Publication: Voluntary exercise opposes insulin resistance of skeletal muscle glucose transport during liquid fructose ingestion in rats
Issued Date
2018-08-01
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18778755
11387548
11387548
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2-s2.0-85048080400
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Mahidol University
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SCOPUS
Bibliographic Citation
Journal of Physiology and Biochemistry. Vol.74, No.3 (2018), 455-466
Suggested Citation
Yupaporn Rattanavichit, Jariya Buniam, Juthamard Surapongchai, Vitoon Saengsirisuwan Voluntary exercise opposes insulin resistance of skeletal muscle glucose transport during liquid fructose ingestion in rats. Journal of Physiology and Biochemistry. Vol.74, No.3 (2018), 455-466. doi:10.1007/s13105-018-0639-8 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/45085
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Title
Voluntary exercise opposes insulin resistance of skeletal muscle glucose transport during liquid fructose ingestion in rats
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Abstract
© 2018, University of Navarra. We have recently reported that male rats given liquid fructose ingestion exhibit features of cardiometabolic abnormalities including non-obese insulin resistance with impaired insulin signaling transduction in skeletal muscle (Rattanavichit Y et al. Am J Physiol Regul Integr Comp Physiol 311: R1200-R1212, 2016). While exercise can attenuate obesity-related risks of cardiometabolic syndrome, the effectiveness and potential mechanism by which exercise modulates non-obese insulin resistance have not been fully studied. The present investigation evaluated whether regular exercise by voluntary wheel running (VWR) can reduce cardiometabolic risks induced by fructose ingestion. Moreover, the potential cellular adaptations following VWR on key signaling proteins known to influence insulin-induced glucose transport in skeletal muscle of fructose-ingested rats were investigated. Male Sprague-Dawley rats were given either water or liquid fructose (10% wt/vol) without or with access to running wheel for 6 weeks. We demonstrated that VWR restored insulin-stimulated glucose transport in the soleus muscle by improving the functionality of several signaling proteins, including insulin-stimulated IRβ Tyr 1158 /Tyr 1162 /Tyr 1163 (82%), IRS-1 Tyr 989 (112%), Akt Ser 473 (56%), AS160 Thr 642 (76%), and AS160 Ser 588 (82%). These effects were accompanied by lower insulin-stimulated phosphorylation of IRS-1 Ser 307 (37%) and JNK Thr 183 /Tyr 185 (49%), without significant changes in expression of proteins in the renin-angiotensin system. Intriguingly, multiple cardiometabolic abnormalities were not observed in fructose-ingested rats with access to VWR. Collectively, this study demonstrates that the development of cardiometabolic abnormalities as well as insulin resistance of skeletal muscle and defective signaling molecules in rats induced by fructose ingestion could be opposed by VWR.