학술논문

Cyanidin and delphinidin modulate inflammation and altered redox signaling improving insulin resistance in high fat-fed mice
Document Type
article
Source
Subject
Biochemistry and Cell Biology
Biological Sciences
Nutrition
Diabetes
Complementary and Integrative Health
Obesity
Prevention
Metabolic and endocrine
Animals
Anthocyanins
Diet
High-Fat
Fatty Liver
Inflammation
Insulin Resistance
Male
Mice
Inbred C57BL
Oxidation-Reduction
Oxidative Stress
Signal Transduction
Medical Biochemistry and Metabolomics
Pharmacology and Pharmaceutical Sciences
Biochemistry and cell biology
Medicinal and biomolecular chemistry
Language
Abstract
Consumption of diets high in fat and/or fructose content promotes tissue inflammation, oxidative stress, and insulin resistance, activating signals (e.g. NF-κB/JNK) that downregulate the insulin cascade. Current evidence supports the concept that select flavonoids can mitigate obesity and type 2 diabetes (T2D). This work investigated if supplementation with the anthocyanidins (AC) cyanidin and delphinidin could attenuate the adverse consequences of consuming a high fat diet (HFD) in mice. Consumption of an AC-rich blend mitigated HFD-induced obesity, dyslipidemia and insulin resistance (impaired responses to insulin and glucose). HFD-fed mice were characterized by increased liver lipid deposition and inflammation, which were also attenuated upon AC supplementation. HFD caused liver oxidative stress showing an increased expression of NADPH oxidases, generators of superoxide and H2O2, and high levels of oxidized lipid-protein adducts. This was associated with the activation of the redox sensitive signals IKK/NF-κB and JNK1/2, and increased expression of the NF-κB-regulated PTP1B phosphatase, all known inhibitors of the insulin pathway. In agreement with an improved insulin sensitivity, AC supplementation inhibited oxidative stress, NF-κB and JNK activation, and PTP1B overexpression. Thus, cyanidin and delphinidin consumption either through diet or by supplementation could be a positive strategy to control the adverse effects of Western style diets, including overweight, obesity, and T2D. Modulation of inflammation, oxidative stress, and NF-κB/JNK activation emerge as relevant targets of AC beneficial actions.