Scope
To assess the impact of ginger extract (GIN) in stimulating the production of quality HDL and the cholesterol efflux in the small intestine (SI), key processes in the management of hyperlipidemia (HL)‐induced hepatic steatosis, and atherosclerosis.
Methods and results
Three groups of hamsters are used: (i) N, fed standard diet, (ii) HL, fed high‐fat diet for 21 weeks, and (iii) HL‐GIN, HL treated with GIN for the last 5 weeks of diet. Apolipoprotein A‐I (apoA‐I), malondialdehyde‐apoA‐I (MDA‐apoA‐I), paraoxonase1 (PON1), and myeloperoxidase (MPO) are measured in plasma and SI. ATP‐binding cassette A1 transporter (ABCA1), ABCG5/G8, liver X receptor α/β (LXRα/β), peroxisome proliferator‐activated receptor γ (PPARγ), and sirtuin1 (SIRT1) are assessed in the SI. Results show that in HL plasma, GIN decreases MDA‐apoA‐I, MPO/PON1 ratio and increases HDL‐cholesterol/total cholesterol. In HL‐SI, GIN decreases MDA‐apoA‐I and MPO, increases ApoA‐I, PON1, and ABCA1, and restores cholesterol efflux disturbed by HL (SIRT1‐LXRα/β‐PPARγ‐ABCG8). GIN administration is associated with the reduction of the aortic valves lipid‐deposits.
Conclusion
In HL conditions, GIN stimulates the functional HDL production by restoring apoA‐I quality and quantity through inhibition of the oxidative stress, and increases cholesterol efflux in the SI. These effects are associated with the restoration of SIRT1‐LXRα/β‐PPARγ pathway.