Biomedical subjects

A D McNall

Publications and source records attributed to A D McNall.

3 recordsLinked to original sources

PubMed1996

Zinc status does not affect aluminum deposition in tissues of rats.

To examine whether zinc deficiency would increase the toxicity of dietary aluminum, weanling, male Sprague-Dawley rats were fed purified diets containing either 2 or 30 mg Zn/kg diet, with or without 500 mg Al/kg diet for 28 d. Individually pair-fed rats were fed the 30 mg Zn/kg diet with or without added aluminum to control for inanition secondary to zinc deficiency. Rats fed the 2 micrograms Zn/kg diet showed evidence of zinc deficiency, including anorexia, growth retardation, and depressed concentrations of zinc in tibias and livers. Zinc deficiency did not significantly increase the concentrations of aluminum in the tibias, livers, kidneys, or regions of the brain examined (cerebrum, cerebellum, midbrain, and hippocampus). Inclusion of aluminum in the diet did not alter aluminum concentrations in the various tissues. Under the conditions of this study, zinc deficiency did not result in greater sensitivity to dietary aluminum exposure.

Aluminum↗

PubMed1996

The growth hormone-dependent decrease in hepatic fatty acid synthase mRNA is the result of a decrease in gene transcription.

The present study was conducted to determine the chronic effects of porcine growth hormone administration on fatty acid synthase (FAS) mRNA abundance and gene transcription in growing rats. Growth hormone treatment increased growth rate approximately 27% (P<0.01). Porcine growth hormone decreased FAS mRNA levels by 55%. The reduction in FAS mRNA was due to a marked decrease in transcription of the FAS gene (decreased by 80%). In contrast, porcine growth hormone did not affect mRNA abundance or transcription rate of another insulin-regulated gene, phosphoenolpyruvate carboxykinase. In summary, our results have established that chronic treatment with growth hormone decreases FAS mRNA by decreasing the transcription rate of the gene. Furthermore, they suggest that the effects of growth hormone are specific and are not mediated by general changes in insulin-responsive gene expression in liver.

Animals↗

PubMed1995

The impaired growth induced by zinc deficiency in rats is associated with decreased expression of the hepatic insulin-like growth factor I and growth hormone receptor genes.

This study was conducted to determine whether dietary zinc status affects the expression of the insulin-like growth factor I and growth hormone receptor/growth hormone binding protein genes in the liver of growing rats. Weanling male Sprague-Dawley rats were randomly allotted to zinc-deficient, pair-fed or ad libitum-fed dietary treatments and fed diets containing no added zinc for 14 d. Zinc acetate was added to the deionized, distilled water (30 mg/L) provided to pair-fed and ad libitum-fed rats. As expected, zinc deficiency significantly reduced growth rate by 60% and was associated with a significantly lower serum insulin-like growth factor I concentration (46 and 67% lower than pair-fed and ad libitum-fed rats, respectively). The reduction in serum insulin-like growth factor I concentration was associated with a decrease in insulin-like growth factor I gene expression. The abundance of the 7.5-kb insulin-like growth factor I mRNA transcript in zinc-deficient and pair-fed rats was 14 and 31% that of the ad libitum-fed rats. The 0.8-1.2-kb insulin-like growth factor I transcript also was significantly lower in the zinc-deficient and pair-fed rats. In contrast, the abundance of the 1.8-kb insulin-like growth factor I transcript was unaffected by zinc deficiency. The growth hormone receptor mRNA levels of zinc-deficient and pair-fed rats were 17 and 50% and their growth hormone binding protein mRNA levels were 46 and 65% those of the ad libitum-fed rats. In summary, zinc deficiency markedly decreases expression of the insulin-like growth factor I and growth hormone receptor genes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