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, 35 (4), 403-410

Theracurmin (Highly Bioavailable Curcumin) Prevents High Fat Diet-Induced Hepatic Steatosis Development in Mice

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Theracurmin (Highly Bioavailable Curcumin) Prevents High Fat Diet-Induced Hepatic Steatosis Development in Mice

Jin Won Yang et al. Toxicol Res.

Abstract

Curcumin, a hydrophobic polyphenol isolated from the Curcuma longa L. plant, has many pharmacological properties, including antioxidant, anti-inflammatory, and chemo-preventive activities. Curcumin has been shown to have potential in preventing nonalcoholic fatty liver disease (NAFLD). However, the low bioavailability of curcumin has proven to be a major limiting factor in its clinical adoption. Theracurmin, a highly bioavailable curcumin that utilizes micronized technology showed improved biological absorbability in vivo. The aim of this study was to investigate the role of theracurmin in modulating hepatic lipid metabolism in vivo. A fatty liver mouse model was produced by feeding mice a high fat diet (HFD; 60% fat) for 12 weeks. We found that treatment for 12 weeks with theracurmin significantly lowered plasma triacylglycerol (TG) levels and reduced HFD-induced liver fat accumulation. Theracurmin treatment lowered hepatic TG and total cholesterol (T-CHO) levels in HFD-fed mice compared to controls. In addition, theracurmin administration significantly reduced lipid peroxidation and cellular damage caused by reactive oxygen species in HFD-fed mice. Overall, these results suggest that theracurmin has the ability to control lipid metabolism and can potentially serve as an effective therapeutic remedy for the prevention of fatty liver.

Keywords: Curcumin; Fatty liver; High fat diet (HFD); Nonalcoholic fatty liver disease (NAFLD); Steatosis; Theracurmin.

Conflict of interest statement

CONFLICT OF INTEREST The Authors who have taken part in this study declared that they do not have anything to disclose regarding funding or conflict of interest with respect to this manuscript. Hee Hye Yun is former employee of HANDOK, Inc.

Figures

Fig. 1
Fig. 1
Effects of theracurmin on hepatic lipid accumulation in mice fed with HFD. (A) Liver sections were stained with H&E or oil-Red O staining. The mice were fed either a ND or HFD for 12 weeks. theracurmin (500, 1,000, and 2,000mg/kg) or silymarin (25mg/kg) (reference control) was administered to the mice at the same time. H&E staining. The livers of the mice were stained with H&E after a treatment with 500, 1,000, and 2,000mg/kg theracurmin for 12 weeks. CV, Central vein; PT, Portal triad area; Scale bars = 100 μm. Oil Red O staining. Each photo represents their groups after staining with Oil Red O in the liver. Scale bars = 100 μm. (B) Histomorphometric analysis. Measurement of hepatic steatosis region (%/mm2 of hepatic parenchyma) and diameter of hepatocyte (mm/hepatocyte). Data were expressed as mean ± SEM statistically analyzed by LSD-test methods. Significant versus normal control, ##p< 0.01; significant versus HFD-fed group, **p< 0.01 (n = 10). G1: ND (normal saline), n = 10; G2: HFD + vehicle (normal saline), n = 10; G3: HFD + theracurmin (500 mg/kg/day), n = 10; G4: HFD + theracurmin (1,000 mg/kg/day), n = 10; G5: HFD + theracurmin (2,000 mg/kg/day), n = 10; G6: HFD + reference control (silymarin 25 mg/kg/day), n = 10.
Fig. 2
Fig. 2
Effects of theracurmin on the accumulation of hepatic TG and CHO in HFD-fed mice. (A, B) Measurement of accumulation of TG and CHO in the liver from mice of each group. Data were expressed as mean ± SEM statistically analyzed by LSD-test methods. Significant versus normal control, ##p< 0.01; significant versus HFD-fed group, **p< 0.01 (n = 10). G1: ND (normal saline), n = 10; G2: HFD + vehicle (normal saline), n = 10; G3: HFD + theracurmin (500 mg/kg/day), n = 10; G4: HFD + theracurmin (1,000 mg/kg/day), n = 10; G5: HFD + theracurmin (2,000 mg/kg/day), n = 10; G6: HFD + reference control (silymarin 25 mg/kg/day), n = 10.
Fig. 3
Fig. 3
Effects of theracurmin on the serum TG, CHO, LDL, and HDL in HFD-fed mice. (A–D) serum TG levels (A), serum CHO levels (B), serum LDL levels (C), serum HDL levels (D) in mice fed a normal diet or high-fat-diet for 12 weeks. Data were expressed as mean ± SEM statistically analyzed by Q-test and LSD-test methods. Significant versus normal control, ##p< 0.01; significant versus HFD-fed group, **p< 0.01 (n = 10). G1: ND (normal saline), n = 10; G2: HFD + vehicle (normal saline), n = 10; G3: HFD + theracurmin (500mg/kg/day), n = 10; G4: HFD + theracurmin (1,000 mg/kg/day), n = 10; G5: HFD + theracurmin (2,000 mg/kg/day), n = 10; G6: HFD + reference control (silymarin 25mg/kg/day), n = 10.
Fig. 4
Fig. 4
Effects of theracurmin on oxidative stress in HFD-fed mice. Measurement of hepatic MDA and GSH contents in the liver from mice of each group. Data were expressed as mean ± SEM statistically analyzed by Q-test and LSD-test methods. Significant versus normal control, ##p< 0.01; significant versus HFD-fed group, *p< 0.05; **p< 0.01 (n = 10). G1: ND (normal saline), n = 10; G2: HFD + vehicle (normal saline), n = 10; G3: HFD + theracurmin (500 mg/kg/day), n = 10; G4: HFD + theracurmin (1,000 mg/kg/day), n = 10; G5: HFD + theracurmin (2,000 mg/kg/day), n = 10; G6: HFD + reference control (silymarin 25 mg/kg/day), n = 10.

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