Preventive Effects of Health-Food Drinks on the Obesity and DNA Damage of Mice Fed a High-Fat Diet under a Mild Stress

Authors

  • Minoru Higashimoto Graduate School of Human Life & Science, Nagoya Keizai University
  • Chikako Toda Department of Food & Nutrition, Suzugamine Women’s College, Hiroshima, Japan
  • Nao Tokumoto Department of Food & Nutrition, Suzugamine Women’s College, Hiroshima, Japan
  • Arinobu Yamauchi Department of Food & Nutrition, Suzugamine Women’s College, Hiroshima, Japan

DOI:

https://doi.org/10.6000/1929-4247.2016.05.03.3

Keywords:

health-food drinks, high-fat diet, restraint stress, obesity, DNA damage, dyslipidemia.

Abstract

The body weight gain of mice fed an obesity-inducing diet is suppressed by a mild restraint stress, but at the same time, as previously reported, the stress induces DNA damage in the cells of multiple organs. In the present study, we attempted to prevent not only the obesity but also the DNA damage of mice fed an obesity-inducing diet under a mild restraint with commercially available health-food drinks such as fruit and vegetable juices, soymilks, vinegars and lactic acid bacteria drinks, which are rich in antioxidants. The body weight gain of young female mice fed a high-fat diet containing 20% fat for 4 weeks was considerably inhibited by restraint for 15 min per day in weeks 2 to 4 of 4-week period. The inhibition was further promoted with the concomitant administration of health-food drinks noted above, and was accompanied by a decrease of periovular fat, a major abdominal fat in the female mice. The definite loss of energy intake in the mice given health-food drinks was approximately compensated by the energy of the drink administered. On the other hand, the increase of DNA damage generated by restraint in the cells of five organs – the liver, pancreas, spleen, heart and bone marrow – was markedly suppressed with the administration of these drinks. The results suggest that a combination of mild stress and intake of suitable health-food containing some antioxidants may inhibit lifestyle-related diseases including hyperlipidemia and obesity, which may contribute to the inhibition of metabolic syndrome and childhood obesity.

