BACKGROUND:In the condition of exercise physiology, adenosine triphosphate-sensitive potassium (KATP) channel plays an important role in many aspects, such as regulation of coronary artery tension, exercise-induced myocardial protection effect and delay of skeletal muscle fatigue. OBJECTIVE:To review and investigate the role of KATP in exercise in order to provide theoretical reference for understanding mechanism underlying exercise regulation of body’s metabolism. METHODS: A computer-based online search of PubMed and VIP databases was performed for articles related to molecular structure, biological function and regulatory role of KATP as wel as correlation of KATP with coronary artery, myocardium, skeletal muscle fatigue and exercise ability published from January 1991 to June 2014. The keywords were “KATP channels; adenosine triphosphate; sports; myocardium; ion channels” in English and Chinese, respectively. Finaly, 42 relevant articles were included in result analysis. RESULTS AND CONCLUSION: Coupling with celular energy metabolism and cel membrane excitability, KATP channel is one of the effectors for myocardial protection in response to various physiological and pathological stresses. Prolonged endurance training can increase the expression of skeletal muscle and myocardial KATP, which may be an adaptive performance of the myocardium and skeletal muscle in response to exercise stress. KATP may participate in regulation of coronary blood flow. Myocardial KATP plays an important protective role for aleviating myocardial ischemia-reperfusion injury induced by exercise. When skeletal muscle fatigue occurs, the activation of KATP is helpful to prevent muscle fiber damage and cel death due to excessive consumption of ATP, in favor for the fast recovery from fatigue. The relation between KATP and exercise ability stil needs further research.

OBJECTIVE To systematically evaluate the regulatory effect of liraglutide on hypoglycemia in patients with type 1 diabetes mellitus （T1DM） and provide evidence for the prevention and control of hypoglycemia in the clinical treatment of T1DM. METHODS Electronic databases including The Cochrane Library， PubMed， Embase， Web of Science， China Biology Medicine Disc （CBM）， CNKI， Wanfang database， and VIP database were searched from the inception of the databases to June 30， 2023. The clinical randomized controlled trials （RCTs） of liraglutide on hypoglycemia in T1DM patients were screened according to inclusion and exclusion criteria. Data extraction， grouping， and subgroup meta-analysis were conducted for the included studies. RESULTS A total of 11 RCTs involving 1 685 patients were ultimately included. Meta-analysis results showed that treatment with 1.2 mg liraglutide could reduce the frequency of hypoglycemia in patients with T1DM [OR＝0.81， 95%CI （0.74， 0.88）， P＜0.01]， while treatment with 1.8 mg liraglutide could increase the frequency of hypoglycemia [OR＝1.33， 95%CI （1.23， 1.44）， P＜0.01]. The effect of liraglutide on hypoglycemia in patients with T1DM was not correlated with the duration of hypoglycemia [MD＝ －0.29， 95%CI （－1.21， 0.63）， P＝0.53]， and did not increase the incidence of severe hypoglycemia in these patients [OR＝0.87， 95%CI （0.57， 1.33）， P＝0.53]. Liraglutide could reduce the levels of glycated hemoglobin [MD＝－1.39， 95%CI （－2.65， －0.13）， P＝0.03]， weight [MD＝－4.28， 95%CI （－5.01， －3.55）， P＜0.01]， and body mass index [MD＝－1.20， 95%CI （－1.80， －0.60）， P＜0.01] in them. CONCLUSIONS Liraglutide has a bidirectional regulatory effect on hypoglycemia in patients with T1DM， which is correlated with the dose of liraglutide. An appropriate dose of liraglutide （1.2 mg） can inhibit hypoglycemia in these patients， while an increased dose of liraglutide （1.8 mg） can promote hypoglycemia in them.