Abstract

Induced impairment of growth rate and mature size in the rat was used to characterize and compare histological and biochemical indices of skeletal muscle hyperplastic and hypertrophic growth. Maternal nutritional restriction during gestation and lactation caused a 54% reduction in progeny body weight before realimentation was begun at weaning. A compensatory growth response was observed in restricted male progeny. Muscle fiber number in soleus and extensor digitorum longus (EDL) were not different between treatments, sexes or muscles after 12 wk of realimentation. Muscle nuclei per fiber transverse section was greater in soleus than EDL, but was unaffected by early nutritional restriction or sex. Capacity for protein synthesis (RNA:DNA ratio) and translational activity per ribosome (RNA:protein ratio) were not less in restricted progeny after realimentation. Therefore, it was concluded that phenotypic expression of genetic potential for cell size, but not cell number, is affected by prenatal and early postnatal nutritional restriction that causes permanent growth impairment in the rat. The significantly greater DNA concentration in the soleus, which is also reflected in nuclear counts, and markedly different pattern of growth exhibited by it, suggest that the soleus may be atypical compared with most hind limb muscles of the rat and may not be the best model for further study of the regulation of skeletal muscle growth.

Full Text
Paper version not known

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 call

Disclaimer: 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.