NEUROENDOCRINE ALTERATIONS IN THE SOMATOTROPIC AND LACTOTROPIC AXES IN UREMIC MEN

被引:45
作者
VELDHUIS, JD
IRANMANESH, A
WILKOWSKI, MJ
SAMOJLIK, E
机构
[1] UNIV VIRGINIA, HLTH SCI CTR,NATL SCI FDN,CTR BIOL TIMING, DEPT INTERNAL MED,DIV METAB & NEPHROL, CHARLOTTESVILLE, VA 22908 USA
[2] SALEM VET AFFAIRS HOSP, DEPT INTERNAL MED, ENDOCRINE SECT, SALEM, VA USA
[3] NEWARK BETH ISRAEL MED CTR, DEPT MED, NEWARK, NJ USA
关键词
D O I
10.1530/eje.0.1310489
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
To investigate the pathophysiology of altered growth hormone (GH) and prolactin secretion in endstage renal disease, we sampled blood at 10-min intervals for 24 h and applied deconvolution analysis to calculate hormone half-lives and pulsatile secretion rates. Two-site immunoradiometric assays were employed to quantitate presumptively intact GH and prolactin in nine middle-aged men with chronic renal failure and 14 gender-, age-, body weight- and community-matched controls. We observed that the half-lives of endogenous GH and prolactin were prolonged significantly in uremia: for GH, control 17 +/- 1.4 versus uremia 21 +/- 1.3 min (p < 0.05); for prolactin, control 66 +/- 9.3 versus uremia 112 +/- 10 min (p < 0.01). Daily GH secretion rates exceeded sex-, age- and weight-predicted values in eight of nine uremic individuals, while values for prolactin were variable but on average twofold higher in uremia. In both the somatotropic and lactotropic axes, the frequency of secretory bursts was increased significantly (for GH, control 11 +/- 1.1 versus uremia 15 +/- 0.84 secretory events/24 h; for prolactin, control 20 +/- 0.90 versus uremia 27 +/- 1.3 pulses/24 h, p < 0.05). Although there were no significant alterations in the mean amplitude, duration or mass of GH secretory bursts, prolactin secretory burst amplitudes were elevated threefold in uremia (p < 0.01). These distinctive mechanisms brought about higher 24-h mean serum concentrations of GH (0.70 +/- 0.17 control versus 1.22 +/- 0.32 mu g/l uremia) and prolactin (7.3 +/- 2.4 control versus 26 +/- 6.1 mu g/l uremia, p < 0.05). Lastly, serum concentrations of estradiol were increased but those of unconjugated estriol decreased in uremia. We conclude that hypersomatotropinemia and hyperprolactinemia in uremic men result from prolonged hormone half-lives combined with increased frequencies of secretory events driven by unknown stimuli within the respective axes, and/or by defects in their negative-feedback regulation. We postulate that the latter may arise from partial tissue resistance to hormone action in hemodialyzed men.
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页码:489 / 498
页数:10
相关论文
共 60 条
[1]   DOWN REGULATION OF PROLACTIN RECEPTORS IN THE LIVER, MAMMARY-GLAND AND KIDNEY OF FEMALE VIRGIN RAT, INFUSED WITH OVINE PROLACTIN OR HUMAN GROWTH-HORMONE [J].
BARASH, I ;
MADAR, Z ;
GERTLER, A .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1983, 116 (02) :644-650
[2]   THE METABOLIC-CLEARANCE, DISTRIBUTION, AND DEGRADATION OF DIMERIC AND MONOMERIC GROWTH-HORMONE (GH) - IMPLICATIONS FOR THE PATTERN OF CIRCULATING GH FORMS [J].
BAUMANN, G ;
STOLAR, MW ;
BUCHANAN, TA .
ENDOCRINOLOGY, 1986, 119 (04) :1497-1501
[3]   SOMATOMEDIN-C MEDIATES GROWTH-HORMONE NEGATIVE FEEDBACK BY EFFECTS ON BOTH THE HYPOTHALAMUS AND THE PITUITARY [J].
BERELOWITZ, M ;
SZABO, M ;
FROHMAN, LA ;
FIRESTONE, S ;
CHU, L ;
HINTZ, RL .
SCIENCE, 1981, 212 (4500) :1279-1281
[4]  
BLUM WF, 1991, ACTA PAEDIATR, P24
[5]  
BROYER M, 1982, PEDIATR CLIN N AM, V29, P991
[6]   METABOLIC CLEARANCE OF HUMAN GROWTH-HORMONE IN PATIENTS WITH HEPATIC AND RENAL-FAILURE, AND IN ISOLATED PERFUSED PIG LIVER [J].
CAMERON, DP ;
BURGER, HG ;
CATT, KJ ;
WATTS, JM ;
GORDON, E .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1972, 21 (10) :895-+
[7]   INCREASED GROWTH-HORMONE RESPONSE TO GROWTH-HORMONE RELEASING HORMONE INDUCED BY ERYTHROPOIETIN IN UREMIC PATIENTS [J].
CANTALAMESSA, L ;
CREMAGNANI, L ;
ORSATTI, A ;
VIGNA, L ;
BUCCIANTI, G .
CLINICAL ENDOCRINOLOGY, 1991, 34 (01) :85-89
[8]   ALBUMIN METABOLISM IN CHRONIC RENAL FAILURE [J].
COLES, GA ;
PETERS, DK ;
JONES, JH .
CLINICAL SCIENCE, 1970, 39 (03) :423-&
[9]   HYPOTHALAMIC-PITUITARY FUNCTION IN UREMIA [J].
COWDEN, EA ;
RATCLIFFE, WA ;
RATCLIFFE, JG ;
KENNEDY, AC .
ACTA ENDOCRINOLOGICA, 1981, 98 (04) :488-495
[10]   ABNORMAL TSH, PRL AND GH RESPONSE TO TSH RELEASING FACTOR IN CHRONIC RENAL-FAILURE [J].
CZERNICHOW, P ;
DAUZET, MC ;
BROYER, M ;
RAPPAPORT, R .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1976, 43 (03) :630-637