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Review
. 2014 Jul 14;5(4):404-17.
doi: 10.3945/an.113.005603. Print 2014 Jul.

Effect of citrus flavonoids, naringin and naringenin, on metabolic syndrome and their mechanisms of action

Affiliations
Review

Effect of citrus flavonoids, naringin and naringenin, on metabolic syndrome and their mechanisms of action

M Ashraful Alam et al. Adv Nutr. .

Abstract

Flavonoids are important natural compounds with diverse biologic activities. Citrus flavonoids constitute an important series of flavonoids. Naringin and its aglycone naringenin belong to this series of flavonoids and were found to display strong anti-inflammatory and antioxidant activities. Several lines of investigation suggest that naringin supplementation is beneficial for the treatment of obesity, diabetes, hypertension, and metabolic syndrome. A number of molecular mechanisms underlying its beneficial activities have been elucidated. However, their effect on obesity and metabolic disorder remains to be fully established. Moreover, the therapeutic uses of these flavonoids are significantly limited by the lack of adequate clinical evidence. This review aims to explore the biologic activities of these compounds, particularly on lipid metabolism in obesity, oxidative stress, and inflammation in context of metabolic syndrome.

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Conflict of interest statement

Author disclosures: M. A. Alam, N. Subhan, M. M. Rahman, S. J. Uddin, H. M. Reza, and S. D. Sarker, no conflicts of interest.

Figures

FIGURE 1
FIGURE 1
Effect of citrus fruits on various pathologic conditions in human health. MCP-1, monocyte chemotactic protein 1; PGC-1α, peroxisome proliferator-activated receptor γ coactivator 1α.
FIGURE 2
FIGURE 2
Basic structure of flavonoids (I), naringin (II), and naringenin (III).
FIGURE 3
FIGURE 3
Transcriptional regulation of fat metabolism and mitochondrial biogenesis via AMPK-PGC-1α–mediated pathway. PGC-1α, in combination with the nuclear hormone receptor PPAR-γ, promotes the expression of NRF, UCP-1, mtTFA, and components of the respiratory chain complex. mtTFA translocates to mitochondria where it regulates the expression of mitochondrial genes and mitochondrial DNA replication. AMPK, AMP-activated protein kinase; mtTFA, mitochondrial transcription factor A; NRF, nuclear respiratory; factor; pAMPK, phosphorylated AMPK; PGC-1α, peroxisome proliferator-activated receptor γ coactivator 1α ROS, reactive oxygen species; UCP-1, uncoupling protein 1.

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