Objectives:
CNM (CNM) polyphenol has antioxidant and anti-inflammatory properties. Therefore, we hypothesized CNM decrease heart disease risk factors and may enhance anti- inflammatory properties in rats fed a diet containing CNM. In this study, we evaluated the effects of CNM polyphenol on insulin resistance (IR), hyperlipidemia, hepatic transcription factors expressions [sterol regulatory element-binding protein1c (SREBP-1c), liver X receptor-α (LXR-α), nuclear factor kappa B p65 (NF-κB p65), nuclear factor-E2-related factor-2 (Nrf2)] in rats fed high fat diet (HFD).
Method:
Twenty-eight Wistar rats were allocated into four groups; (i) normal control; animals fed with normal chow (C ) (ii) CNM (C+CNM 100 mg/kg b.wt.), (iii) HFD (42% of calories as fat, high fat diet [HFD]), and (iv) HFD + CNM for 12 weeks. Blood analysis for triglycerides (TG) and cholesterol (CHOL), glucose, insulin, malonaldehyde (MDA a marker of oxidative stress [OS]) were estimated. Body weight, visceral fat and liver weight recorded and liver MDA assessed. SREBP-1c, LXR-α, ATP-citrate lyase (ACLY), fatty acid synthase (FAS), NF-κB p65 expressions and decreased the PPAR-α, p-IRS-1, Nrf2, HO-1 proteins were evaluated by Western blotting.
Results:
HFD rats of the liver had increased SREBP-1c, LXR-α, ATP-citrate lyase (ACLY), fatty acid synthase (FAS), NF-κB p65 expressions and decreased the PPAR-α, p-IRS-1, Nrf2, HO-1 expressions compared to control group. CNM supplementation decreased body weight (8.4%), visceral fat (36.6%), liver weight (17.7%), serum glucose and insulin concentrations, lipid profile (
P
< 0.05), and serum and liver MDA (23.3% and 25.4 %) concentration compared to HFD rats (
P
< 0.05). CNM decreased hepatic SREBP-1c (18.1 %), LXRα (27.9%), ATP-citrate lyase (ACLY, 22.7 %), fatty acid synthase (FAS, 15.8 %), NF-κB p65 (23.3%) and enhanced the PPAR-α, IRS-1 (72.7 %), Nrf2 (111.7 %) and HO-1 (72.1 %) proteins in HFD rat livers (
P
< 0.05).
Discussion:
These results suggest CNM supplementation reduces hyperlipidemia, inflammation, and oxidative stress through activating transcription factors (SREBP-1c, LXR-α, NF-κB, and Nrf2) and anti-oxidative defense signaling pathway.