. Among the many different causes that are associated with altered nutritional status in ESRD, the hemodialysis (HD) procedure has been associated clearly with net whole-body (WB) protein and skeletal muscle (SM) protein loss (3). This catabolic process can be reversed acutely by administration of intradialytic parenteral nutrition (IDPN) (4). Despite its shown anabolic effects, IDPN administration is costly, and patient eligibility for this type of nutrition support is widely restricted. In addition, the anabolic effects of IDPN seem to be limited to the period of administration, with no evidence of persistent anabolism once its infusion is shut off (4).Oral nutritional supplementation (PO) is a promising anabolic intervention in chronic HD (CHD) patients because of its potentially more physiologic and affordable characteristics. Despite its potential benefits, only limited studies have evaluated the effects of intradialytic PO administration on protein metabolism in CHD patients, and none to our knowledge has compared its metabolic effects with those of IDPN in CHD patients with deranged nutritional status.In this study, we hypothesized that administration of intradialytic PO supplementation would compensate WB and SM protein derangements as a result of the HD procedure, resulting in net protein anabolism. We further hypothesized that these beneficial effects would be less than what is observed with IDPN administration. To test these hypotheses, we studied protein metabolism in eight CHD patients with deranged nutritional status during three separate HD sessions-with PO, with IDPN, and with no intervention (control)-using stable isotope infusion techniques. Materials and Methods PatientsPatients were recruited from the Vanderbilt University Outpatient Dialysis Unit. Inclusion criteria consisted of patients who were on CHD for Ͼ6 mo, were using a biocompatible HD membrane (Fresenius F80; Fresenius USA, Lexington, MA), had double-pool Kt/V Ն1.4, were on a thrice-weekly HD program, and had signs of deranged nutrition status, as defined by levels of several serum proteins below National Kidney Foundation Kidney Disease Outcomes Quality Initiative (K/DOQI) Nutritional Guidelines recommended targets, including serum albumin Ͻ4 g/dl, serum prealbumin Ͻ30 mg/dl, cholesterol Ͻ150 mg/dl, and serum transferrin Ͻ150 mg/dl for 3 consecutive months
Deranged protein metabolism is known to complicate uremia. Insulin resistance is evident in chronic hemodialysis (CHD) patients. We hypothesized that the degree of insulin resistance would predict protein catabolism in non-diabetic CHD patients. We examined the relationship between Homeostasis Model Assessment (HOMA) and fasting whole-body and skeletal muscle protein turnover in 18 non-diabetic CHD patients using primed-constant infusions of L-(1-(13)C) leucine and L-(ring-(2)H(5)) phenylalanine. Mean+/-s.d. fasting glucose and body mass index were 80.6+/-9.8 mg/dl and 25.4+/-4.4 kg/m(2), respectively. Median (interquartile range) HOMA was 1.6 (1.4, 3.9). Mean+/-s.e.m. skeletal muscle protein synthesis, breakdown, and net balance were 89.57+/-11.67, 97.02+/-13.3, and -7.44+/-7.14 microg/100 ml/min, respectively. Using linear regression, a positive correlation was observed between HOMA and skeletal muscle protein synthesis (R(2)=0.28; P=0.024), and breakdown (R(2)=0.49; P=0.001). An inverse association between net skeletal muscle protein balance and HOMA was also noted (R(2)=0.20; P=0.066). After adjustment for C-reactive protein, only the relationship between HOMA and skeletal muscle protein breakdown persisted (R(2)=0.49; P=0.006). There were no significant associations between components of whole-body protein turnover and HOMA. This study demonstrates that insulin resistance is evident in non-diabetic dialysis patients, is associated with skeletal muscle protein breakdown, and represents a novel target for intervention in uremic wasting.
The results of this study demonstrate that CHD patients with T2DM under a suboptimal metabolic control display accelerated muscle protein loss compared with a matched group of non-DM CHD patients.
