Mechanism Of Growth Retardation Research Articles

Interactions between diurnal temperature fluctuations and salinity on expansion growth and water status of young tomato plants

SummaryExpansion growth is limited if the difference between day and night temperature (DIF) is negative. Growth is also limited high salinity. Expansion growth of tomato seedlings was studied under day/night temperatures of 16/24°C and 24/16°C, and nutrient solution salinities of 3 and 15 mS cm‐1 to ascertain whether interactions exist between the two stress forms. Water status was also studied in order to assess possible mechanisms of growth retardation. A significant interaction between DIF and salinity was found for all recorded growth variables. Hypocotyl length, plant height, leaf area and fresh and dry weight were lower at negative DIF than at positive, the reduction being greater at low salinity than at high. Increased salinity also reduced growth, more so at positive DIF than at negative. Growth reduction at negative DIF was accompanied increased shoot water and osmotic potentials. Pressure potential was unaffected DIF. Growth reduction at high salinity was accompanied reduced water and osmotic potentials. Pre‐dawn pressure potential was increased at high salinity, whereas no effect of salinity on pressure potential at midday was found. The differences in effects on water status between the two stress forms may suggest differing mechanisms of growth retardation.

Mechanisms of Growth Retardation, Drug Therapy, and Nutritional Support in Pediatric Inflammatory Bowel Disease: A Workshop Sponsored by the North American and European Societies for Pediatric Gastroenterology and Nutrition

: Growth retardation is common in children with inflammatory bowel disease (IBD). The most sensitive measure of impaired growth, growth velocity, is abnormal in 65% of children with Crohn's disease. With treatment, growth velocity may return to normal, but catch-up growth is often incomplete and ultimate height lower than predicted. In some patients delayed puberty may compensate for poor growth earlier in life, and there is good evidence that even after menarche, significant growth can occur. Surgery may have a favorable impact on growth in the short term, but final height often remains reduced. The mechanism for growth failure in IBD is thought to be related to both prolonged periods of suboptimal nutritional intake and persistent inflammation. Growth throughout childhood is dependent on growth hormone and insulin-like growth factors (IGF). At puberty, androgens and estrogens also play a significant role in normal growth. Both malnutrition and inflammatory bowel disease result in low levels of IGF-1. With recovery, levels return to normal. Although little work has been done to measure the effects of chronic maintenance drug therapy on growth, it is known that children taking alternate-day prednisone grow normally and can exhibit catch-up growth. Nutritional therapy with tube feeding of elemental diets also improves nutrition and decreases inflammation. Children with either small-bowel Crohn's or Crohn's ileocolitis respond to tube feedings of both elemental or semielemental diets.

Insulin-like growth factor and growth hormone receptor in nephrotic rats.

In an attempt to elucidate the mechanism of growth retardation in the nephrotic syndrome, specific serum and hepatic growth factors were measured in Sprague-Dawley rats in which nephrotic syndrome was produced by administration of puromycin (1.5 mg.100 g body wt-1.day-1) for 12 days. On the 13th day, the results of these nephrotic animals were compared with those of an equal number of pair-fed and control animals: the mean dietary intake of the nephrotic group was 71% that of the control group (P < 0.001). Serum insulin-like growth factor (IGF) binding protein-3 was significantly reduced (P < 0.005) in the nephrotic rats, compared with the pair-fed and the control groups. Hepatic IGF-I mRNA in the nephrotic rats averaged 36% that of control (P < 0.001) and 46% that of the pair-fed animals (P < 0.001). Hepatic growth hormone receptor (GHr) mRNA in the nephrotic rats averaged 19% of that of the control (P < 0.001) and 27% of that of the pair-fed rats (P < 0.001). These results indicate that the growth retardation of the nephrotic rats may be associated with the significant decrease in IGF-I mRNA and reduction in GHr mRNA.

Metabolic acidosis inhibits growth hormone secretion in rats: mechanism of growth retardation

To test the hypothesis that growth retardation in nonanion gap acidosis may be associated with impairment of growth hormone (GH) secretory patterns, we examined GH secretion in rats made acidotic with ammonium chloride ingestion. Considerable growth retardation was demonstrated in pair-fed and acidotic rats after 1 wk of ammonium chloride ingestion compared with control. With stable metabolic acidosis sustained on the 8th day of experiment, pulsatile secretion of GH was evaluated by blood samples drawn every 10 min for 6 h. Using deconvolution analysis to quantitate in vivo GH secretory rates, we found significant inhibition of pulsatile GH secretion in acidotic rats. Changes in amplitude of GH pulses and mean mass of GH pulses correlated with changes in body weight. These studies showed that chronic metabolic acidosis causes growth impairment, reduced food efficiency, and amplitude-specific inhibition of pulsatile secretion of GH. We propose that this GH axis suppression, whether mediated by decreased nutrients or not, contributes significantly to growth failure in children with renal tubular acidosis. Because a similar degree of inhibition of GH secretion was seen in pair-fed rats, we infer that insufficient calorie intake in metabolic acidosis may contribute to disruption of normal GH secretion patterns. These changes in GH secretion were specific, because acidotic rats were different from pair-fed controls in that they showed no change in either half-life of GH in circulation or in pulse frequency. Such observations offer a rationale for more detailed clinical investigations into the impact of metabolic acidosis on physiological regulation of pulsatile GH secretion in humans.

