Pathological changes in chickens, ducks and turkeys fed high levels of rapeseed oil.
Rations containing 25% of either regular rapeseed oil (36% erucic acid), Oro rapeseed oil (1.9% erucic acid), soybean oil or a mixture of lard and corn oil were fed to chickens, ducks and turkeys. The regular rapeseed oil ration caused growth depression, increased feed conversion and anemia in all species. All the ducks and some of the chickens fed the regular rapeseed oil ration died. These dead birds were affected with hydropericardium and ascites. No deaths in the turkeys could be attributed to the regular rapeseed oil ration but some turkeys fed this ration had degenerative foci characterized by infiltrations of histiocytic and giant cells in the myocardium. Severe fatty change in the heart, skeletal muscles, spleen and kidney was found at an early age in all birds fed the regular rapeseed oil ration. Less severe fatty change but no other lesions were found in birds fed the Oro rapeseed oil and soybean oil rations. (+info)
Changes in body composition and leptin levels during growth hormone (GH) treatment in short children with various GH secretory capacities.
OBJECTIVE: The aim of this study was to follow changes in body composition, estimated by dual-energy X-ray absorptiometry (DXA), in relation to changes in leptin during the first year of GH therapy in order to test the hypothesis that leptin is a metabolic signal involved in the regulation of GH secretion in children. DESIGN AND METHODS: In total, 33 prepubertal children were investigated. Their mean (S.D.) chronological age at the start of GH treatment was 11.5 (1.6) years, and their mean height was -2.33 (0.38) S.D. scores (SDS). GH was administered subcutaneously at a daily dose of 0.1 (n=26) or 0.2 (n=7) IU/kg body weight. Ten children were in the Swedish National Registry for children with GH deficiency, and twenty-three children were involved in trials of GH treatment for idiopathic short stature. Spontaneous 24-h GH secretion was studied in 32 of the children. In the 24-h GH profiles, the maximum level of GH was determined and the secretion rate estimated by deconvolution analysis (GHt). Serum leptin levels were measured at the start of GH treatment and after 10 and 30 days and 3, 6 and 12 months of treatment. Body composition measurements, by DXA, were performed at baseline and 12 months after the onset of GH treatment. RESULTS: After 12 months of GH treatment, mean height increased from -2.33 to -1.73 SDS and total body fat decreased significantly by 3.0 (3.3)%. Serum leptin levels were decreased significantly at all time points studied compared with baseline. There was a significant correlation between the change in total body fat and the change in serum leptin levels during the 12 months of GH treatment, whereas the leptin concentration per unit fat mass did not change. In a multiple stepwise linear regression analysis with 12 month change in leptin levels as the dependent variable, the percentage change in fat over 12 months, the baseline fat mass (%) of body mass and GHt accounted for 24.0%, 11.5% and 12.2% of the variability respectively. CONCLUSIONS: There are significant correlations between changes in leptin and fat and endogenous GH secretion in short children with various GH secretory capacities. Leptin may be the messenger by which the adipose tissue affects hypothalamic regulation of GH secretion. (+info)
Separate and joint effects of micronutrient deficiencies on linear growth.
Recent studies have investigated the effect of micronutrient deficiencies on growth stunting, with special attention toward the effect of zinc, iron, vitamin A and iodine deficiencies. In Mexico, the prevalence of growth stunting in children <5 y old is approximately 24%; it is higher in rural areas and lower in urban areas. In an initial study, the effect of zinc and/or iron supplementation on linear growth was investigated in a longitudinal, placebo-controlled design. After 12 mo of supplementation, there was no difference between the groups supplemented with zinc, iron or zinc plus iron and the placebo group. At baseline, 82% of the children in this study were deficient in at least two out of the five micronutrients that were determined, and 73% were anemic. In another study, a mixture of those micronutrients that were documented to be lacking in Mexican children was formulated in a supplement and given to Mexican children over a period of 12 mo in a longitudinal, placebo-controlled, supplementation design. Children in the low and medium socioeconomic status grew about 1 cm more than similar children in the placebo group. This difference was not found in children of high socioeconomic status. It is suggested that, in most cases, growth stunting is associated with marginal deficiencies of several micronutrients and that in populations with multiple micronutrient deficiencies, the effect on linear growth of supplementation with single nutrients will not be significant. Supplementation with multiple micronutrients is expected to be more effective, but even in that case the actual increment in height was less than the expected potential increment. (+info)
Burden of infection on growth failure.
