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. 2014 Jul 7;5(4):404–417. doi: 10.3945/an.113.005603

TABLE 2.

Effects of naringin and naringenin on hyperlipidemia, body weight gain, and adipose tissue in metabolic syndrome1

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)
1

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.