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The Journal of Exercise Nutrition & Biochemistry
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eISSN : 2233-6842

Special Article


pISSN : 2233-6834
eISSN : 2233-6842
Editor in Chief : Jonghoon Park
The Journal of Exercise Nutrition & Biochemistry - Vol. 22 , No. 3

Treadmill running suppresses the vulnerability of dopamine D2 receptor deficiency to obesity and metabolic complications: a pilot study

Jinkyung Cho, Donghyun Kim, Jungmoon Jang, Jeonghyeon Kim, Hyunsik Kang

[Purpose] To investigate the effect of treadmill running on D2R deficiency related susceptibility to high fat diet (HFD )-induced obesity and its metabolic complications.

[Methods] D2R-/- and +/- mice were obtained by backcrossing D2R+/- heterozygotes on wild type (WT) littermates (C57BL/6J background) for >10 generations. Mice were randomly assigned to 1) WT mice with standard chow (SC) (WT+SC); 2) WT mice with high-fat diet (WT+HFD); 3) WT mice with high-fat diet plus exercise (WT+HFD+EX), 4) heterozygous (HET) D2R mice with SC (HET+SC); 5) heterozygous D2R mice with HFD (HET+HFD); and 6) heterozygous D2R mice with HFD plus exercise (HET+HFD+EX). In addition, mice assigned to EX groups were subjected to running on a motor-driven rodent treadmill with a frequency of 5 days per week.

[Results] After a 10-week HFD treatment, HET D2R (+/-) mice exhibited significantly higher values for hepatic steatosis (p<0.001), areas under the curves (AUCs) for the glucose tolerance test (GTT) and the insulin tolerance test (ITT) (p<0.001 & p<0.001 respectively), serum leptin (p=0.005) and total cholesterol (TC ) (p=0.009), in conjunction with decreased locomotor activity (p=0.031), compared to HET mice exposed to standard chow. However, these HFD-induced elevations in hepatic steatosis (p<0.001), AUCs for GTT and ITT (p=0.032 & p=0.018, respectively), serum leptin (p=0.038) and TC (p=0.038) were significantly alleviated after 10 weeks of treadmill running.

[Conclusion] The current findings of the study provide experimental evidence of treadmill running as an effective and non-pharmacologic strategy to treat the susceptibility of brain D2R deficiency to HFD-induced obesity and metabolic disorders.




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