Nutr Res Pract.  2023 Oct;17(5):870-882. 10.4162/nrp.2023.17.5.870.

Mentha canadensis attenuates adiposity and hepatic steatosis in high-fat diet-induced obese mice

Affiliations
  • 1Biological Clock-based Anti-aging Convergence Regional Leading Research Center of National Research Foundation of Korea, Korea University, Sejong 30019, Korea
  • 2Department of Food and Nutrition, Chosun University, Gwangju 61452, Korea
  • 3Department of Food Science and Nutrition, Kyungpook National University, Daegu 41566, Korea
  • 4Center for Food and Nutritional Genomics Research, Kyungpook National University, Daegu 41566, Korea
  • 5Center for Beautiful Aging, Kyungpook National University, Daegu 41566, Korea

Abstract

BACKGROUND/OBJECTIVES
Obesity is a major risk factor for metabolic syndrome, a global public health problem. Mentha canadensis (MA), a traditional phytomedicine and dietary herb used for centuries, was the focus of this study to investigate its effects on obesity.
MATERIALS/METHODS
Thirty-five male C57BL/6J mice were randomly divided into 2 groups and fed either a normal diet (ND, n = 10) or a high-fat diet (HFD, n = 25) for 4 weeks to induce obesity. After the obesity induction period, the HFD-fed mice were randomly separated into 2 groups: one group continued to be fed HFD (n = 15, HFD group), while the other group was fed HFD with 1.5% (w/w) MA ethanol extract (n = 10, MA group) for 13 weeks.
RESULTS
The results showed that body and white adipose tissue (WAT) weights were significantly decreased in the MA-supplemented group compared to the HFD group. Additionally, MA supplementation enhanced energy expenditure, leading to improvements in plasma lipids, cytokines, hepatic steatosis, and fecal lipids. Furthermore, MA supplementation regulated lipid-metabolism-related enzyme activity and gene expression, thereby suppressing lipid accumulation in the WAT and liver.
CONCLUSIONS
These findings indicate that MA has the potential to improve diet-induced obesity and its associated complications, including adiposity, dyslipidemia, hepatic steatosis, and inflammation.

Keyword

Obesity; metabolic syndrome; herbal medicine; nonalcoholic fatty liver disease; diet; high-fat

Figure

  • Fig. 1 Effects of 13-week Mentha Canadensis extract supplementation on body and adipocyte weights and eWAT morphology in C57BL/6J mice fed a HFD. (A) Changes in BW, (B) BWG, (C) FI and EI, (D) WAT weight, and (E) eWAT morphology. Data are presented as the mean ± SE. Representative eWAT photomicrographs shown at 200× magnification.ND, normal diet; HFD, high-fat diet (20% fat and 1% cholesterol); MA, high-fat diet + Mentha canadensis ethanol extract (1.5%, w/w); H&E, hematoxylin and eosin-stained transverse section of epididymal white adipose tissue; eWAT, epididymal white adipose tissue; BW, body weight; BWG, body weight gain; FI, food intake; EI, energy intake; SUB, subcutaneous; VIS, visceral.Mann Whitney U t-test; *P < 0.05, **P < 0.01, ***P < 0.001 vs. control.

  • Fig. 2 Effects of 13-week Mentha canadensis extract supplementation on energy expenditure in C57BL/6J mice fed a HFD. (A) Measures of energy expenditure. (B) Immunohistochemistry of UCP1 staining in BAT (magnification 200×). (C) Measures of epididymal white adipose tissue mRNA expression of genes related to lipid metabolism. Data are presented as the mean ± SE.ND, normal diet; HFD, high-fat diet (20% fat and 1% cholesterol); MA, high-fat diet + Mentha canadensis ethanol extract (1.5%, w/w); BAT, brown adipose tissue; GAPDH, glyceraldehyde-3-phosphate dehydrogenase.Mann Whitney U t-test; *P < 0.05, **P < 0.01, ***P < 0.001 vs. control.

  • Fig. 3 Effects of 16-week Mentha canadensis supplementation on hepatic steatosis-related biomarkers in C57BL/6J mice fed a HFD. (A) Measures of liver weight. (B) Photomicrographs showing hepatic morphology (magnification 200×). Measures of (C) hepatic lipid contents and (D) hepatic enzyme activities related to lipid metabolism. (E, F) Hepatic mRNA expression levels of genes involved in lipid metabolism. Data are presented as the mean ± SE.ND, normal diet; HFD, high-fat diet (20% fat and 1% cholesterol); MA, high-fat diet + Mentha canadensis ethanol extract (1.5%, w/w); FAS, fatty acid synthase, G6PD, glucose-6-phosphatedehydrogenase; PAP, phosphatidate phosphatase; ME, malic enzyme; CPT, carnitine palmitoyl-coenzyme A reductase; BW, body weight; TG, triglyceride; FA, fatty acid; FAS, fatty acid synthase; GAPDH, glyceraldehyde-3-phosphate dehydrogenase.Mann Whitney U t-test; *P < 0.05, **P < 0.01, ***P < 0.001 vs. control.

  • Fig. 4 Effects of 16-week Mentha canadensis supplementation on plasma and fecal lipid contents in C57BL/6J mice fed a HFD. (A) Plasma lipid profiles. (B) Plasma leptin levels. (C) Fecal lipid contents. Data are presented as the mean ± SE.ND, normal diet; HFD, high-fat diet (20% fat and 1% cholesterol); MA, high-fat diet + Mentha canadensis ethanol extract (1.5%, w/w); TG, triglyceride; FFA, free fatty acid; PL, phospholipid; TC, total cholesterol; C, cholesterol; HDL, high-density lipoprotein; Apo, apolipoprotein.Mann Whitney U t-test; *P < 0.05, **P < 0.01, ***P < 0.001 vs. control.

  • Fig. 5 Effects of 16-week Mentha canadensis supplementation on inflammation and fibrosis biomarkers in C57BL/6J mice fed a HFD. (A) Plasma cytokine levels. (B) MT staining of eWAT and hepatic tissue (magnification 200×). (C) Hepatic mRNA expression levels of inflammation-related genes. Data are presented as the mean ± SE.ND, normal diet; HFD, high-fat diet (20% fat and 1% cholesterol); MA, high-fat diet + Mentha canadensis ethanol extract (1.5%, w/w); IL-6, interleukin 6; MCP1, monocyte chemoattractant protein-1; eWAT, epididymal white adipose tissue; MT, Masson’s trichrome; GAPDH, glyceraldehyde-3-phosphate dehydrogenase.Mann Whitney U t-test; *P < 0.05, **P < 0.01, ***P < 0.001 vs. control.


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