William M. Wallace
Case Western Reserve University
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Annals of the New York Academy of Sciences | 2006
William B. Weil; William M. Wallace
The studies to be described here had their inception in an attempt to reconcile observations on the changes in body composition obtained by indirect methods, particularly metabolic balance measurements, with direct whole body analysis by classical analytical techniques in the study of growth and certain types of protein deficiency states. Direct chemical analysis of experimental animals under a variety of conditions of growth and suboptimal nutrient intake have indicated a remarkable constancy of body composition. The make-up of the body appears to achieve an independence from the nutritional environment and it can be said that compositional homeostasis appears to be the rule. If correction for fat content be made the homeostasis is more precise. On the other hand many studies of man and animals using indirect methods for determining composition during growth and recovery from nutritional deficit have indicated that extensive changes in compositional make-up can occur. Nitrogen and minerals appear to be lost or gained to the body without parallel changes in body weight. The divergence between results obtained by direct and indirect approaches to body composition under certain conditions have been discussed in detail e l se~here . ’*~*~,~ One possibility for explaining gain of nitrogen and minerals without concomitant gain of weight during growth is that “maturation” of body composition is occurring and that this process can be hastened or retarded by the quantity of protein fed.5 It is well established that a newborn animal has a lower nitrogen content than does a mature animal. This is also true for the newborn human infant. At birth the newborn rat has a nitrogen content of 1.5 per cent of its fat-free body; this increases to 3.5 per cent at maturity. Using 6.25 as a conversion factor for protein, this corresponds to a change from 9.5 per cent to 22.5 per cent during the period of growth. If this change could be accelerated or decelerated by alterations in diet it might explain some of the alterations in nitrogen balance which appear to occur independently of changes in weight. The experiments to be described were designed to test whether or not, in growing animals, the changing protein to weight ratio is a function of age or weight and whether or not this change can be modified by diet independently of changes in age or weight. The data indicate that the change in the ratio can be accelerated by high protein feeding but only if concomitant change in weight occurs.
Archives of Biochemistry and Biophysics | 1976
Joseph W. Mayo; William M. Wallace; LeRoy W. Matthews; Don M. Carlson
Submandibular secretions collected from children with cystic fibrosis (CF) showed increased protein concentration (milligrams/milliliter) and increased amylase specific activity (units/milligram of protein) relative to normal secretions. These differences between normal (N) and CF secretions were as follows: protein, 1.25 ± 0.51 (N), 1.75 ± 0.35 (CF) (P < 0.02); and amylase, 58 ± 18 (N), 80 ± 19 (CF) (P < 0.001). To determine the basis for elevated protein in CF saliva, several major proteins resolved by polyacrylamide disc gel electrophoresis were quantitated by densitometry. These included four phosphoproteins (PP), serum albumin, an acid phosphatase-containing fraction, amylase, and an unidentified protein referred to as PI-7.1. Together, these proteins comprise greater than 75% of the total protein in the secretion. Differences in individual protein concentrations (milligrams/milliliter) resolved from normal and CF secretions, respectively, were as follows: PP2, 0.02 ± 0.01, 0.03 ± 0.02 (NS, not significant); PP3, 0.06 ± 0.04, 0.05 ± 0.03 (NS); acid phosphatase fraction, 0.06 ± 0.04, 0.12 ± 0.07 (P < 0.05); amylase, 0.09 ± 0.04, 0.27 ± 0.16 (P < 0.01); and pI-7.1, 0.04 ± 0.02, 0.13 ± 0.08 (P < 0.02). Amylase, the most significant contributor to the elevated protein, comprised 26% of the total protein of normal secretions and 38% of the total protein of CF secretions. Thus, our results do not support the concept of a generalized increase in all organic components in CF submandibular secretions but, rather, increases in specific proteins, namely amylase, component pI-7.1, and an acid phosphatase-containing fraction.
Metabolism-clinical and Experimental | 1964
L. Leighton Hill; William B. Weil; Michael Bennett; Margaret Hetrick; Irving Miller; William M. Wallace
Abstract This study was undertaken to examine the influence of the prior level of protein intake on the capability of rats to withstand extreme dietary stresses. In Part 1, weanling rats were prefed 24 per cent (HP) or 12 per cent (LP) protein diets and then starved or starved and thirsted. The HP animals grew much larger with feeding, but the body composition of HP and LP control animals (killed at the end of the feeding periods) was similar. Prefasting body size seemed to exert a marked influence on survival, the larger animals surviving the longest. When adjusted statistically to the same prefasting weight, a superiority of the LP groups in resisting both stresses was indicated. In the second and third parts of the experiment, age and caloric intake were varied for HP animals in order to create 2 groups of animals having the same mean prefasting weight as additional groups of LP animals. When subjected to the same stresses as in Part 1, the LP animals of Parts 2 and 3 survived longer. Carcasses of the stressed animals of the first experiment were practically devoid of fat and were dehydrated when compared to control groups. Comparison of the HP and LP stressed groups revealed strikingly lower concentrations of water in the LP carcasses. The availability of water during starvation made no difference in this regard. The results indicate an influence of the level of prior protein intake on survival and on the terminal body composition of the stressed animals.
Journal of Clinical Investigation | 1954
William H. Bergstrom; William M. Wallace
Pediatrics | 1956
William B. Weil; William M. Wallace
Journal of Clinical Investigation | 1953
George Nichols; Nancy Nichols; William B. Weil; William M. Wallace
Pediatrics | 1965
Thomas M. Teree; Eduardo Mirabal-Font; Antonio Ortiz; William M. Wallace
American Journal of Clinical Pathology | 1953
William M. Wallace
Pediatrics | 1964
William M. Wallace
Pediatrics | 1960
William M. Wallace