC inhibited hepatic inflammation by reducing TLR4/NF-κB/JNK in the liver tissues and ameliorated oxidative stress by activating the Nrf2/HO-1/NQO1 pathway. Thus, AC might activate IRS-1/AKT and prevent HFD-induced gluconeogenesis and IR by ameliorating inflammation and oxidative stress. Modulation of inflammation and oxidative stress with AC may represent a promising target for the treatment of IR and provide insight into the mechanism by which AC protects against obesity.
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Authors | Baoming Tian, Jianhua Zhao, Xiaoqing Xie, Tao Chen, Yan Yin, Ruohan Zhai, Xinlei Wang, Wei An, Juxiu Li |
Journal | Food & function
(Food Funct)
Vol. 12
Issue 9
Pg. 3855-3871
(May 11 2021)
ISSN: 2042-650X [Electronic] England |
PMID | 33704297
(Publication Type: Journal Article)
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Chemical References |
- Anthocyanins
- Blood Glucose
- Insulin Receptor Substrate Proteins
- Irs1 protein, mouse
- NF-kappa B
- Tlr4 protein, mouse
- Toll-Like Receptor 4
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Topics |
- Animals
- Anthocyanins
(administration & dosage)
- Blood Glucose
(metabolism)
- Diet, High-Fat
(adverse effects)
- Dietary Supplements
- Fruit
(chemistry)
- Gluconeogenesis
- Homeostasis
- Inflammation
- Insulin Receptor Substrate Proteins
(metabolism)
- Insulin Resistance
- Lipid Metabolism
- Liver
(metabolism, pathology)
- Lycium
- Male
- Mice
- Mice, Inbred C57BL
- NF-kappa B
(metabolism)
- Obesity
(prevention & control)
- Oxidative Stress
- Signal Transduction
- Toll-Like Receptor 4
(metabolism)
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