Vitamin A deficiency is one of the most common dietary deficiencies in the developing world and is a major health concern where it is associated with increased risk of fetal and infant mortality and morbidity. Early studies in the rat demonstrated that, in addition to respiratory problems, neonates showed evidence of mobility problems in response to moderate vitamin A deficiency. This study investigated whether moderate deficiency of this vitamin plays a role in regulating key skeletal muscle regulatory pathways during development. Thirty female rats were fed vitamin A-moderate (VAM) or vitamin A-sufficient diets from weaning and throughout pregnancy. Fetal and neonatal hindlimb and muscle samples were collected on days 13.5, 15.5, 17.5, and 19.5 of pregnancy and 1 day following birth. Mothers fed the VAM diet had reduced retinol concentrations at all time points studied (P Ͻ 0.01), and neonates had reduced relative lung weights (P Ͻ 0.01). Fetal weight and survival did not differ between groups but neonatal survival was lower in the VAM group where neonates had increased relative heart weights (P Ͻ 0.05). Analysis of myogenic regulatory factor expression and calcineurin signaling in fetuses and neonates demonstrated decreased protein levels of myf5 [50% at 17.5 dg (P Ͻ 0.05)], myogenin [70% at birth (P Ͻ 0.001)], and myosin heavy chain fast [50% at birth (P Ͻ 0.05)] in response to moderate vitamin A deficiency. Overall, these changes suggest that vitamin A status during pregnancy may have important implications for fetal muscle development and subsequent muscle function in the offspring. retinoic acid; calcineurin; skeletal muscle; neonate VITAMIN A IS AN ESSENTIAL nutritional factor required for a wide range of physiological processes including the promotion of general growth, maintenance of the immune and visual systems, regulation of epithelial tissues, and embryonic development. Vitamin A itself exists in three oxidation states: retinol (alcohol
Certain beta(2)-adrenoceptor agonists, such as clenbuterol, are known to elicit a muscle-specific anabolism or hypertrophy in both normal and catabolic muscle in a wide variety of species. However, the underlying mechanism(s) of the beta(2)-agonist-induced anabolism remains unclear. This study aimed to determine the effects of clenbuterol administration in utero on skeletal muscle and to examine the underlying molecular mechanisms. Pregnant rats were fed clenbuterol (2 mg/kg diet) from Day 4 of gestation (4 dg) until weanling and fetal samples were taken from 13.5, 15.5, 17.5, and 19.5 dg and from 1d neonatal pups. Muscles were analyzed for total DNA, RNA and protein and sections examined morphologically for changes in muscle development. Western and immunohistochemical analyses were performed to identify changes in known myogenic signaling proteins. Clenbuterol increased the size of both fast and slow fibers in utero which was associated with a decreased DNA:protein ratio (28%) and an increased RNA:DNA ratio (36%). Additionally, drug treatment in utero induced a decrease in the fast:slow fiber ratio (38%). These myogenic changes were correlated with an increase in the GATA-2 hypertrophic transcription factor at both 17.5 dg (by 250%) and 19.5 dg (by 40%) in fetuses from clenbuterol treated dams. In addition, drug treatment resulted in increased membrane association of PKC-micro at 17.5 dg (325%) and increased PKC-alpha cytosolic abundance (40%) and PKC-theta membrane abundance at 19.5 dg (250%). These results are the first demonstration that beta(2)-agonists such as clenbuterol may act through upregulating the GATA-2 transcription factor and implicate certain PKC isoforms in the drug-induced regulation of skeletal muscle development.
This study was conducted with 16 subjects to detertnitie whether the topical application of betatnethasone dipropionate (Diprosotie) 0,05% creatn, iti amounts of 30 or 60 g daily for a period of four weeks, would lead to adrenocortical suppre.s.sion. Five patietits were given 60 g daily, six patietits given 30 g daily and five nortnal subjects 30 g daily. Adrenocortical futiction was assessed weekly by tneatis of plastna cortisol levels. The results showed that transient adretiocortical suppression may follow the use of betatnethasone dipropiotiate 0.05% cream daily at these dosage levels and this tnay be a futiction of heightetied absorption in some individuals.It is intended to carry out a further trtal using both plastna cortisol detertnination atid itisulin-induced hypoglycaetnia as a measure of hypothakuntis-pituitary-adrenal axis suppression, as it is believed that mittor atid moderate degrees of adrenal suppression tnay not becotne obvious from plastna cortisol determinations.
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