Alterations of serum Insulin-like Growth Factor-I (IGF-I) and IGF-binding proteins (IGFBPS) in swine infected with the protozoan parasite Sarcocystis miescheriana

The effects of a Sarcocystis miescheriana infection on insulin-like growth factor-I (IGF-I) and insulin-like growth factor binding proteins (IGFBPs) were investigated to determine possible mechanisms of growth retardation in growing pigs. Sixteen pigs averaging 14 kg body weight were divided into 4 groups of 4 pigs each and infected either with 0.5, 1.0, or 3.0 × 10 6 sporocysts of S. miescheriana. Four pigs were retained as non-infected controls; however, they became serologically positive during the course of the infection. Effects also were investigated in 2 groups of 3 pregnant sows. One group was infected with 0.5 × 10 6 sporocysts and the other group was retained as uninfected controls. Body weights of infected growing pigs were depressed as compared to controls following the acute phase 15 d after infection (dai). Serum concentrations of IGF-I dropped significantly (p < 0.05) during the acute phase of infection in all infected groups of growing pigs. Conversely, the amounts of unsaturated serum IGFBPs were elevated significantly (p < 0.05) during the acute phase of infection. Specifically, serum concentrations of IGFBP-1, IGFBP-2, and IGFBP-4 were elevated at this time, as determined by ligand blot analysis. There was no association between growth factor alterations and tissue damage as measured by serum creatinine kinase and aspartate aminotransferase levels. The extent of effects in growing pigs was related to the amount of the original parasite inoculum. During the acute phase of infection 2 of 3 pregnant sows aborted. The third sow went to term, but piglets were stillborn or died within 24 hr. Compared to uninfected controls, serum concentrations of IGF-I in infected pregnant sows were depressed during and after the acute phase of the infection. Levels of unsaturated serum IGFBPs in pregnant sows were not affected. These data suggest that decreased IGF-I levels and/or elevated levels of specific forms of IGFBPs may be a mechanism by which growth is affected in feeder pigs infected with S. miescheriana.

Mechanism of Growth Retardation following Chronic Administration of β-Adrenoceptor Antagonists to Developing Rats

A total of 112 3-week old Wistar rats were separated into eight groups: control groups I-IV (n = 62) and propranolol-treated groups V-VIII (n = 50). Propranolol hydrochloride (100 mg/kg) was present in the rats' drinking water until 26 weeks of age and growth rates of all groups were monitored daily until 53 days of age and thereafter every third day throughout the study. Chronic oral propranolol administration produced growth retardation (P less than 0.05) in both sexes that was reversible when treatment was discontinued. Organ weights were generally smaller in propranolol-treated rats; on the other hand, the ratio of most organ weights per 100 g of body weight was greater in propranolol-treated rats (especially females). The radio-immunological determination of plasma growth hormone showed increased concentrations of growth hormone in propranolol-treated rats (P less than 0.05), whereas hypothalamic somatostatin content was not significantly changed. The results showed that the retarded growth rate following chronic oral propranolol administration to growing rats was independent of changes in plasma growth hormone and hypothalamic somatostatin concentrations, and that retardation was entirely reversible when the beta-adrenoceptor antagonist was discontinued.

Growth in Children With Cerebral Palsy Fed Via Gastrostomy

Growth characteristics of 57 children with feeding gastrostomies attending the cerebral palsy clinic at a regional medical facility were evaluated. All children had severe neuromotor and orofacial involvement and mental retardation. More than 90% of the patients were less than fifth percentile for height and weight, and 80% were underweight for height before gastrostomy tube placement. Following gastrostomy, 33% remained underweight for height and 21% became overweight for height. The majority of children remained at less than the fifth percentile for height and weight. Improvement in linear growth was much less common than improvement in weight. Children with gastrostomies placed in the first year of life were most likely to exceed the fifth percentile for height and weight. The mechanisms of growth retardation in children severely affected by cerebral palsy are not known, but poor nutrition is thought to be the major contributor. Gastrostomy feeding in children severely affected by cerebral palsy can improve nutritional status but does not eliminate growth retardation. The importance of growth and adequate nutrition in reducing morbidity in children with severe neuromotor involvement remains to be established.