References

[1] Olinski R, Siomek A, Rozalski R, et al. Oxidative damage to DNA and antioxidant status in aging and age-related diseases. Acta Biochim Polonica 2007; 54: 11-26.
[2] Palafox-Carlos H, Ayala-Zavala JF, González-Aguilar GA. The role of dietary fiber in the bioaccessibility and bioavailability of fruit and vegetable antioxidants. J Food Sci 2011; 76: R6-R15.
http://dx.doi.org/10.1111/j.1750-3841.2010.01957.x
[3] Poljsak B. Strategies for reducing or preventing the genera-tion of oxidative stress. Oxid Med Cell Longev 2011; 1-15.
http://dx.doi.org/10.1155/2011/194586
[4] Marseglia L, Manti S, D’Angelo G, et al. Oxidative stress in obesity: a critical component in human diseases. Int J Mol Sci 2015; 16: 378-400.
http://dx.doi.org/10.3390/ijms16010378
[5] Fukuda S, Morimoto K. Lifestyle, stress and cortisol response: Review I, mental stress. Environ Health Prev Med 2001; 6: 9-14.
http://dx.doi.org/10.1007/BF02897303
[6] Fukuda S, Morimoto K. Lifestyle, stress and cortisol response: Review II, lifestyle. Environ Health Prev Med 2001; 6: 15-21.
http://dx.doi.org/10.1007/BF02897304
[7] Meydani M, Hasan ST. Dietary polyphenols and obesity. Nutrients 2010; 2: 737-51.
http://dx.doi.org/10.3390/nu2070737
[8] Güngör NK. Overweight and obesity in children and adolescents. J Clin Res Pediatr Endocrinol 2014; 6: 129-43.
http://dx.doi.org/10.4274/jcrpe.1471
[9] Pulgaron ER, Delamater AM. Obesity and type 2 diabetes in children: epidemiology and treatment. Curr Diab Rep 2014; 14: 508.
http://dx.doi.org/10.1007/s11892-014-0508-y
[10] Kondoh M, Tsukada M, Kuronaga M, et al. Induction of hepatic metallothionein synthesis by endoplasmic reticulum stress in mice. Toxicol Lett 2004; 148: 133-9.
http://dx.doi.org/10.1016/j.toxlet.2003.12.066
[11] Suzuki S, Tohma S, Futakawa N, Higashimoto M, Takiguchi M, Sato M. Induction of hepatic metallothionein by mitocho-ndrial oxidative stress in mice. J Health Sci 2005; 51: 533-7.
http://dx.doi.org/10.1248/jhs.51.533
[12] Futakawa N, Kondoh M, Ueda S, et al. Involvement of oxi-dative stress in the synthesis of metallothionein induced by mitochondrial inhibitors. Biol Pharm Bull 2006; 29: 2016-20.
http://dx.doi.org/10.1248/bpb.29.2016
[13] Higashimoto M, Isoyama N, Ishibashi S, et al. Tissue-dependent preventive effect of metallothionein against DNA damage in dyslipidemic mice under repeated stresses of fasting or restraint. Life Sci 2009; 84: 569-75.
http://dx.doi.org/10.1016/j.lfs.2009.01.022
[14] Sato M, Ishibashi S, Higashimoto M, Kadota Y, Kawakami T, Suzuki S. Early changes induced by environmental stresses in insulin sensitivity-related genes. Eur J Pharmaco 2011; l668: 472-6.
[15] Higashimoto M, Isoyama N, Ishibashi S, et al. Preventive effects of metallothionein against DNA and lipid metabolic damages in dyslipidemic mice under repeated mild stress. J Med Invest 2013; 60: 240-8.
http://dx.doi.org/10.2152/jmi.60.240
[16] Kouda K, Iki M. Beneficial effects of mild stress (hormetic effects): Dietary restriction and health. J Physiol Anthropol 2010; 29: 127-32.
http://dx.doi.org/10.2114/jpa2.29.127
[17] Machlin LJ, Bendich A. Free radical tissue damage: protec-tive role of antioxidant nutrients. FASEB J 1987; 1: 441-5.
[18] Jacob RA, Burri BJ. Oxidative damage and defense. Am J Clin Nutr 1996; 63: 985S-90.
[19] Bieri JG, Stoewsand GS, Briggs GM, Phillips RW, Woodard JC, Knapka JJ. Report of the American Institute of Nutrition Ad Hoc Committee on standards for nutritional studies. J Nutr 1977; 107: 1340-8.
[20] Sasaki YF, Tsuda S, Izumiyama F, Nishidate E. Detection of chemically induced DNA lesions in multiple mouse organs (liver, lung, spleen, kidney, and bone marrow) using the alkaline single cell gel electrophoresis (Comet) assay. Mutat Res 1997; 388: 33-44.
http://dx.doi.org/10.1016/S1383-5718(96)00133-7
[21] Collins AR. The comet assay for DNA damage and repair. Mol Biotech 2004; 26: 249-61.
http://dx.doi.org/10.1385/MB:26:3:249
[22] IDF Diabetes Atlas 7th ed., 2015.
[23] Katz DL. Diet and diabetes: lines and dots. J Nutr 2014; 144: 567s-70.
http://dx.doi.org/10.3945/jn.113.182923
[24] Lamprecht M, Obermayer G, Seebauer W. Influence of mixed fruit and vegetable concentrates on redox homeostasis and immune system of exercising people. Antioxidants in Sport Nutrition. Chapter 12: Florida; Boca Raton: CRC Press/Taylor & Francis 2015.
[25] Rui Hai Liu. Potential synergy of phytochemicals in cancer pre-vention: mechanism of action. J Nutr 2004; 134: 3479S-85.
[26] Diplock AT, Charleux JL, Crozier-Villi G, et al. Functional food science and defence against reactive oxidative species. Br J Nutr 1998; 80(Suppl 1): S77-112.
http://dx.doi.org/10.1079/BJN19980106
[27] Juan CA, Veronica F-S, Pedro M-R, Maria LV, et al. Frontiers in aging. Neurosc 2015; 7: 1-7.

Downloads

Published

2016-09-02

Issue

Section

Special Issue: The Metabolic Syndrome and Childhood Obesity: A Critical Public Health Issue