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      Beneficial Effects of Caloric Restriction on Chronic Kidney Disease in Rodent Models: A Meta-Analysis and Systematic Review

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          Numerous studies have demonstrated the life-extending effect of caloric restriction. It is generally accepted that caloric restriction has health benefits, such as prolonging lifespan and delaying the onset and progression of CKD in various species, especially in rodent models. Although many studies have tested the efficacy of caloric restriction, no complete quantitative analysis of the potential beneficial effects of reducing caloric intake on the development and progression of CKD has been published.


          All studies regarding the relationship between caloric restriction and chronic kidney diseases were searched in electronic databases, including PubMed/MEDLINE, EMBASE, Science Citation Index (SCI), OVID evidence-based medicine, Chinese Bio-medical Literature and Chinese science and technology periodicals (CNKI, VIP, and Wan Fang). The pooled odds ratios (OR) and 95% confidence intervals (95% CI) were calculated by using fixed- or random-effects models.


          The data from 27 of all the studies mentioned above was used in the Meta analysis. Through the meta-analysis, we found that the parameter of blood urea nitrogen, serum creatinine and urinary protein levels of the AL group was significant higher than that of the CR group, which are 4.11 mg/dl, 0.08mg/dl and 33.20mg/kg/24h, respectively. The incidence of the nephropathy in the caloric restriction (CR) group was significantly lower than that in the ad libitum—fed (AL) group. We further introduced the subgroup analysis and found that the effect of caloric restriction on the occurrence of kidney disease was only significant with prolonged intervention; the beneficial effects of CR on the 60%-caloric-restriction group were greater than on the less-than-60%-caloric-restriction group, and caloric restriction did not show obvious protective effects in genetically modified strains. Moreover, survival rate of the caloric restriction group is much higher than that of the ad libitum—fed (AL) group.


          Our findings demonstrate for the first time that compared with the AL group, the caloric restriction indeed decreased urea nitrogen, creatinine, urine protein, incidence of kidney diseases and increased the survival rate on 700~800 days.

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          Most cited references 15

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          Species and strain differences in rodent sciatic nerve anatomy: implications for studies of neuropathic pain.

          Hindlimb pain models developed in rats have been transposed to mice, but assumed sciatic nerve neuroanatomic similarities have not been examined. We compared sciatic nerve structural organization in mouse strains (C57BL/6J, DBA/2J, and B6129PF2/J) and rat strains (Wistar, Brown Norway, and Sprague-Dawley). Dissection and retrograde labeling showed mouse sciatic nerve origins predominantly from the third lumbar (L3) and L4 spinal nerves, unlike the L4 and L5 in rats. Proportionate contributions by each level differed significantly between strains in both mice and rats. Whereas all rats had six lumbar vertebrae, variable patterns in mice included mostly five vertebrae in DBA/2J, mostly six vertebrae in C57BL/6J, and a mix in B6129PF2/J. Mice with a short lumbar vertebral column showed a rostral shift in relative contributions to the sciatic nerve by L3 and L4. Ligation of the mouse L4 nerve created hyperalgesia similar to that in rats after L5 ligation, and motor changes were similar after mouse L4 and rat L5 ligation (foot cupping) and after mouse L3 and rat L4 ligation (flexion weakness). Thus, mouse L3 and L4 neural segments are anatomically and functionally homologous with rat L4 and L5 segments. Neuronal changes after distal injury or inflammation should be sought in the mouse L3 and L4 ganglia, and the spinal nerve ligation model in mice should involve ligation of the L4 nerve while L3 remains intact. Strain-dependent variability in segmental contributions to the sciatic nerve may account in part for genetic differences in pain behavior after spinal nerve ligation.
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            Nutrients, not caloric restriction, extend lifespan in Queensland fruit flies (Bactrocera tryoni).

