Angiotensin II (ANGII) plays a central role in the enhanced sodium reabsorption in early type 1 diabetes in man and in streptozotocin-induced (STZ) diabetic rats. This study investigates the effect of untreated STZ-diabetes leading to diabetic nephropathy in combination with ANGII treatment, on the abundance and localization of the renal Na + ,K + -ATPase (NKA), a major contributor of renal sodium handling. After 7 weeks of STZ-diabetes (i.v. 65 mg kg −1 ) a subgroup of control (C) and diabetic (D7) Wistar rats were treated with ANGII (s.c. minipump 33 μg kg −1 h −1 for 24 h; CA and D7A). We measured renal function and mRNA expression, protein level, Serin23 phosphorylation, subcellular distribution, and enzyme activity of NKA α-1 subunit in the kidney cortex. Diabetes increased serum creatinine and urea nitrogen levels (C versus D7), as did ANGII (C versus CA, D7 versus D7A). Both diabetes (C versus D7) and ANGII increased NKA α-1 protein level and enzyme activity (C versus CA, D7 versus D7A). Furthermore, the combination led to an additive increase (D7 versus D7A, CA versus D7A). NKA α-1 Ser23 phosphorylation was higher both in D7 and ANGII-treated rats in the non-cytoskeletal fraction, while no signal was detected in the cytoskeletal fraction. Control kidneys showed NKA α-1 immunopositivity on the basolateral membrane of proximal tubular cells, while both D7 and ANGII broadened NKA immunopositivity towards the cytoplasm. Our study demonstrates that diabetes mellitus (DM) increases the mRNA expression, protein level, Ser23 phosphorylation and enzyme activity of renal NKA, which is further elevated by ANGII. Despite an increase in total NKA quantity in diabetic nephropathy, the redistribution to the cystosol suggests the Na + pump is no longer functional. ANGII also caused translocation from the basolateral membrane, thus in diabetic states where ANGII level is acutely elevated, the loss of NKA will be exacerbated. This provides another mechanism by which ANGII blockade is likely to be protective.
230Main text: 2938 Tables: 4 3 ABSTRACT Objectives: Popular belief holds that the lunar cycle affects human physiology, behavior and health, including sleep. To date, only a few and conflicting analyses have been published about the association between lunar phases and sleep. Our aim was to analyze the relationship between lunar phases and sleep characteristics. Methods:In this retrospective, cross-sectional analysis data from 319 patients who had been referred for sleep study were included. Individuals with apnea-hypopnea index≥15/h were excluded. Sociodemographic parameters were recorded. All participants underwent one-night standard polysomnography. Associations between lunar cycle (new moon, full moon and alternate moon) and sleep parameters were examined in unadjusted and adjusted models.Results: 57% of patients were males. Mean age for men was 45±14 years and 51±12 years for women. 224 persons had their sleep study done during alternate moon, 47 during full moon and 48 during new moon. There were no significant differences regarding age and gender between groups.Full moon was associated with lower sleep efficiency (median(%) [ Conclusion:Our results are consistent with a recent report and the widely held belief that sleep characteristics may be associated with the full moon.
Obstructive sleep apnea(OSA) is one of the most common sleep disorders in kidney transplant recipients, however its long-term consequences have only rarely been investigated. Here, we hypothesized that the presence of OSA would be associated with higher risk of mortality and faster decline of graft function in kidney transplant recipients. In a prospective cohort study 100 prevalent kidney transplant recipients who underwent one-night polysomnography at baseline and were followed for a median 75 months. Generalized linear mixed-effects models and Cox regression models were used to assess the association between OSA and the rate of progression of chronic kidney disease(CKD) and mortality. The estimated slopes of estimated glomerular filtration rate(eGFR) in patients with and without OSA were compared using a two-stage model of eGFR change including only OSA as a variable. In this model patients with OSA (eGFR versus time was −0.93 ml/min/1.73 m2/yr(95%CI:−1.75 to−0.11) had a similar slope as compared to patients without OSA(eGFR versus time was −1.24 ml/min/1.73 m2/yr(95%CI: −1.67 to −0.81). In unadjusted Cox proportional regression analyses OSA was not associated with higher all-cause mortality risk (Hazard Ratio(HR) = 1.20; 95% Confidence Interval(CI): 0.50–2.85). No association was found between the presence of OSA and the rate of progression of CKD or all-cause mortality in prevalent kidney transplant recipients.