The high prevalence of infections among children living in poor areas of developing countries impairs linear growth in these populations. Acute, invasive infections, which provoke a systemic response (e.g., dysentery and pneumonia), and chronic infections, which affect the host over a sustained period (e.g., gut helminth infections), have a substantial effect on linear growth. Such infections can diminish linear growth by affecting nutritional status. This occurs because infections may decrease food intake, impair nutrient absorption, cause direct nutrient losses, increase metabolic requirements or catabolic losses of nutrients and, possibly, impair transport of nutrients to target tissues. In addition, induction of the acute phase response and production of proinflammatory cytokines may directly affect the process of bone remodeling that is required for long bone growth. Infection of cells directly involved in bone remodeling (osteoclasts or osteoblasts) by specific viruses may also directly affect linear growth. Many interventions are possible to diminish the effect of infection on growth. Prevention of disease through sanitation, vector control, promotion of breast-feeding and vaccination is crucial. Appropriate treatment of infections (e.g., antibiotics for pneumonia) as well as supportive nutritional therapy (again including breast-feeding) during and after recovery, is also important. Targeted therapeutic interventions to decrease the prevalence of gut helminth infections may also be appropriate in areas in which such infections are widespread. Such interventions are of public health benefit not only because they reduce the incidence or severity of infections, but also because they decrease the long-term detrimental effect of malnutrition on populations. (+info)
Retarded growth and deficits in the enteric and parasympathetic nervous system in mice lacking GFR alpha2, a functional neurturin receptor.
Glial cell line-derived neurotrophic factor (GDNF) and a related protein, neurturin (NTN), require a GPI-linked coreceptor, either GFR alpha1 or GFR alpha2, for signaling via the transmembrane Ret tyrosine kinase. We show that mice lacking functional GFR alpha2 coreceptor (Gfra2-/-) are viable and fertile but have dry eyes and grow poorly after weaning, presumably due to malnutrition. While the sympathetic innervation appeared normal, the parasympathetic cholinergic innervation was almost absent in the lacrimal and salivary glands and severely reduced in the small bowel. Neurite outgrowth and trophic effects of NTN at low concentrations were lacking in Gfra2-/- trigeminal neurons in vitro, whereas responses to GDNF were similar between the genotypes. Thus, GFR alpha2 is a physiological NTN receptor, essential for the development of specific postganglionic parasympathetic neurons. (+info)
Cloning and expression of a novel chicken sulfotransferase cDNA regulated by GH.
We have used mRNA differential display to compare gene expression in normal and GH receptor-deficient dwarf chickens, and report here the characterization of one differentially expressed gene, which shows significant sequence identity to the sulfotransferase gene family. Partial cDNA clones were isolated from a chicken liver cDNA library and an additional sequence was obtained using 5' rapid amplification of cDNA ends. A complete cDNA probe hybridizes to three transcripts (2.4, 2.0 and 1.45 kb) on Northern blots of chicken liver RNA, which differ in the length of the 3' untranslated region. All three transcripts are expressed at higher levels in normal vs dwarf chickens, as expected for a GH-regulated gene. The expression of this sulfotransferase mRNA was also detected in skeletal muscle, but not other tissues. The administration of GH to chickens increased the hepatic expression within 1 h, suggesting this sulfotransferase could be directly regulated by GH. Sulfotransferase activity, using estradiol or corticosterone as substrate, is detected in cells transfected with an expression vector containing the full-length cDNA. The sequence of this sulfotransferase does not show significant similarity with any subfamily of the sulfotransferases and its endogenous substrate is presently unknown. However, we speculate that GH activation of sulfotransferase activity could play a role in reducing concentrations of growth-antagonistic steroid hormones in GH target tissues. These results demonstrate the usefulness of differential display in this model system to identify genes that play a role in mediating GH action. (+info)
Growth hormone treatment in young children with Down's syndrome: effects on growth and psychomotor development.
BACKGROUND: Learning disability and short stature are cardinal signs of Down's syndrome. Insulin-like growth factor I (IGF-I), regulated by growth hormone (GH) from about 6 months of age, may be involved in brain development. AIMS: To study long term effects of GH on linear growth and psychomotor development in young children with Down's syndrome. Study design-Fifteen children with Down's syndrome were treated with GH for three years from the age of 6 to 9 months (mean, 7.4). Linear growth, psychomotor development, skeletal maturation, serum concentrations of IGF-I and its binding proteins (BPs), and cerebrospinal fluid (CSF) concentrations of IGF-II were studied. RESULTS: The mean height of the study group increased from -1.8 to -0.8 SDS (Swedish standard) during treatment, whereas that of a Down's syndrome control group fell from -1.7 to -2.2 SDS. Growth velocity declined after treatment stopped. Head growth did not accelerate during treatment. No significant difference in mental or gross motor development was found. The low concentrations of serum IGF-I and IGFBP-3 became normal during GH treatment. CONCLUSIONS: GH treatment results in normal growth velocity in Down's syndrome but does not affect head circumference or mental or gross motor development. Growth velocity declines after treatment stops. (+info)
The generalised form of epimerase deficiency galactosaemia has been described in only two children from unrelated families. Their progress is reported and three other affected children from these families are described. The initial presentation was similar to classic galactosaemia. Despite treatment all have shown poor growth and moderate learning difficulties. Three have sensorineural deafness and four have pronounced dysmorphic features. The two older female patients have normal pubertal development. (+info)