AJCN North Carolina Research Campus
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Miller, M.
Right arrow Articles by Shepherd, R. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Miller, M.
Right arrow Articles by Shepherd, R. W.
Agricola
Right arrow Articles by Miller, M.
Right arrow Articles by Shepherd, R. W.

American Journal of Clinical Nutrition, Vol 36, 492-499, Copyright © 1982 by The American Society for Clinical Nutrition, Inc

ORIGINAL RESEARCH COMMUNICATIONS

Altered body composition and muscle protein degradation in nutritionally growth-retarded children with cystic fibrosis

M Miller, L Ward, BJ Thomas, WG Cooksley and RW Shepherd

To investigate nutritional growth retardation and the adaptive response to malnutrition in cystic fibrosis (CF), body composition and muscle protein catabolism were studied in nine malnourished CF children and eight healthy controls by anthropometry, measurement of whole body potassium, urinary creatinine excretion, creatinine height index, and urinary 3-methylhistidine excretion, an index of myofibrillar protein catabolism. CF children had a significant deficit of body mass (p less than 0.001), derived from both the body fat and the fat-free compartments, including a deficit in muscle mass (p less than 0.005). A deficit of muscle mass in CF was also reflected by a lower creatinine height index (mean +/- 1 SEM = 0.66 +/- 0.04 in CF, versus 0.85 +/- 0.5 in controls, p less than 0.02). Urinary 3-methylhistidine excretion was elevated in CF children and the mean (+/- 1 SEM) rate of muscle protein catabolism was 0.82 +/- 0.06 versus 0.53 +/- 0.04 kg-1 24 h-1 in CF and controls, respectively (p less than 0.01). 3-Methylhistidine excretion rates did not correlate with severity of disease as assessed by clinical score. We conclude that nutritional growth retardation in CF is characterized by a protein energy deficit resembling that of protein- energy malnutrition, but that in contrast to the normal adaptive response to protein-energy malnutrition, muscle protein catabolism is markedly increased. These data may have important implications regarding the clinical course and prognosis of CF and the design of optimal therapy.


This article has been cited by other articles:


Home page
 ChestHome page
A. A. Ionescu, W. D. Evans, R. J. Pettit, L. S. Nixon, M. D. Stone, and D. J. Shale
Hidden Depletion of Fat-Free Mass and Bone Mineral Density in Adults With Cystic Fibrosis
Chest, December 1, 2003; 124(6): 2220 - 2228.
[Abstract] [Full Text] [PDF]

Home page
 ThoraxHome page
C E Bolton, A A Ionescu, W D Evans, R J Pettit, and D J Shale
Altered tissue distribution in adults with cystic fibrosis
Thorax, October 1, 2003; 58(10): 885 - 889.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
A. Moran, C. Milla, R. Ducret, and K. S. Nair
Protein Metabolism in Clinically Stable Adult Cystic Fibrosis Patients With Abnormal Glucose Tolerance
Diabetes, June 1, 2001; 50(6): 1336 - 1343.
[Abstract] [Full Text]

Home page
 Am. J. Respir. Crit. Care Med.Home page
C. E. MILLA, W. J. WARWICK, and A. MORAN
Trends in Pulmonary Function in Patients with Cystic Fibrosis Correlate with the Degree of Glucose Intolerance at Baseline
Am. J. Respir. Crit. Care Med., September 1, 2000; 162(3): 891 - 895.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1982 by The American Society for Nutrition