TABLE 2.
Derivative and dose | Model | Experimental outcome | Reference |
Naringin | |||
0.02 g/100 g | Cholesterol-fed LDLR-knockout mice | Hepatic HMG-CoA reductase activity was reduced | (62) |
Increases the excretion of fecal sterol | |||
100 mg · kg−1 · d−1 | High-fat/high-carbohydrate–fed Wister rat | Decreased total cholesterol, TGs and NEFAs | (64) |
Preserved hepatic mitochondrial respiration | |||
0.2 g/kg of diet | High-fat-diet–fed C57BL/6 mice | Inhibited the synthesis way and increased FA oxidation | (60) |
Upregulated AMPK. | |||
0.003%, 0.006%, and 0.012% of diet for 6 wk | Male Long-Evans hooded rats | Reduced total TGs and cholesterol in plasma and liver | (54) |
Increased expression of PPARα, CPT-1, and UCP-2. | |||
100 mg · kg−1 · d−1 | High-fat/high-carbohydrate–fed Wister rat | Lowered abdominal fat deposition | (64) |
Body weight was not affected, probably due to increasing muscle mass | |||
Naringenin | |||
1% or 3% wt:wt of diet | LDLR-null mice | Increased hepatic FA oxidation through a PGC1α/PPARα–mediated transcription program | (63) |
Prevented SREBP-1c–mediated lipogenesis in both liver and muscle by reducing fasting hyperinsulinemia | |||
0.003%, 0.006%, and 0.012% of diet for 6 wk | Male Long-Evans hooded rats | Lowered adiposity and TG contents in parametrial adipose tissue | (54) |
AMPK, AMP kinase; CPT-1, carnitine palmitoyltransferase 1; HMG-CoA, 3-hydroxy-3-methyl coenzyme A; LDLR, LDL receptor; NEFA, nonesterified FA; PGC-1α, peroxisome proliferator-activated receptor γ coactivator 1α SREBP-1c, sterol regulatory element–binding protein 1c; UCP-2, uncoupling protein 2.