Nutritional Growth Retardation Research Articles

Immunoreactive somatomedin C in children from Morocco: a biological marker of nutritional growth retardation ?

Somatomedin C (Sm-C) is supposed to be a sensitive marker of malnutrition. Its relationship to growth and protein intake was investigated in 47 Moroccan children. The children (mean age: 7.5 ± 2 yr) had no endocrine abnormality. Anthropometric parameters were measured, together with blood levels of Sm-C and growth hormone (GH). Lower values of Sm-C were found in the following situations: ( a) growth retardation ( more than −2 Sd, N = 23; Sm-C = 3.61 ± 0.42 nmol l vs. 13.38 ± 1.52, P < 0.02) ; ( b) body weight less than 80% of expected weight for height ( N = 8; Sm-C = 4.84 ± 0.97 vs. 10.33 ± 1.19, P < 0.02); ( c) boys with meat consumption less than 3 times per wk ( N = 15; Sm-C = 4.03 ± 0.71 vs. 12.35 ± 2.01, P < 0.002). Thus, lower values of Sm-C are found in association with weight insufficiency and lower protein intake. As has previously been assumed, serum Sm-C, which is regulated by nutrition, may be a sensitive tool in the assessment of nutritional status in developing countries such as Morocco. Furthermore, it could explain some cases of growth retardation in states of malnutrition.

Nutritional rehabilitation in cystic fibrosis: Controlled studies of effects on nutritional growth retardation, body protein turnover, and course of pulmonary disease

The effects of a sustained increase in energy and protein intake on weight gain, growth, body protein metabolism, and the course of pulmonary disease were studied in 10 undernourished patients with cystic fibrosis unable to maintain nutrition and growth by the oral route and with declining nutritional and pulmonary status in the year prior to study. A 1-year course of nutrient supplementation using a semielemental high-nitrogen formula was delivered by nocturnal intragastric feeding or as an orally administered supplement; progress was compared with that of 14 height-, sex- and FEV1-matched patients with cystic fibrosis receiving conventional therapy. Supplementation resulted in a catch-up weight gain and sustained improvement in linear growth, with fewer pulmonary infections per year than during the initial observation period. Better weight gain and linear growth than in the comparison group were observed, as well as a significant reversal of the trend for deteriorating lung function. Compared with data from healthy children, 15N-glycine kinetics demonstrated increased protein breakdown and negligible net protein deposition in the treatment group prior to supplementation. After supplementation, synthesis in excess of breakdown, with net protein accretion, occurred by 1 month of supplementation. By 6 to 12 months a significant reduction in the previously high rate of mean synthesis and breakdown was observed, with maintenance of net anabolism. These dynamic changes in whole-body protein turnover reflect a long-term improvement in energy and protein intake, which can favorably affect nutrition, growth, and the course of pulmonary disease in problem cases of cystic fibrosis.

Intrauterine Growth Retardation

Intrauterine growth retardation can result from a variety of environmental and genetic influences on fetal growth. The sequelae of intrauterine growth retardation resulting from impairment of nutrient flow include low birth weight with sparing of brain growth, polycythemia, and hypoglycemia resulting from decreased storage fuels and defective gluconeogenesis. Available data suggest that the vast majority of nutritionally growthretarded infants have normal postnatal development without significant difference in IQ or neurologic scores from normal infants. The outcome of infants in whom there is decreased growth potential relates to the condition underlying growth retardation and may, of course, result in later severe handicap. Infants with nutritional intrauterine growth retardation may exhibit decreased fetal size and sparing of brain growth as an adaptive stage in the presence of lower oxygen and substrate availability. Under such conditions, a smaller size may decrease substrate and oxygen needs and improve outcome. All infants with intrauterine growth retardation, however, require follow-up and careful developmental evaluation.

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

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.

Nutritionally Small-for-Dates Rats: Their Subsequent Growth, Regional Brain 5-Hydroxytryptamine Turnover, and Behavior

Rats were subjected to nutritional growth retardation either from conception to 5 postnatal days of age (fetal and neonatal restriction (FNR) group), or from 5 to 25 postnatal days of age (infantile restriction (IR) group). The FNR group may serve as a model for the human small-for-dates baby. At 20 weeks of age cerebellum, midbrain, and cerebrum were significantly reduced in weight by 4%, 5%, and 4%, respectively, in FNR animals when compared with controls. Only cerebellum and midbrain were affected in IR rats of the same age, but in both regions the percentage deficits (8% and 9%, respectively) were greater than in FNR animals. Both cerebellum and midbrain weighed significantly less in IR than in FNR rats. The timing of nutritional growth retardation appeared to be of little consequence to the regional brain turnover of 5-hydroxytryptamine in adulthood. The rate of synthesis in the hippocampus of both FNR and IR animals was significantly faster (67% and 75% respectively) than in controls. The increased turnover could perhaps represent "overactivity" of those 5-hydroxytryptaminergic neurons terminating in the hippocampus. Some differences in the behavior of the previously undernourished adult animals were also evident. On the fifth day of testing, control rats were most venturesome in the open field. Eighteen control rats left the edge zone within 2 min, whereas only 8 FNR and 11 IR rats did so. Most animals froze immediately after a 7-sex exposure to a loud electric bell. The delay before moving about again differentiated the three groups. FNR rats took longest to move out of the area in which they froze.

Vulnerability of developing brain. IX. The effect of nutritional growth retardation on the timing of the brain growth-spurt.

Vulnerability of developing brain. IX. The effect of nutritional growth retardation on the timing of the brain growth-spurt.

What Does Nutritional Growth Retardation Imply?

What Does Nutritional Growth Retardation Imply?