Dennis R. Campion

Animal growth regulation.

1 Placental Regulation of Fetal Growth.- 1. Introduction.- 2. Placental Anatomy and Pattern of Blood Flow.- 3. Placental Growth.- 4. Growth of Uteroplacental Blood Flow.- 5. Regulation of Blood Flow.- 6. Placental Transport.- 7. Hormone Secretion.- 8. Conclusions.- References.- 2 Endocrinology of Bone Formation.- 1. Introduction.- 1.1. Unique Aspects of Bone Physiology.- 1.2. Bone Structure.- 1.3. Methods of Investigating Bone Formation.- 2. Hormones.- 2.1. Somatomedins.- 2.2. PTH.- 2.3. Vitamin D.- 2.4. Calcitonin.- 2.5. Insulin.- 2.6. Thyroid Hormones.- 2.7. Sex Steroids.- 2.8 Glucocorticoids.- 3. Local Regulators of Bone Formation.- 3.1. Prostaglandins.- 3.2. Noncollagen Proteins.- 3.3. Growth Factors.- References.- 3 Endocrine Regulation of Adipogenesis.- 1. Introduction.- 2. Insulin.- 3. Growth Hormone.- 4. Insulinlike Growth Factors.- 5. Glucocorticoids.- 6. Indomethacin, Prostaglandins, and AMP.- 7. Thyroid Hormones.- 8. Cachectin.- 9. Autocrine Control.- 10. Perspectives on Integrated Endocrine Control.- References.- 4 Autocrine, Paracrine, and Endocrine Regulation of Myogenesis.- 1. Introduction.- 2. Muscle Structure.- 3. Myogenesis.- 4. Factors Affecting Myogenesis.- 4.1. Insulinlike Growth Factors (Somatomedins).- 4.2. Insulin.- 4.3. Transforming Growth Factor-? (TGF-?) (Differentiation Inhibitor).- 4.4. Transferrin.- 4.5. Fibroblast Growth Factor (FGF).- 4.6. Somatotropin.- 4.7. Glucocorticoids.- 4.8. Thyroid Hormone.- 5. Summary.- References.- 5 The Expression of Protooncogenes in Skeletal Muscle.- 1. Introduction.- 2. Categories of Oncogenes.- 2.1. Tyrosine Kinases.- 2.2. GTP-Binding Proteins.- 2.3. Nuclear Proteins.- 2.4. Peptide Hormones.- 3. Oncogene Expression in Skeletal Muscle.- References.- 6 Regulation of Myofibrillar Protein Gene Expression.- 1. Introduction.- 2. Multigene Families.- 3. Major Myofibrillar Proteins of the Sarcomere.- 3.1. Actin.- 3.2. Tropomyosin (TM).- 3.3. Troponin (TN).- 3.4. Myosin Light Chains (MLC).- 3.5. Myosin Heavy Chains (MHC).- 4. Isolation and Characterization of MHC Sequences.- 5. Effects of Various Stimuli on MHC Gene Expression.- 5.1. Thyroid Hormone.- 5.2. Exercise/Electrical Stimulation.- 6. Alternative Splicing and MHC Gene Structure.- 7. Conclusions.- References.- 7 Regulation of Growth by Negative Growth Regulators.- 1. Introduction.- 2. Transforming Growth Factor-?.- 3. Platelet-Derived Inhibitors.- 3.1. 37-kDa Protein.- 3.2. 27-kDa Protein.- 3.3. Proteins Greater than 200 kDa.- 4. Interferons.- 5. Liver-Derived Inhibitors.- 6. Mammary-Derived Inhibitor.- 7. Glycopeptide Inhibitors.- 8. Density-Dependent Inhibitors.- 9. Summary.- References.- 8 Skeletal Muscle Proteases and Protein Turnover.- 1. Introduction.- 2. General Features of Intracellular Protein Degradation.- 3. Intracellular Degradation of Muscle Proteins.- 4. Neutral and Alkaline Proteolytic Activities.- 4.1. Neutral and Alkaline Proteolytic Activities in Muscle Cells.- 4.2. The ATP-Stimulated and ATP-Dependent Proteinases.- 4.3. The Ca2 +-Dependent Proteinases.- 5. Protease Inhibitors.- 6. Summary.- References.- 9 Regulation of Protein Turnover.- 1. Introduction.- 2. Factors That Affect Tissue Growth and Protein Turnover.- 2.1. Protein Turnover in Different Tissues and the Effect of Developmental Age.- 2.2. Nutrient Intake.- 2.3. Functional Load.