期刊
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
卷 473, 期 4, 页码 673-682出版社
SPRINGER HEIDELBERG
DOI: 10.1007/s00424-021-02543-0
关键词
Lithium; Exercise; T1DM; Glycogen breakdown; GSK3β AKT
类别
资金
- Ministry of Education of the Republic of Korea
- National Research Foundation of Korea [NRF-2017S1A5A2A01024319]
- National Research Foundation of Korea [2017S1A5A2A01024319] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
The study found that lithium can lower blood glucose levels in T2DM and T1DM animal models by enhancing glucose uptake, as well as enhancing exercise-induced glycogen breakdown and insulin-induced AKT activation.
The purpose of this study was to investigate the effect of lithium on glucose disposal in a high-fat diet-induced type 2 diabetes mellitus (T2DM) and streptozotocin-induced type 1 diabetes mellitus (T1DM) animal model along with low-volume exercise and low-dose insulin. Lithium decreased body weight, fasting plasma glucose, and insulin levels when to treat with low-volume exercise training; however, there were no adaptive responses like an increase in GLUT4 content and translocation factor levels. We discovered that lithium enhanced glucose uptake by acute low-volume exercise-induced glycogen breakdown, which was facilitated by the dephosphorylation of serine 473-AKT (Ser473-AKT) and serine 9-GSK3 beta. In streptozotocin-induced T1DM mice, Li/low-dose insulin facilitates glucose uptake through increase the level of exocyst complex component 7 (Exoc7) and Ser473-AKT. Thus, lithium enhances acute exercise-induced glycogen breakdown and insulin-induced AKT activation and could serve as a candidate therapeutic target to regulate glucose level of DM patients.
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