Hemodialysis stimulates muscle and whole body protein loss and alters substrate oxidation

被引:230
作者
Ikizler, TA
Pupim, LB
Brouillette, JR
Levenhagen, DK
Farmer, K
Hakim, RM
Flakoll, PJ
机构
[1] Vanderbilt Univ, Med Ctr, Div Nephrol, Dept Med, Nashville, TN 37232 USA
[2] Vanderbilt Univ, Med Ctr, Dept Surg, Nashville, TN 37232 USA
[3] Vanderbilt Univ, Med Ctr, Dept Biochem, Nashville, TN 37232 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM | 2002年 / 282卷 / 01期
关键词
catabolism; malnutrition; inflammation; energy expenditure; metabolism;
D O I
10.1152/ajpendo.2002.282.1.E107
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The hemodialysis (HD) procedure has been implicated as a potential catabolic factor predisposing the chronic HD (CHD) patients to protein calorie malnutrition. To assess the potential effects of HD on protein and energy metabolism, we studied 11 CHD patients 2 h before, during, and 2 h after HD by use of primed constant infusion of L-[1-C-13] leucine and L-[ring-H-2(5)] phenylalanine. Our results showed that HD led to increased whole body (10%) and muscle protein (133%) proteolysis. Simultaneously, whole body protein synthesis did not change, and forearm synthesis increased (120%). The net result was increased net whole body protein loss (96%) and net forearm protein loss (164%). During the 2-h post-HD period, the muscle protein breakdown trended toward baseline, whereas whole body protein breakdown increased further. Substrate oxidation during the post-HD was significantly altered, with diminished carbohydrate and accelerated lipid and amino acid oxidation. These data demonstrate that hemodialysis is an overall catabolic event, decreasing the circulating amino acids, accelerating rates of whole body and muscle proteolysis, stimulating muscle release of amino acids, and elevating net whole body and muscle protein loss.
引用
收藏
页码:E107 / E116
页数:10
相关论文
共 38 条
  • [1] TRACER PRIMING BICARBONATE POOL
    ALLSOP, JR
    WOLFE, RR
    BURKE, JF
    [J]. JOURNAL OF APPLIED PHYSIOLOGY, 1978, 45 (01) : 137 - 139
  • [2] The acidosis of chronic renal failure activates muscle proteolysis in rats by augmenting transcription of genes encoding proteins of the ATP-dependent ubiquitin-proteasome pathway
    Bailey, JL
    Wang, XN
    England, BK
    Price, SR
    Ding, XY
    Mitch, WE
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1996, 97 (06) : 1447 - 1453
  • [3] CHRONIC METABOLIC-ACIDOSIS DECREASES ALBUMIN SYNTHESIS AND INDUCES NEGATIVE NITROGEN-BALANCE IN HUMANS
    BALLMER, PE
    MCNURLAN, MA
    HULTER, HN
    ANDERSON, SE
    GARLICK, PJ
    KRAPF, R
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1995, 95 (01) : 39 - 45
  • [4] BERGSTROM J, 1995, J AM SOC NEPHROL, V6, P1329
  • [5] Maintaining muscle protein anabolism after a metabolic stress: Role of dextrose vs amino acid availability
    Borel, MJ
    Williams, PE
    Jabbour, K
    Hibbard, JC
    Flakoll, PJ
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 1997, 272 (01): : E36 - E44
  • [6] Protein turnover and energy expenditure increase during exogenous nutrient availability in sickle cell disease
    Borel, MJ
    Buchowski, MS
    Turner, EA
    Goldstein, RE
    Flakoll, PJ
    [J]. AMERICAN JOURNAL OF CLINICAL NUTRITION, 1998, 68 (03) : 607 - 614
  • [7] EXPRESSION OF INSULIN-LIKE GROWTH FACTOR-I IN UREMIC RATS - GROWTH-HORMONE RESISTANCE AND NUTRITIONAL INTAKE
    CHAN, W
    VALERIE, KC
    CHAN, JCM
    [J]. KIDNEY INTERNATIONAL, 1993, 43 (04) : 790 - 795
  • [8] Flakoll P.J., 2000, DIABETES MELLITUS FU, P148
  • [9] PROTEIN AND GLUCOSE-METABOLISM DURING ISOLATED CLOSED-HEAD INJURY
    FLAKOLL, PJ
    WENTZEL, LS
    HYMAN, SA
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 1995, 269 (04): : E636 - E641
  • [10] INFUSION OF TUMOR NECROSIS FACTOR CACHECTIN PROMOTES MUSCLE CATABOLISM IN THE RAT - A SYNERGISTIC EFFECT WITH INTERLEUKIN-1
    FLORES, EA
    BISTRIAN, BR
    POMPOSELLI, JJ
    DINARELLO, CA
    BLACKBURN, GL
    ISTFAN, NW
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1989, 83 (05) : 1614 - 1622