            Caloric restriction (CR) has been widely accepted as a mechanism explaining increased lifespan (LS) in organisms subjected to dietary restriction (DR), but recent studies investigating the role of nutrients have challenged the role of CR in extending longevity. Fuelling this debate is the difficulty in experimentally disentangling CR and nutrient effects due to compensatory feeding (CF) behaviour. We quantified CF by measuring the volume of solution imbibed and determined how calories and nutrients influenced LS and fecundity in unmated females of the Queensland fruit fly, Bactocera tryoni (Diptera: Tephritidae). We restricted flies to one of 28 diets varying in carbohydrate:protein (C:P) ratios and concentrations. On imbalanced diets, flies overcame dietary dilutions, consuming similar caloric intakes for most dilutions. The response surface for LS revealed that increasing C:P ratio while keeping calories constant extended LS, with the maximum LS along C:P ratio of 21:1. In general, LS was reduced as caloric intake decreased. Lifetime egg production was maximized at a C:P ratio of 3:1. When given a choice of separate sucrose and yeast solutions, each at one of five concentrations (yielding 25 choice treatments), flies regulated their nutrient intake to match C:P ratio of 3:1. Our results (i) demonstrate that CF can overcome dietary dilutions; (ii) reveal difficulties with methods presenting fixed amounts of liquid diet; (iii) illustrate the need to measure intake to account for CF in DR studies and (iv) highlight nutrients rather than CR as a dominant influence on LS.
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              Beneficial effects of weight loss in overweight patients with chronic proteinuric nephropathies.

              Proteinuria is a recognized complication of obesity, but no study has investigated the effect of weight loss in overweight patients with chronic proteinuric nephropathies of different causes. We randomly assigned (in a 2:1 ratio) 30 overweight patients (body mass index [BMI] > 27 kg/m(2)) with diabetic and nondiabetic proteinuric nephropathies to either follow a low-calorie normoproteinic diet or maintain their usual dietary intake for 5 months. The primary outcome was change in urinary protein excretion. Secondary outcomes were changes in renal function (serum creatinine level and Cockcroft-Gault creatinine clearance) and lipid profile. Patients in the diet group showed a significant decrease in body weight and BMI, whereas patients in the control group showed a significant increase in body weight and BMI (between-group comparison, P < 0.05). Mean weight loss in the diet group was 4.1% +/- 3%, and 14 of 20 patients in this group lost more than 3%. Proteinuria decreased by 31.2% +/- 37% in the diet group (from protein of 2.8 +/- 1.4 to 1.9 +/- 1.4 g/24 h; P < 0.005), whereas it tended to increase in the control group (between-group comparison, P < 0.05). Changes in renal function did not differ significantly between groups, although renal function remained stable in the diet group and showed significant worsening in the control group. Serum triglyceride levels remained stable in the diet group and tended to increase in the control group (between-group comparison, P < 0.05). Moderate weight loss in overweight patients with chronic proteinuric nephropathies induces a significant decrease in proteinuria. Am J Kidney Dis 41:319-327. Copyright 2003 by the National Kidney Foundation, Inc.

                Author and article information

                Role: Editor
                PLoS One
                PLoS ONE
                PLoS ONE
                Public Library of Science (San Francisco, CA USA )
                22 December 2015
                : 10
                : 12
                [1 ]Department of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing, China
                [2 ]School of Medicine, Nankai University, Tianjin, China
                University of Utah School of Medicine, UNITED STATES
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Conceived and designed the experiments: XMX GYC XYB XFS XMC. Performed the experiments: XMX WJW. Analyzed the data: XMX. Contributed reagents/materials/analysis tools: XMX RB. Wrote the paper: XMX GYC.

                © 2015 Xu et al

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

                Page count
                Figures: 6, Tables: 2, Pages: 15
                This work was funded by Aging Biology of Individual and Organs and Risk Evaluation System of Geriatric Diseases, National Key Basic Research Program of China (973 Program), No. 2013CB530805 (to Prof. Cai Guangyan), and Beijing Municipal Natural Science Foundation (CN) 81171645. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
                Research Article
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