89 EXPERIMENTAL ZINC DEPLETION IN HUMANS: EFFECT ON PLASMS SOMATOMEDIN-C

Zinc (Zn) has been shown to be essential for growth and development of the microorganism, animal and man. However, the mechanism by which Zn promotes growth has not been well defined. We have previously reported a significant decrease in the level of plasma somatomedin-C (PSM-C) in zinc-deficient rats (Experientia 40:498-500, 1984 and Brit.J.Nutr. 56:163-169, 1986). Four healthy volunteers participated in this experiment which was designed so that each subject served as his own control. During a 1-wk baseline period subjects were fed a semi-purified diet containing 1.2 mg Zn/d and were supplemented with Zn-acetate so that their total daily intake of Zn was equal to their habitual daily intake prior to the study period. The baseline period was followed by a 12-wk depletion period where subjects consumed the semi-purified diet with no Zn supplement. By the end of depletion, we observed a significant decrease (p<0.005) in plasma-Zn, whole blood-Zn, urinary-Zn (μg/24 h), plasma-NH3 (p<0.01), plasma-Alk.phosphatase (p<0.01) and PSM-C (p<0.01). In conclusion, the present study suggests that somatomedin-C is Zn-dependent. It provides an insight into the mechanism of growth retardation associated with Zn-deficiency in humans.

Renal tubular acidosis: diagnostic work-up treatment and mechanisms of growth retardation.

Astute clinical observations, careful evaluation of laboratory results, together with research aimed at understanding the mechanisms of growth failure in children with the various types of renal tubular acidosis, have led to a more cogent approach to the management of children with renal tubular acidosis. This review examines the different clinical presentations of renal tubular acidosis, the diagnostic workup, the recent advances in our understanding of the mechanisms of growth failure and current therapeutic modalities.

Paternal employment in solvent related occupations and adverse pregnancy outcomes.

Washington State birth certificates were examined for associations between adverse pregnancy outcomes and paternal employment in solvent exposed occupations. Four cohorts defined by live, singleton births to fathers usually employed as auto body shop workers, painters (construction and maintenance), printers, or fibreglass workers were compared retrospectively with both a systematically selected control cohort and a low solvent exposed, occupationally defined control cohort (paternal electricians). The effects of maternal race and medical illness were controlled by sample restriction; maternal age and gravidity by stratified analysis. There was evidence of increased risk of low birth weight for infants born to fathers employed as body shop workers (relative risk = 1.6; 95% confidence interval = 1.1-2.4) or painters (RR = 1.4; CI = 0.9-2.1) when compared with the systematically selected controls but not with the electrician controls. The excess risk appeared stronger when only term infants were analysed suggesting a mechanism of growth retardation rather than prematurity. There was no evidence of increased risk among the other exposed cohorts or for other adverse pregnancy outcomes. Several design features limit the interpretation of the findings and confirmation by other studies is needed.

Mechanism of growth retardation of the adenocarcinoma EO 771.

Growth retardation of tumors has been predominantly described by an increase of the "cell loss factor" phi. However, this cell loss factor alone merely reflects the growth deceleration without giving information on the mechanism that causes growth retardation. In the present study a quantitative analysis of the mechanism causing growth retardation of the adenocarcinoma EO 771 has been carried out by determining separately the components of the cell loss factor phi, namely the cell production rate and the cell loss rate of the tumor cell population. For this purpose the alteration of the histology of the tumor (proportion of necrotic tumor tissue, tumor cell density) and the proliferative capacity of the tumor cell population as a function of the tumor size was studied by applying morphometric and cell kinetic methods. The results show that growth deceleration is due to a decrease of the cell production rate kappa p and a simultaneous increase of the cell loss rate kappa l. Both processes contribute to about the same extent to the growth deceleration of the tumor cell population. In early tumor growth deceleration is mainly due to a prolongation of the cycle time of the tumor cells, in later phases of tumor growth to an increasing probability of the tumor cells to decycle leading to a decrease of the growth fraction GF and an increase of the cell loss rate kappa l.

Physiological mechanism of growth retardation in rice seedlings as affected by low temperture.

Physiological mechanism of growth retardation in rice seedlings as affected by low temperture.

461 ROLE OF DIETARY PROTEIN AND AMINO ACIDS IN THE MODULATION OF PLASMA SOMATOMEDIN ACTIVITY IN RATS

The mechanism of growth retardation in many nutritional deficiency states has not been delineated. Somatomedin (SM) is depressed after prolonged fasting or in severe malnutrition despite elevated growth hormone (GH) concentrations, suggesting both nutrition and GH may act as modulators of SM. We have studied the effects of varying concentrations of dietary protein (2.5, 5, 10, 20%) and specific dietary amino acid deficiencies on body and organ weights, GH, SM, cartilage glycosaminoglycans (GAGS) and biochemical composition of brain and liver. Changes in body weights and organ weights were similar for 2.5% protein, a valine deficient or a tryptophane deficient diet (-10%). An increase of 177% was observed for animals on a complete amino acid diet or a 20% protein diet. Arginine deficiency had an intermediate effect. Biochemical alterations were more striking in liver than in brain. Serum SM ranged from 0.20 units for rats on the valine and tryptophane deficient diet to 1.44 units for the rats on the complete diet. SM was positively correlated with the protein content of the diet, body and organ weight changes, food efficiency and cartilage GAGS content and negatively correlated with GH concentrations. These data suggest that dietary protein and amino acids play a direct role in the modulation of SM activity and the growth retardation associated with some nutritional deficiency states may be related to its additional effect on SM activity.