Stress affects the oscillation of blood glucose levels in rodents

ABSTRACT

Background

The baseline of glucose level is one of the most fundamental metrics of glucose metabolism assessments and diabetes diagnosis. Under the demands of maintaining physical activity levels and stimulation from various external factors, blood glucose levels are in a fractal fluctuation state and maintain a day-night rhythm in physical condition. Although several stressors stimulation has been considered to increase glucose levels, how stress affects the glucose oscillation is unknown. Methods: In the study, we measure the glucose levels of mice by glucometer for exploring how the blood collection affect the fractal fluctuation of glucose. Furthermore, we monitor the glucose levels of rats by the continuous glucose monitoring system to study the change of glucose day-night rhythm underlying external stress. Results: We found that stressors (i.e., blood collection) expand the fractal fluctuation of blood glucose. Strikingly, external stress stimulation irreversibly erases the circadian rhythm of glucose levels. The cycle of activity and body temperature, which are tested simultaneously, are also disturbed by stress stimulation. Conclusions: These results reveal a novel insight that stress stimulation leads to an irreversible disruption of the glucose cycle and provides vital implications for the pathogenesis and treatment of long-term stress-induced glucose metabolic disorders.

KEYWORDS:

• Circadian rhythm
• glucose
• termpreature
• activity
• fractal fluctuation

Highlights

Stressors (i.e. blood collection) expanded the fractal fluctuation of blood glucose.

External stress irreversibly erased the circadian rhythm of glucose level in physical condition.

The cycle of activity and body temperature were disturbed by stress stimulation.

Acknowledgments

We thank Zhonghua Lu, Hong Wang, and Fan Yang for their helpful comments, Ningning Li for the intragastric administration in rats, and Zhanhong Du for the data analysis advice. The authors would like to thank the National Natural Science Foundation of China (NSFC) 81425010 (L.W.), NSFC 31630031 (L.W.), NSFC 91632303 (L.W.); the Strategic Priority Research Program of the Chinese Academy of Sciences XDB02050003 (L.W.); External Cooperation Program of the Chinese Academy of Sciences GJHZ1508 (L.W.); International Partnership Program of Chinese Academy of Sciences 172644KYS820170004 (L.W.); Guangdong Key Lab of Brain Connectome and Behavior 2017B030301017 (L.W.); Shenzhen Governmental Basic Research Grant JCYJ20150529143500959 (L.W.) JCYJ20170413164535041 (L.W.); Shenzhen Discipline Construction Project for Neurobiology DRCSM [2016]1379 (L.W.). The Science, Technology and Innovation Commission of Shenzhen Municipality No. JCYJ20150401150223647 (P.W.) for supporting the project.

Disclosure statement

No potential conflict of interest was reported by the authors.

Supplementary material

Supplementary data for this article should be accessed at 10.1080/09291016.2018.1558734

Additional information

Funding

The authors would like to thank National Natural Science Foundation of China (NSFC) 81425010 (L.W.), NSFC 31630031(L.W.), NSFC 91632303(L.W.); the Strategic Priority Research Program of the Chinese Academy of Sciences XDB02050003 (L.W.); External Cooperation Program of the Chinese Academy of Sciences GJHZ1508 (L.W.); International Partnership Program of Chinese Academy of Sciences 172644KYS820170004 (L.W.); Guangdong Key Lab of Brain Connectome and Behavior 2017B030301017 (L.W.); Shenzhen Governmental Basic Research Grant JCYJ20150529143500959 (L.W.) JCYJ20170413164535041 (L.W.); Shenzhen Discipline Construction Project for Neurobiology DRCSM [2016]1379 (L.W.). The Science, Technology and Innovation Commission of Shenzhen Municipality No. JCYJ20150401150223647 (P.W.) for supporting the project.