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. 2020 Dec 3;10(1):21102.
doi: 10.1038/s41598-020-78166-9.

Short-term Cudrania tricuspidata fruit vinegar administration attenuates obesity in high-fat diet-fed mice by improving fat accumulation and metabolic parameters

Jun-Hui Choi  1 , Myung-Kon Kim  2 , Soo-Hwan Yeo  3 , Seung Kim  4
Affiliations

Short-term Cudrania tricuspidata fruit vinegar administration attenuates obesity in high-fat diet-fed mice by improving fat accumulation and metabolic parameters

Jun-Hui Choi et al. Sci Rep. .

Abstract

Previous studies have suggested that vinegar intake can help to reduce body fat and hyperglycemia. Therefore, this study aimed to evaluate the anti-obesity efficacy of vinegar fermented using Cudrania tricuspidata fruits (CTFV) and its main phenolic constituents and to analyze its molecular mechanism and changes in obesity-related metabolizing enzymatic activities. We found that HFD significantly caused hepatic steatosis; increases in body fats, feed efficiency, liver mass, lipids, insulin, oxidative parameters, cardiovascular-associated risk indices, lipase and α-amylase activities, whereas CTFV efficaciously attenuated HFD-induced oxidant stress, fat accumulation, obesity-related enzymatic activity, and the activation or reduction of obesity-related molecular reactions via improving metabolic parameters including phosphorylated insulin receptor substrate 1, protein tyrosine phosphatase 1B, phosphorylated phosphoinositide 3-kinase/protein kinase B, phosphorylated mitogen-activated protein kinases, sterol regulatory element-binding protein 1c, CCAAT/enhancer-binding protein, and fatty acid synthase; and decreases in adiponectin receptor 1, leptin receptor, adenosine monophosphate-activated protein kinase, acetyl-CoA carboxylase, and peroxisome proliferator-activated receptor, subsequently ameliorating HFD-induced obesity. Therefore, CTFV might provide a functional food resource or nutraceutical product for reducing body fat accumulation.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Figure 1
Figure 1
HPLC analysis (A–E) and inhibitory effects (F–L) in CTF and CTFV. (A) Mixture of authentic standards. (B) CTF juice before sterilization. (C) CTF juice after sterilization. (D) CTF wine. (E) CTF vinegar. X-axis is retention time in minutes and Y-axis is absorbance unit (AU). (1) gastrodin; (2) p-hydroxybenzyl alcohol; (3) parishin E; (4) parishin B; (5) parishin C; (6) Parishin A (upper-left panel). (1) gallic acid; (2) protocatechuic acid; (3) chlorogenic acid; (4) p-hydroxybenzoic acid; (5) caffeic acid; (6) isovanillic acid; (7) rutin; (8) p-coumaric acid; (9) ferulic acid; (10) taxifolin; (11) trans-coumaric acid; (12) rosmarinic acid; (13) quecertin; 14, trans-cinnamic acid (upper-right panel). After pretreatment with CTFV and the compounds, the mixtures were incubated for 10 or 30 min. After incubation, the activity of the reaction mixtures was determined by the absorbance values read at 405, 412, or 580 nm. The inhibitory effect was expressed as the percent difference from the residual activity by Eq. (1) (Inhibitory effect (%) = [(Absorbance control without sample − Absorbance control with sample)/Absorbance control without sample] × 100) or Eq. (2) ([1 − Vmax control with sample/Vmax control without sample] × 100). Each value is the mean ± SD of triplicate measurements. *p < 0.05 and **p < 0.01, compared to non-treated each enzyme groups. αA, α-amylase; PL, pancreatic lipase; LPL, lipoprotein lipase; ALP, alkaline phosphatase; βG, β-glucosidase; CS, citrate synthase; PDE IV, phosphodiesterase IV.
Figure 2
Figure 2
