Magnesium-responsive genes are downregulated in diabetic patients after a three-month exercise program on a bicycle ergometer. Issue 6 (June 2019)

• Record Type: Journal Article
• Authors: Chiang, Yueh-Feng; Chen, Hsuan-Ying; Lee, I-Te; Chien, Li-Sheng; Huang, Jui-Hua; Kolisek, Martin; Cheng, Fu-Chou; Tsai, Sen-Wei
• Is Part Of: Journal of the Chinese Medical Association. Volume 82:Issue 6(2019)
• Publication Date: 2019-06
• Subjects: Blood glucose -- Exercise -- Magnesium -- Magnesium transporter -- Type 2 diabetes mellitus; Medicine -- Periodicals; 610.5
• DOI: 10.1097/JCMA.0000000000000112
• Languages: English
• ISSNs: 1726-4901

Abstract

Abstract : Background: Exercise is an effective therapy for the management of diabetes because it helps regulate glucose and magnesium homeostasis. Nevertheless, the mechanisms by which exercise exerts effects on magnesium transport remain unclear. This study investigated the expression of genes encoding magnesium transporters (GMTs) after a three-month exercise program in diabetic patients. Methods: This study was conducted with a within-subject pre-post design. A total of 15 adult patients with type 2 diabetes mellitus (T2DM) were recruited and underwent a three-month indoor bicycle exercise program. The expression of five GMTs ( CNNM2, TRPM6, TRPM7, SLC41A1, and SLC41A3 ) was determined in blood samples. Relevant anthropometric values and biochemical parameters were also determined. Results: Although the body weight and body mass index decreased after three months exercise, there were no significant differences. Fasting blood glucose, glycated hemoglobin (HbA1c), waist circumference, and magnesium levels decreased after the exercise program ( p < 0.05). The expression of SLC41A1 and SLC41A3 were downregulated after exercise, but only CNNM2, TRPM6, and TRPM7 showed significantly decreased expression levels compared with those before the exercise program ( p < 0.05). Conclusion: The three-month exercise program ameliorated blood glucose levels and downregulated the expression of magnesium-responsive genes in patients with T2DM.