Although leptin has been shown to increase blood pressure (BP), it is however unclear if this increase can be prevented by exercise. This study therefore investigated the effect of leptin treatment with concurrent exercise on blood pressure (BP), sodium output, and endothelin-1 (ET-1) levels in normotensive rats. Male Sprague-Dawley rats weighing 250-270 g were divided into four groups consisting of a control group (n = 6), leptin-treated (n = 8), non-leptin-treated exercise group (n = 8), and a leptin-treated exercise group (n = 8). Leptin was given subcutaneously daily for 14 days (60 μg/kg/day). Animals were exercised on a treadmill for 30 min at a speed of 0.5 m/s and at 5° incline four times per week. Measurement of systolic blood pressure (SBP) and collection of urine samples for estimation of sodium and creatinine was done once a week. Serum samples were collected at the end of the experiment for determination of sodium, creatinine and ET-1. At day 14, mean SBP and serum ET-1 level in the leptin-treated group was significantly higher than that in the control group whereas mean SBP and serum ET-1 level was significantly lower in the leptin-treated exercise group than those in leptin-treated and control groups. Creatinine clearance, urinary sodium excretion, and urine output were not different between the four groups. Regular treadmill exercise prevents leptin-induced increases in SBP in rats, which might in part result from increased urinary sodium excretion and preventing the leptin-induced increases in serum ET-1 concentration.
Introduction. Chronic kidney disease (CKD) is associated with high mortality rates, mainly as a result of cardiovascular complications. Meanwhile, recent studies have suggested a role of a homodimer protein called activin A in chronic kidney disease-mineral and bone disorder (CKD-MBD) conditions that may exist in the vascular calcification and osteolytic process. Ultrasound examination of the carotid intima-media thickness (cIMT) is a noninvasive method to assess vascular calcification. This study aimed to analyze the relationship between the activin A serum level and cIMT in patients with CKD at Mohammad Hoesin Hospital, Palembang, Indonesia. Methods. We conducted a hospital-based, cross-sectional study of consecutive CKD patients at the Department of Internal Medicine, Mohammad Hoesin Hospital, from July to November 2019. The level of activin A was measured by enzyme-linked immunosorbent assay. Meanwhile, cIMT measurements were collected by B-mode ultrasound imaging. Results. A total of 55 patients with CKD were included in this investigation. The median serum activin A level in these patients was 236.17 (116.33–283) pg/mL, while the median cIMT was 0.8 (0.6–1.45) mm. A relationship between the serum activin A level and cIMT (r = 0.449; p = 0.001 ) was observed. During multivariate analysis with linear regression, triglyceride p = 0.049 , phosphate p = 0.005 , and activin A p = 0.020 serum levels were factors associated with cIMT. Conclusion. In this study, a relationship between the activin A serum level and cIMT in patients with CKD was identified. Vascular calcification should be screened for in all CKD patients by the measurement of cIMT.
Kidney disease affects 800 million children and adults worldwide, and the numbers keep increasing. A better understanding of the pathogenesis in kidney diseases, especially on a biomolecular level, is much needed to identify novel biomarkers and therapeutic targets for kidney diseases. The glomerular filtration barrier comprises endothelial cells, the glomerular basement membrane, and podocytes. The podocyte has a central role in part of the glomerular filtration barrier. The normal functioning of podocytes is particularly important in preventing the heavy proteinuria seen in nephrotic syndrome or diabetic nephropathy, or in the disease process of focal segmental glomerulosclerosis. The podocyte is injured by circulating factors, which finally results in deranged podocyte motility. Soluble urokinase-type plasminogen activator receptor (suPAR) is a circulating form of glycosyl-phosphatidylinositol uPAR domain membrane protein and is known to play a role in the pathogenesis in kidney diseases, specifically focal segmental glomerulosclerosis and diabetic nephropathy. suPAR binds to αvβ3 integrin on podocyte foot processes and causes podocyte structure disorganization leading to glomerular filtration disruption and hence proteinuria. suPAR is also a potential biomarker to predict the incidence of CKD.
Chronic kidney disease is associated with a high mortality rate, especially cardiovascular disease associated with mineral and bone disorders. Sclerostin is an inhibitor of Wnt signaling which has the effect of increasing the occurrence of vascular calcification in patients with chronic kidney disease. There are several studies that show different results. Carotid intima media thickness ultrasound examination is a tool to identify atherosclerosis which is part of vascular calcification. The aim of this study is to look at the correlation of sclerostin with carotid intima media thickness (CIMT) in patients with chronic kidney disease undergoing hemodialysis. In this cross section, the concentration of sclerostin was measured by examination of enzymed linked immunosorbent assay. CIMT measurement by ultrasound mode B examination. There were 40 patients in this study. The mean sclerostin level was 256.68 ± 127.76 pg / ml. Sclerostin levels are declared high if above 162 pg / ml there are 30 people. CIMT thickening was present in 11 patients. There was no significant correlation of serum sclerostin with CIMT in patients with chronic kidney disease undergoing hemodialysis (r-0.32 p0,847). In multivariate linear regression, hemodialysis duration is an independent factor that is significantly significant with CIMT. There was no significant correlation of serum sclerostin with CIMT in patients with chronic kidney disease undergoing hemodialysis.
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