Effect of dietary phosphorus levels on growth and body composition of crucian carp, Carassius auratusunder indoor and outdoor experiments

2016 ◽  
Vol 23 (4) ◽  
pp. 702-709 ◽  
Author(s):  
M.H. Chen ◽  
Y.Y. Sun ◽  
C.M. Kong ◽  
H.J. Tang ◽  
L. Gan
2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Trisha Sachan ◽  
Anita Saxena ◽  
Amit Gupta

Abstract Background and Aims Changes in dietary phosphorus regulate serum FGF-23, parathyroid hormone, 1,25(OH)(2)D and Klotho concentrations . Cardiovascular disease (CVD) is the principal killer of patients with chronic kidney disease and hyperphosphetemia is a potent risk factor it. Of many causative factors for CVD in CKD, dietary interventions involving restriction of dietary phosphorous intake can help reduce onset of CVD at early stages of CKD with other corrective measures. Muscle wasting is a consequence of uremic syndrome which alters body composition. The aim of the study was to study effect of dietary phosphorous restriction on FGF-23, iPTH, Klotho, 1,25(OH)(2)D and body composition in chronic kidney disease patients. Method This is a longitudinal study with 12 months intervention, approved by Ethics Committee of the institute. A total 132 subjects were recruited (66 healthy controls, 66 CKD patient. of 66 patients 33 were in CKD stage 1 and 33 in stage 2. GFR was calculated with the help of MDRD formula. Biochemical parameters of subjects were evaluated at baseline, 6 and 12 months along with the anthropometric measurements (body weight, height, mid upper arm circumference (MUAC), and skin folds). Three days dietary recall was taken to evaluate energy, protein and phosphorous intake. CKD patients whose dietary phosphorous intake was more than 1000 mg/day, were given intense dietary counseling and prescribed dietary modifications by restricting dietary phosphorous between 800-1000 mg/day. Results The mean age of controls and patients was 37.01±9.62 and 38.27±12.06 and eGFR of 136.94±11.77 and 83.69±17.37 respectively. One way ANOVA showed significant difference among controls and the study groups in hemoglobin (p<0.001), s albumin (p<0.001), FGF-23 (p<0.001), klotho (p<0.001), urinary protein (p<0.001) and Nephron Index (p<0.001).The mean energy intake (p = 0.001) and dietary phosphorous intake (p<0.001) of the CKD patients decreased significantly with the decline in the renal function along with the anthropometric measures i.e. BMI (p = 0.041),WHR (p = 0.015) and all four skin folds (p<0.001). On applying Pearson’s correlation, eGFR correlated negatively with urinary protein (-0.739, 0.000), FGF-23 (-0.679, 0.000) and serum phosphorous (-0.697, 0.000) and positively with klotho (0.872, 0.000). FGF-23 correlated negatively with klotho (-0.742, 0.000). Dietary phosphorous was found to be positively correlated with urinary protein (0.496, 0.000), serum phosphorous (0.680, 0.000) and FGF-23 (0.573, 0.000) and negatively with Klotho (-0.602, 0.000). Nephron index revealed a positive correlation with eGFR (0.529, 0.000). Urinary protein correlated negatively with klotho (-0.810, 0.000). A multiple linear regression was run to predict eGFR from anthropometric variables such as BMI, WHR, MUAC, skin folds thickness and handgrip strength. All anthropometric variables predicted decline in eGFR (p<0.05, R2 =0.223). At 6 and 12 months; repeated ANOVAs analysis showed a statistically significant difference in serum creatinine (p=0.000), serum phosphorous (p=0.000), FGF-23(p=0.000) and klotho (p=0.000). Conclusion Elevated levels of FGF-23 and decreased Klotho levels, with the moderate decline in renal function improved with the restricted phosphorous diet at 6 and 12 months emphasizing the importance of phosphorus restriction at an early stage.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 341-341
Author(s):  
Sowmiya Muthuraju ◽  
Derek Miketinas

Abstract Objectives Patients with liver conditions may have increased phosphorus turnover which can increase the risk of severe hypophosphatemia and other complications. The objective of this cross-sectional study was to quantify the usual intake of phosphorus, assess serum phosphorus (SP) levels across levels of liver conditions, and to estimate and assess the odds for having critically low phosphorus levels across adults with and without liver conditions. Methods Data were obtained from the NHANES 2015–2016 cycle. Adults were divided into four groups based on self-reported responses from the NHANES medical history questionnaire: liver cancer (LC), unspecified current liver condition (CLC), unspecified resolved liver condition (RLC), and no liver condition. Usual intake was estimated using the NCI method and all analyses were adjusted to account for the complex, multistage, probability sampling design. Results Usual phosphorus intake was highest in participants with RLC (1399 ± 26.5 mg) and lowest in participants with LC (1267 ± 140.7 mg). Although the percentage of those meeting the EAR for phosphorus was high (>95%), SP levels are lowest in participants with LC. SP levels differed slightly across liver conditions: participants with LC had a SP level of 1.0 ± 0.07 mmol/L, while participants with CLC, RLC, or no liver conditions had SP levels of 1.2 ± 0.01 mmol/L, 1.2 ± 0.01 mmol/L, and 1.2 ± 0.02 mmol/L, respectively. Participants with CLC had a usual phosphorus intake of 1350 ± 49.6 mg, and those who had no liver conditions had a usual phosphorus intake of 1387 ± 18.5 mg. The odds for normal phosphorus levels in participants with LC was low (Odds = 0.06; 95% CI: 0.01–0.45); the odds for CLC participants having normal SP levels was 1.6 (95% CI: 1.2–2.15); the odds for normal SP levels in participants with RLC were 2.2 (95% CI: 1.3–3.75), and the odds for normal SP in participants with no liver conditions odds for low were 1.9, (95% CI: 1.71–2.14). Conclusions These results indicate that patients with liver cancer are at higher risk of hypophosphatemia, and that phosphorus recommendations for patients with liver cancer may need to be adjusted. However, the variability in this subpopulation with liver cancer is high and warrants further investigation. Funding Sources None.


Sign in / Sign up

Export Citation Format

Share Document