To investigate the association between physical activity and health, we need accurate and detailed free-living physical activity measurements. The determination of energy expenditure of activity (EE ACT ) may also be useful in the treatment and maintenance of nutritional diseases such as diabetes mellitus. Minute-to-minute energy expenditure during a 24-h period was measured in 60 sedentary normal female volunteers (35.4 ± 9.0 years, body mass index 30.0 ± 5.9 kg/m 2 ), using a state-of-theart whole-room indirect calorimeter. The activities ranged from sedentary deskwork to walking and stepping at different intensities. Body movements were simultaneously measured using a hip-worn triaxial accelerometer (Tritrac-R3D, Hemokentics, Inc., Madison, Wisconsin) and a wrist-worn uniaxial accelerometer (ActiWatch AW64, MiniMitter Co., Sunriver, Oregon) on the dominant arm. Movement data from the accelerometers were used to develop nonlinear prediction models (separately and combined) to estimate EE ACT and compared for accuracy. In a subgroup (n = 12), a second 24-h study period was repeated for cross-validation of the combined model. The combined model, using Tritrac-R3D and ActiWatch, accurately estimated total EE ACT (97.7 ± 3.2% of the measured values, p = 0.781), as compared with using ActiWatch (86.0 ± 4.7%, p < 0.001) or Tritrac-R3D (90.0 ± 4.6%, p < 0.001) alone. This model was also accurate for all intensity categories during various physical activities. The subgroup cross-validation also showed accurate and reproducible predictions by the combination model. In this study, we demonstrated that movement measured using accelerometers at the hip and wrist could be used to accurately predict EE ACT of various types and intensity of activities. This concept can be extended to develop valid models for the accurate measurement of free-living energy metabolism in clinical populations.
Locally produced 1,25-dihydroxyvitamin D3 may have pleiotropic effects outside of bone. Experimental and observational studies suggest that nutritional vitamin D may enhance erythropoiesis in settings of 25-hydroxy vitamin D (25(OH)D) deficiency. We conducted a double-blind, placebo-controlled, randomized clinical trial to assess the effects of supplementation with ergocalciferol on epoetin utilization and other secondary outcomes in patients on hemodialysis with serum 25(OH)D ,30 ng/ml. In all, 276 patients were randomized to 6 months of ergocalciferol or placebo. Mean6SD serum 25(OH)D increased from 16.065.9 ng/ml at baseline to 39.2614.9 ng/ml in the ergocalciferol arm and did not change (16.966.4 ng/ml and 17.567.4 ng/ml, respectively) in the placebo arm. There was no significant change in epoetin dose over 6 months in the ergocalciferol or placebo arms (geometric mean rate 0.98 [95% confidence interval (95% CI), 0.94 to 1.02] versus 0.99 [95% CI, 0.95 to 1.03], respectively) and no difference across arms (P=0.78). No change occurred in serum calcium, phosphorus, intact parathyroid hormone, or C-reactive protein levels, cinacalcet use, or phosphate binder or calcitriol dose in either study arm. Rates of all-cause, cardiovascular, and infection-related hospitalizations did not differ by study arm, although statistical power was limited for these outcomes. In conclusion, 6 months of supplementation with ergocalciferol increased serum 25(OH)D levels in patients on hemodialysis with vitamin D insufficiency or deficiency, but had no effect on epoetin utilization or secondary biochemical and clinical outcomes.
Background-Environmental factors including seasonal changes are important to guide physical activity (PA) programs to achieve or sustain weight loss. The goal was to determine seasonal variability in the amount and patterns of free-living PA in women.
There were no differences in metabolic hormones, plasma amino acid and whole-body protein balance between the interventions. During the post-HD phase, PO + EX retained a positive total amino acid (TAA) balance (primarily due to essential amino acid) while PO returned to a negative TAA balance although this difference did not reach statistical significance (78 +/- 109 versus -128 +/- 72 nmol/100 ml/min, respectively; P = 0.69). In the post-HD phase, PO + EX had significantly higher net muscle protein balance when compared to PO (19 +/- 16 versus -24 +/- 10 microg/100 ml/min, respectively; P = 0.036) We conclude that a single bout of resistance exercise augments the protein anabolic effects of oral intradialytic nutritional supplementation when examining skeletal muscle protein turnover.
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