Aim: to investigate the effect of acute insulin administration on the subcellular localization of na + /K + -AtPase isoforms in cardiac muscle of healthy and streptozotocin-induced diabetic rats. Methods: Membrane fractions were isolated with subcellular fractionation and with cell surface biotinylation technique. na + /K + -AtPase subunit isoforms were analysed with ouabain binding assay and Western blotting. Enzyme activity was measured using 3-Omethylfluorescein-phosphatase activity. Results: In control rat heart muscle α1 isoform of Na + /K + ATPase resides mainly in the plasma membrane fraction, while α2 isoform in the intracellular membrane pool. Diabetes decreased the abundance of α1 isoform (25 %, P<0.05) in plasma membrane and α2 isoform (50%, P<0.01) in the intracellular membrane fraction. When plasma membrane fractions were isolated by discontinuous sucrose gradients, insulin-stimulated translocation of α2-but not α1-subunits was detected. α1-Subunit translocation was only detectable by cell surface biotinylation technique. After insulin administration protein level of α2 increased by 3.3-fold, α1 by 1.37-fold and β1 by 1.51-fold (P<0.02) in the plasma membrane of control, and less than 1.92-fold (P<0.02), 1.19-fold (not significant) and 1.34-fold (P<0.02) in diabetes. the insulin-induced translocation was wortmannin sensitive.Conclusion: This study demonstrate that insulin influences the plasma membrane localization of Na + /K + -AtPase isoforms in the heart. α2 isoform translocation is the most vulnerable to the reduced insulin response in diabetes. α1 isoform also translocates in response to insulin treatment in healthy rat. Insulin mediates na + /K + -ATPase α1-and α2-subunit translocation to the cardiac muscle plasma membrane via a PI3-kinase-dependent mechanism.
Study Objectives: Both depression and sleep complaints are very prevalent among kidney transplant (kTx) recipients. However, details of the complex relationship between sleep and depression in this population are not well documented. Thus, we investigated the association between depressive symptoms and sleep macrostructure parameters among prevalent kTx recipients. Methods: Ninety-five kTx recipients participated in the study (54 males, mean ± standard devation age 51 ± 13 years, body mass index 26 ± 4 kg/m 2 , estimated glomerular filtration rate 53 ± 19 ml/min/1.73 m 2 ). Symptoms of depression were assessed by the Center for Epidemiologic Studies -Depression Scale (CES-D). After 1-night polysomnography each recording was visually scored and sleep macrostructure was analyzed. Results: The CES-D score was significantly associated with the amount of stage 2 sleep (r = 0.20, P < .05), rapid eye movement (REM) latency (r = 0.21, P < .05) and REM percentage (r = −0.24, P < .05), but not with the amount of slow wave sleep (r = −0.12, P > .05). In multivariable linear regression models the CES-D score was independently associated with the amount of stage 2 sleep (β: 0.205; confidence interval: 0.001-0.409; P = .05) and REM latency (β: 0.234; confidence interval: 0.001-0.468; P = .05) after adjustment for potential confounders. I NTRO DUCTI O NDepression is one of the most prevalent mental health conditions in patients with chronic kidney disease (CKD) [1][2][3][4] ; furthermore, it is an important determinant of impaired quality of life. 5,6 Among kidney transplant (kTx) recipients, depression is associated with reduced adherence and also with increased morbidity, graft loss, and mortality. [7][8][9][10][11][12][13] Poor sleep and various sleep problems are also frequent complaints among kTx recipients.14,15 Earlier we reported that chronic insomnia was independently associated with the presence of depression in kTx recipients. 16 In the general population there is a strong and bidirectional relationship between depression and sleep.17 This is also reflected in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition definition of major depression (MD), 18 as sleep complaints are core symptoms of MD. Several objective sleep parameters are different in patients with MD than in healthy control patients. Patients with MD have decreased amounts of slow wave sleep (SWS) and shortened rapid eye movement (REM) latency with increased amounts of REM sleep. The exact mechanisms and factors that may link depression to poor clinical outcomes among kTx recipients are not yet well defined. In a recent review focusing on kTx and depression, 23 sleep is not mentioned. This may be due to the complete lack of polysomnography (PSG) studies that assess the association between sleep and depression in this population. The frequent co-occurrence of subjective sleep complaints and depression among kTx recipients 16 suggests that the relationship between the two conditions may be similar to the association described in the g...
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