Assessment of cytotoxic effects. MTT assay showing the effect of CTFV on 3T3-L1 (A), HepG2 (B), and Raw264.7 cells (C) viability. Cells were incubated with the compound at different concentrations (0–1000 μg/mL) for 24 h and cell viability was analyzed by MTT reduction assay. Each value is the mean ± SD of triplicate measurements. *p < 0.01, compared with non-treated group.
Figure 3
Figure 3
Effects of CTFV, PFV, and fenofibrate on body weight (A), body weight gain (B), reduction (%) (C), feed intake (D,E), and feed efficiency (F) in high fat-diet (HFD)-induced obese mice. Each value is the mean ± SD (n = 10). #p < 0.01, compared with Control group, *p < 0.01, compared with DIO group, ap < 0.01, compared with DIO + Feno group. Control, non-induced normal group; DIO, diet-induced obesity model group; DIO + Feno, fenofibrate-treated DIO group, DIO + PFV, pomegranate fruit vinegar (PFV)-treated DIO group; DIO + CTFV, C. tricuspidata fruit vinegar (CTFV)-treated DIO group.
Figure 4
Figure 4
Representative histopathological analysis of the livers (A) and adipocyte tissues (B). Effects of CTFV, PFV, and fenofibrate on hepatic fat (C), and size of epididymal adipose tissue (D) in the obese mice were analyzed with H&E, microscope, and ImageJ. Each value is the mean ± SD of triplicate measurements. #p < 0.01, compared with Control group, *p < 0.01, compared with DIO group, ap < 0.01, compared with DIO + Feno group, bp < 0.05, compared with DIO + PFV group. Control, non-induced normal group; DIO, diet-induced obesity model group; DIO + Feno, fenofibrate-treated DIO group, DIO + PFV, pomegranate fruit vinegar (PFV)-treated DIO group; DIO + CTFV, C. tricuspidata fruit vinegar (CTFV)-treated DIO group.
Figure 5
Figure 5
Effects of CTFV, PFV, and fenofibrate on α-amylase (A,G), pancreatic lipase (B), lipoprotein lipase (C,H), alkaline phosphatase (D,I), β-glucosidase (E,J), and phosphadesterase IV (F,K), and citrate synthase (L) in serum and liver from the obese mice. Each value is the mean ± SD of triplicate measurements. #p < 0.05 and ##p < 0.01, compared with Control group, *p < 0.05 and **p < 0.01, compared with DIO group, ap < 0.05 and aap < 0.01, compared with DIO + Feno group. Control, non-induced normal group; DIO, diet-induced obesity model group; DIO + Feno, fenofibrate-treated DIO group, DIO + PFV, pomegranate fruit vinegar (PFV)-treated DIO group; DIO + CTFV, C. tricuspidata fruit vinegar (CTFV)-treated DIO group.
Figure 6
Figure 6
Effects of CTFV, PFV, and fenofibrate on AdipoR1, OBR, IRS1, and PTP1B (A), or PI3K, AKT, ERK, P38, AMPK, and ACC (B) expressions in liver from the obese mice. Each value is the mean ± SD of triplicate measurements. Protein expression was detected by western blotting. #p < 0.01, compared with Control group, *p < 0.05 and **p < 0.01, compared with DIO group, ap < 0.05 and aap < 0.01, compared with DIO + Feno group, bp < 0.01, compared with DIO + PFV group. Control, non-induced normal group; DIO, diet-induced obesity model group; DIO + Feno, fenofibrate-treated DIO group, DIO + PFV, pomegranate fruit vinegar (PFV)-treated DIO group; DIO + CTFV, C. tricuspidata fruit vinegar (CTFV)-treated DIO group.
Figure 7
Figure 7
Effects of CTFV, PFV, and fenofibrate on GLUT4, SREBP1C, PPARα, PPARγ, CEBPα, CEBPβ, and FAS expressions in liver from the obese mice. Each value is the mean ± SD of triplicate measurements. Protein expression was detected by western blotting. #p < 0.01, compared with Control group, *p < 0.01, compared with DIO group (A), ap < 0.05 and aap < 0.01, compared with DIO + Feno group, bp < 0.01, compared with DIO + PFV group. Control, non-induced normal group; DIO, diet-induced obesity model group; DIO + Feno, fenofibrate-treated DIO group, DIO + PFV, pomegranate fruit vinegar (PFV)-treated DIO group; DIO + CTFV, C. tricuspidata fruit vinegar (CTFV)-treated DIO group.
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