BackgroundEnergy and Zinc (Zn) deficiencies have been associated with nutritional related growth retardation as well as growth hormone (GH) resistance. In this study, the relationship between suboptimal energy and/or Zn intake and growth in rats and their response to immunoreactive exogenous recombinant human GH (GHi), was determined.ResultsRats treated with GHi and fed ad-libitum energy and Zn (100/100) had increased IGFBP-3 (p < 0.05) as compared with NSS (215 ± 23 vs. 185 ± 17 ng/ml) along with similar body weight gain. Rats treated with GHi and fed suboptimal energy and full Zn (70/100) had significantly increased weight gain (109.0 ± 18.2 vs. 73.8 ± 11.0 g) and serum IGF-I levels (568 ± 90 vs. 420 ± 85 ng/ml), along with decreased total body water (TBW; 61.0 ± 1.6 vs. 65.7 ± 2.1%) as compared to NSS controls. However, body weight gain was reduced (p < 0.05) as compared with rats fed ad-libitum energy. Growth hormone treated rats fed only suboptimal Zn (100/70), had increased weight gain (217.5 ± 13.2 vs. 191.6 ± 17.9 g; p < 0.05) compared to those given NSS. These rats gained weight in similar amounts to those fed full Zn. Rats treated with GHi and fed both suboptimal energy and Zn (70/70) showed similar results to those fed suboptimal energy with appropriate Zn (70/100), along with significant increases in IGFBP-3 levels (322 ± 28 vs. 93 ± 28 ng/ml). All restricted rats had reduced 24-h EE (kcal/100 g BW) and physical activity index (oscillations/min/kg BW) and GHi did not overcome these effects.ConclusionThese results suggest that GHi enhances weight gain in rats with suboptimal energy and Zn intake but does not modify energy expenditure or physical activity index. Suboptimal Zn intake did not exacerbate the reduced growth or decrease in energy expenditure observed with energy restriction.
This study investigated developmental changes in the contractile system of the mesenteric small arteries of the rabbit. Arteries about 1 mm in length and 100-250 microns in internal diameter were dissected out from the mesenteric bed of the fetus (29 d of gestation), newborn (3-5 d old), and adult rabbit. Vascular contraction was induced by high KCl concentration, and contractile force was measured using a tension transducer. The sensitivity of vascular contraction to high KCl was similar in the three age groups. To determine the role of Ca influx across the sarcolemma in vascular contraction, the vasorelaxant effect of diltiazem was studied in the artery precontracted with high KCl concentration. The vasorelaxant effect of diltiazem in the fetus and newborn was less than in the adult. To estimate the size of the intracellular Ca pool, caffeine-induced and noradrenaline-induced contraction were measured in the Ca- and Na-free solution. In the fetus and newborn, both the caffeine-induced contraction and noradrenaline-induced contraction were greater than in the adult. The ultrastructural study showed that the endoplasmic reticulum was abundant in the fetus and newborn, and it was scarce in the adult. These data indicate that the dependency of vascular contraction on Ca influx across the sarcolemma increases and the intracellular Ca store decreases with development in the mesenteric resistance arteries.
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