ABSTRACT
To investigate the role of IGF in muscle development in vivo, developmental expression and location of IGF-I and -II protein and mRNA were examined in fetal, postnatal, and adult skeletal muscle. Muscle tissue was collected from 30-, 44-, 59-, 68-, 75-, 89-, and 109-d porcine fetuses, 21-d neonatal pigs, and 6-mo-old (adult) pigs. Relative amounts of IGF-II mRNA peaked (P < .05) in 59-d fetal muscle and decreased thereafter. Inversely, muscle IGF-I expression increased (P < .05) to maximal levels around birth. For in situ hybridization, frozen muscle tissue sections (10 microm) were hybridized with a hydrolyzed form of the same riboprobes or incubated with polyclonal or monoclonal antibodies to IGF-I or -II, respectively. The majority of IGF-I and IGF-II mRNA was localized to developing muscle fibers, whereas little signal was found in the surrounding connective tissues. Immunofluorescent localization of IGF-I and -II confirmed that muscle IGF are present in developing muscle fibers. Collectively, these data show that IGF-I and -II are expressed and produced primarily in muscle cells within developing muscle tissue and support the hypothesis that IGF-I and -II modulate fetal muscle development.
Subject(s)
Gene Expression Regulation, Developmental/genetics , Insulin-Like Growth Factor II/genetics , Insulin-Like Growth Factor I/genetics , Muscle, Skeletal/chemistry , Swine/growth & development , Animals , Blotting, Northern/veterinary , Female , Fluorescent Antibody Technique, Indirect/veterinary , Gestational Age , In Situ Hybridization/veterinary , Insulin-Like Growth Factor I/analysis , Insulin-Like Growth Factor II/analysis , Male , Muscle, Skeletal/embryology , RNA, Messenger/analysis , RNA, Messenger/genetics , Swine/embryologyABSTRACT
The physiologic response to infection includes reductions in tissue concentrations of anabolic growth factors as a means of reducing growth and conserving nutrients for immunologic processes. This repartitioning of nutrients is accompanied by anorexia, which has been linked to increased leptin expression. Furthermore, leptin and growth hormone (GH) concentrations are inversely related, with leptin being required for normal GH release. The objective of this study was to determine if pretreatment with GH would influence endotoxin-induced changes in leptin expression or attenuate endotoxin-induced reductions in serum insulin-like growth factor-1 (IGF-1) and IGF-1 expression in liver and longissimus muscle. In experiment 1, 40 pigs were assigned to four treatments (n = 10 per treatment) arranged as a 2x2 factorial with GH (s.c. injection, 2 mg 1 h before challenge and 2 mg 2 h after challenge) and endotoxin (single i.m. injection, 25 microg/kg body weight) as main effect variables. Pretreatment with GH resulted in a marked increase (p<0.001) in serum GH within 1 h that was sustained throughout the study. Endotoxin challenge reduced (p<0.003) serum IGF-1 independent of GH (GH x endotoxin, p>0.682), and reduced (p<0.05) IGF-1 expression in longissimus muscle but not liver. Leptin mRNA abundance was reduced 56% (p<0.005) by GH but was not affected by endotoxin (p>0.81). In experiment 2, 36 pigs (n = 12 per treatment) were either allowed ad libitum feed consumption with no injection or deprived of feed and injected twice with either saline or endotoxin 24 h apart. Feed deprivation reduced leptin expression (p<0.05). However, endotoxin did not change leptin expression but markedly increased (p<0.05) serum haptoglobin. These data indicate that changes in IGF-1 status in endotoxin-challenged pigs are independent of serum GH and that leptin expression is not increased by endotoxin challenge in the pig. These data also indicate a regulatory linkage between GH and leptin in vivo.
Subject(s)
Adipose Tissue/drug effects , Growth Hormone/pharmacology , Lipopolysaccharides/pharmacology , Protein Biosynthesis , Adipose Tissue/metabolism , Animals , Female , Insulin-Like Growth Factor I/biosynthesis , Leptin , Liver/drug effects , Liver/metabolism , Male , Muscle, Skeletal/drug effects , Muscle, Skeletal/metabolism , SwineABSTRACT
Other tissue involvement has been described in Darier's disease, eg: susceptibility to infection. In order to know if this susceptibility is due to abnormal phagocytosis and if this can revert by administration of retinoic acid (RA), blood monocyte-derived macrophages, from four individuals with Darier's disease were obtained prior and after administration of RA to determine in them morphological, cytochemical and phagocytic activity changes. It was observed that phagocytosis was diminished and RA administration increased it, without changes in enzyme distribution. This modification of phagocytosis could be due to a reordenation of cytoskeleton.
