Objective. Physical exercise can provide many health benefits in humans. Exercise-induced reactive oxygen species (ROS) formation and its downstream signaling cascades are reported to induce mitochondrial biogenesis in exercising tissues. Selenoprotein P (SELENOP) is the antioxidant hepatokine, whose hypersecretion is associated with various metabolic diseases. It was reported to impair exercise-induced reactive oxygen species signaling and inhibit subsequent mitochondrial biogenesis in mice. However, the relationship between selenoprotein P and mitochondrial dynamic in humans has not yet been reported. While reduction of plasma selenoprotein P becomes an attractive therapeutic target for metabolic diseases, the role of regular exercise in this regard is still unknown. This study aimed to analyze the influence of regular habitual exercise on plasma selenoprotein P levels and its association with leucocyte mitochondrial DNA copy number in healthy young adults.Methodology. Plasma selenoprotein P levels and leucocyte mitochondrial DNA copy numbers were compared in 44 regularly exercising subjects and 44 non-exercising controls, and the correlation between the two parameters was analyzed. Plasma selenoprotein P levels were measured by Enzyme-linked Immunosorbent Assay, and leucocyte mitochondrial DNA copy numbers were measured using the qPCR method.Results. The regular-exercise group had lower plasma selenoprotein P levels with higher leucocyte mitochondrial DNA copy numbers than the non-exercise group. There was a tendency of negative correlation between the two variables in our studied population. Conclusion.Regular habitual exercise has a beneficial effect on reducing plasma selenoprotein P levels while raising mitochondrial DNA copy numbers.
Introduction: There is alarming problem in increasing incidence of hypertension and its complications in Myanmar. The genetic background of hypertension is not known well in Myanmar population. The present study aimed to find out the association with angiotensinogen gene M235T polymorphism, plasma angiotensinogen level, BMI and essential hypertension in local area. Methods: There were 144 subjects, 72 hypertensive and 72 normotensives from internal medicine unit of Mandalay General Hospital and Mandalay area. After getting informed consents, determination of blood pressure and BMI were done. The AGT M235T genotypes were determined by polymerase chain reaction followed by digestion of the products with Tth111I. The determination of plasma angiotensinogen level was done by ELISA method. Results: The odd ratio for essential hypertension of TT genotype was 4.93 (95% CI-1.97-5.40) and genotype frequency was statistically significant between hypertensive and normotensives, p<0.001. And subjects carrying T allele has 2.5 times greater chance for essential hypertension [OR=2.56 (95% CI-1.59-4.13)]. The plasma angiotensinogen level in hypertensive was 65.00 ± 27.73 ng/ml and 24.87 ± 15.06 ng/ml in normotensives (p<0.001). Moreover, subjects carrying TT genotype have increased plasma angiotensionogen than other genotypes in both hypertensive and normotensives (P<0.001). Determination of their BMI, there was found that significance difference between hypertensive than that of normotensives (p<0.001). In normotensives, 9.7% has TT genotypes and interestingly they have increased BMI than other genotypes. Conclusion: In fact, the study noted that there was association between AGT M235T polymorphism and increased plasma angiotensinogen and increased BMI in essential hypertension.
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