Dietary fiber intake is associated with chronic kidney disease (CKD) progression and cardiovascular risk, but not protein nutritional status, in adults with CKD.

BACKGROUND AND OBJECTIVES: Evidence suggests that dietary fiber benefits patients with chronic kidney disease (CKD); however, this conclusion requires further validation. In this study, we examined the effects of dietary fiber on kidney function, inflammation, indoxyl sulfate, nutritional status, and cardiovascular risk in patients with advanced CKD. METHODS AND STUDY DESIGN: We performed linear regressions to assess the association between dietary fiber intake and CKD parameters. The aforementioned parameters were compared over an 18-month follow- up period. Kaplan-Meier analysis was used to investigate the association between fiber intake and Cardiac vascular disease (CVD). RESULTS: In total, 157 patients were included in this study. Dietary fiber and inflammatory indices were associated (interleukin [IL]-6: ß=-0.024, p=0.035). The differential estimated glomerular filtration rate (ΔeGFR) as well as levels of C-reactive protein, IL-6, indoxyl sulfate, and serum cholesterol in the higher fiber intake (>=25 g/day) group were lower than those in the lower fiber intake (<25 g/day) group (p<0.05). Differences in IL-6 and indoxyl sulfate levels were more significant in patients in the higher protein intake group (p<0.05). Dietary fiber intake may be a protective factor associated with CVD (hazard ratio=0.537 and 0.305- 0.947). The protein nutritional status was not different between the two groups (p>0.05). CONCLUSIONS: Our results suggest that increasing fiber intake can retard the decrease in the eGFR; can reduce the levels of proinflammatory factors, indoxyl sulfate, and serum cholesterol; and is negatively associated with cardiovascular risk, but does not disrupt the nutritional status of patients with CKD.

Astragalus polysaccharides decrease muscle wasting through Akt/mTOR, ubiquitin proteasome and autophagy signalling in 5/6 nephrectomised rats.

ETHNOPHARMACOLOGICAL RELEVANCE: Existing evidences suggest that Radix Astragali and its polysaccharides composition (APS) can improve muscle mass, but the mechanisms need more research. AIM OF THE STUDY: In this study, we aimed to examine the effects of APS on muscle wasting at molecular level in 5/6 nephrectomised rats. MATERIALS AND METHODS: We performed 5/6 nephrectomy or sham operation in 160 6-week-old Sprague-Dawley rats, and feed animals with or without 2% APS for 155 days. After treatment, we compared the change of weight, muscle fibre, protein metabolism, pro-inflammatory factors (TNF-α, IL-15, CRP) and oxidative factors (MDA, SOD) among each group. In addition, we detected the Akt/mTOR, ubiquitin proteasome, autophagy signalling and AA transporters in vivo and in vitro. RESULTS: Data in vivo show 2% APS could alleviate weight loss and improve protein metabolism in nephrectomised rats. The levels of serum pro-inflammatory factors and oxidative factors were restored by APS treatment. In molecular levels, APS restored Akt/mTOR, MAFbx, MuRF1, Atg7, LC3B-II/LC3B-I and SLC38A2 which changed in nephrectomised rats. Data in vitro show the optimal dose of APS is 0.2mg/mL, and SLC38A2 siRNA attenuated the effects of 0.2mg/mL APS on atrophy and autophagy. CONCLUSIONS: Our results suggested APS could improve muscle wasting through Akt/mTOR, ubiquitin proteasome and autophagy signalling, and SLC38A2 may be one of potential targets.

Effects of Astragalus Polysaccharides on Dysfunction of Mitochondrial Dynamics Induced by Oxidative Stress.

This paper studied the chronic fatigue induced by excessive exercise and the restoration effects of Astragalus polysaccharides (APS) on mitochondria. In vivo, we found that excessive exercise could cause oxidative stress statue which led to morphological and functional changes of mitochondria. The changes, including imbalance between mitochondria fusion-fission processes, activation of mitophagy, and decrease of PGC-1α expression, could be restored by APS. We further confirmed in vitro, and what is more, we found that APS may ameliorate mitochondrial dysfunction through Sirt1 pathway. Based on the results, we may figure out part of the molecular mechanism of mitochondrial amelioration by APS.