Location: Location not imported yet.Title: The effects of the in utero glucocorticoid (GLC) exposure on fetal skeletal muscle growth in rats) Author
Submitted to: Pediatric Academic Society
Publication Type: Abstract only
Publication Acceptance Date: 11/18/2009
Publication Date: 5/1/2010
Citation: Gokulakrishnan, G., Estrada, I., Fiorotto, M.L. 2010. The effects of the in utero glucocorticoid (GLC) exposure on fetal skeletal muscle growth in rats [abstract]. In: Proceedings of the 2010 Pediatric Academic Societies Annual Conference, May 1-4, 2010, Vancouver, British Columbia, Canada. Paper No. 3670.2. Interpretive Summary:
Technical Abstract: Data from epidemiological studies suggest that adult muscle strength and lean body mass are related to birth weight and therefore, are influenced by the intra-uterine environment. The degree to which the effects on the musculature result from a nutrient deficit or its consequent exposure to above normal GLC levels is unclear. To test the hypothesis that exposure of the fetus to GLC results in a reduction in muscle growth that is independent of the effects of maternal nutrient intake. The objective is to quantify the effects of exposure to GLC during gestation on skeletal muscle mass and fiber size, rates of protein synthesis rate and myonuclear accretion as well as maturation in term fetuses. Three groups (n=6-10/group) of timed-pregnant Sprague-Dawley (SD) rats were studied: Control (CON): ad libitum food intake; no dexamethasone; Dexamethasone (DEX): ad libitum food intake; dexamethasone (1 mg/L, in drinking water) ad lib from embryonic day (ED)13 to 21. Pair-fed (PF): pair-fed to DEX group from ED 13 to 21; no DEX given. Body weights, food, and water intake were measured daily. On ED 22, pups were surgically delivered, weighed, and the quadriceps and diaphragm muscles dissected quantitatively. DEX intake (89 +/- 6 microg/(kg.d)) reduced maternal food intake by 13% (P<0.001) and weight gain by 82% (P<0.001). Nutritional effects contributed only to 25% of the dam weight gain deficit. Pups/litter was not altered by treatment. DEX reduced pup body and muscle weights (P<0.001) compared to CON or PF pups but the effects on quadriceps weight was less than its effect on body weight. Quadriceps weights in PF and CON pups were similar. The diaphragm was significantly lighter in both DEX and PF pups (P<0.03) compared to CON, and the deficit was not accounted for by body weight differences. In conclusion, these data support the hypothesis that fetal exposure to GLC results in growth retardation that is independent of its effects on maternal food intake. The consequences for the musculature were muscle-specific, with the diaphragm, unlike the quadriceps, being sensitive to both DEX and maternal nutrient intake. Quadriceps growth was also impaired by GLC, but to a lesser degree than the diaphragm and other body tissues.