Endocrine journalJul 12, 2019

Ellagic acid helps turn white fat into brown fat in obese rats by reducing genes that keep fat cells white

Regenerative Health Weekly Brief ↗PubMed ↗DOI ↗

Updated Mar 28, 2026

Abstract

Supplementation with Ellagic Acid (EA) for 24 weeks improved metabolic health in high-fat diet-induced obesity in rats.

High-fat diet intake resulted in overweight, glucose intolerance, and white adipocyte enlargement.
EA treatment mitigated the negative effects associated with a high-fat diet.
Supplementation with EA reduced serum resistin levels and improved liver fat accumulation and lipid profiles.
EA decreased the expression of genes associated with maintaining white adipose tissue.
Increased expression of brown adipocyte markers and mitochondrial function was observed with EA supplementation.
EA significantly elevated the expression of UCP1, a specific protein of brown adipocytes, in inguinal white adipose tissue.

Simplified

Promoting brown adipose tissue (BAT) formation and function reduces obesity. Ellagic Acid (EA), located abundantly in plant extracts and fruits, has been shown to modulate formation and differentiation of adipocytes, although its role in the process of browning of white adipose tissue (WAT) has not been elucidated. In this study, fifty-six five-week old SD rats were randomly assigned to receive normal diet (ND, 10% lipids) or high-fat diet (HFD, 60% lipid) with or without various dosages of EA for 24 weeks. Our results showed that high fat diet intake triggered overweight, glucose intolerance and white adipocyte hypertrophy, the effects of which were mitigated by EA treatment. Meanwhile, EA supplementation reduced serum resistin levels, improved hepatic steatosis and serum lipid profile in DIO (high fat diet induced obesity) rats. Moreover, EA supplementation significantly decreased mRNA expression of Zfp423 and Aldh1a1, the key determinants of WAT plasticity. EA also increased mRNA expression of brown adipocyte markers including UCP1, PRDM16, Cidea, PGC1α, Ppar-α; beige markers including CD137and TMEM26; mitochondrial biogenesis markers including TFAM in inguinal WAT (iWAT) when compared to their counterparts. EA treatment significantly improved mitochondrial function, as measured by citrate synthase activity. More importantly, EA markedly elevated the expression of UCP1 in iWAT, which is a specific protein of brown adipocyte. In conclusion, our results provided evidence that EA improved obesity-induced dyslipidemia and hepatic steatosis in DIO rats via browning of iWAT through suppressing white adipocyte maintaining genes and promoting expression of key thermogenic genes. These findings suggest that EA could be a promising therapeutic avenue to treat metabolic diseases.

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Ellagic acid helps turn white fat into brown fat in obese rats by reducing genes that keep fat cells white

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