Abstract
Effect of metabolic acidosis on the expression of insulin-like growth factor and growth hormone receptor. To further our understanding of the growth failure in metabolic acidosis, we examined the insulin-like growth factor (IGF-I and IGF-II), the IGF binding protein-3 (IGFBP-3), and the hepatic IGF mRNA and growth hormone receptor mRNA in control, pair-fed and acidotic rats. The rats in the last group were made acidotic by using ammonium chloride (1.5%) as their sole fluid intake for eight days. Metabolic acidosis was confirmed by a blood pH of 7.11 ± 0.10 (mean ± SD). The mean starting weights for all rats were 167.1 ± 3.4 grams. Growth impairment was observed in the acidotic rats after one week of ammonium chloride intake. The body weights of the acidotic rats compared to those of the control rats were 155.5 ± 18.9 g versus 222.8 ± 9.7 g, P < 0.001; the pair-fed rats weighed 156.8 ± 19.6 grams. All rats were bled and sacrificed on day 8. Sera and tissue were analyzed with the following results: compared to the ad libitum controls, the same IGF-I concentrations were significantly decreased in the acidotic animals (P < 0.02) as well as pair-fed controls (P < 0.005). The serum IGF-II and IGF-binding protein-3 concentrations were unchanged by acidosis or food restriction. The hepatic IGF-I mRNA was significantly reduced by acidosis (P < 0.01) and pair-feeding (P < 0.01). Compared to control, the mean hepatic IGF mRNA in acidosis was significantly lower (P < 0.01). However, there was no significant difference between the acidotic and the pair-fed groups. The growth hormone receptor mRNA was depressed in acidosis (P < 0.02), but the data in the pair-fed group did not differ significantly from that of the control group. We conclude that the growth retardation of metabolic acidosis is related to significantly decreased values of serum IGF-I, inhibition of hepatic IGF-I gene expression and hepatic growth hormone receptors mRNA. Reduced nutritional intake may be an additional factor in the causal relationships.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