- 3. Factors That Control Protein Turnover.- 3.1. Substrates and Hormones and Their Relation to Nutritional Control.- 3.2. The Role of Initiation and Ribosomal Accretion in the Control of Translation.- 3.3. Comments on the Link between Receptor Activation and Protein Synthesis.- 4. Conclusion.- References.- 10 Energy Balance Regulation.- 1. Introduction.- 2. Evidence for Energy Balance Regulation in Farm Animals.- 2.1. Lactation.- 2.2. Growing Animals.- 2.3. Compensatory Growth.- 2.4. Egg Production.- 3. Mechanisms of Energy Balance Regulation.- 3.1. Lactation.- 3.2. Brown Adipose Tissue Metabolism.- 3.3. Compensatory Growth.- 4. CNS Control of Food Intake.- 4.1. Brain Areas Involved.- 4.2. Mechanisms of Action.- 5. CNS Control of Peripheral Metabolism.- 5.1. Brain Areas Involved.- 5.2. Direct Regulation.- 5.3. Indirect Regulation.- 6. Theories of Signals Regulating Food Intake.- 6.1. Short-Term Mechanisms.- 6.2. Long-Term Mechanisms.- 7. Role of Neurotransmitters and Neuropeptides.- 8. Summary.- References.- 11 Central Regulation of Growth Hormone Secretion.- 1. Introduction.- 2. Patterns of GH Secretion.- 3. Hypothalamic Peptides Involved in GH Regulation.- 3.1. Somatostatin.- 3.2. GH-Releasing Factor (GRF).- 3.3. Other Peptides That Increase GH Secretion.- 4. Hypothalamic Regions Involved in GH Regulation.- 5. Interaction of Somatostatin and GRF in Episodic GH Secretion.- 6. Neuropharmacological Regulation of GH Secretion.- 6.1. Norepinephrine (NE).- 6.2. Dopamine (DA).- 6.3. Serotonin (5-HT).- 6.4. Other Neurotransmitters.- 7. Gonadal Steroid Modulation of GH Secretion.- 8. Feedback Regulation of GH Secretion.- References.- 12 Mechanisms of Action for Somatotropin in Growth.- 1. Introduction.- 2. Chemical Nature of Somatotropin.- 2.1. Variants of Somatotropin.- 2.2. Fragments of Somatotropin.- 2.3. Receptor Mediation of Somatotropin Effects.- 3. Biological Response to Somatotropin.- 3.1. Nutrient Partitioning.- 3.2. Pattern of Administration.- 3.3. Dose-Response Relationships: Growth Model.- 4. Mechanisms of Action.- 4.1. General Considerations.- 4.2. Carbohydrate Metabolism.- 4.3. Bone and Mineral Metabolism.- 4.4. Adipose Tissue Lipid Metabolism.- 4.5. Muscle and Protein Metabolism.- 5. Summary and Perspectives.- References.- 13 Regulation of Somatomedin Production, Release, and Mechanism of Action.- 1. Origin of the Somatomedin Hypothesis.- 2. Methods of Analyses.- 3. Gene Expression and the Insulin Peptide Family.- 4. Site of Synthesis.- 5. Somatomedin Research in Domestic Animals.- References.- 14 Sexual Differentiation and the Growth Process.- 1. Introduction.- 2. Rats.- 3. Cattle and Sheep.- 4. Swine.- 5. Chickens.- 6. Sexual Differences in Growth-Related Endocrine Processes.- 7. Conclusions.- References.- 15 Potential Mechanisms for Repartitioning of Growth by ss-Adrenergic Agonists.- 1. Introduction.- 2. Biology of Adrenergic Hormones and Neurotransmitters.- 2.1. Endogenous Adrenergic Agents.- 2.2. Synthesis and Removal.- 2.3. Adrenergic Receptors.- 2.4. Coupling of Adrenergic Receptors to Intracellular Function.- 2.5. Physiological Effects of Adrenergic Agonists.- 3. Administration of ss-Adrenergic Agonists to Animals.- 3.1. Effects.- 3.2. Adipose Tissue.- 3.3. Muscle.- 3.4. Other Mechanisms.- References.- 16 Gene Transfer for Enhanced Growth of Livestock.- 1. Introduction.- 2. Identification of Genes for Transfer.- 3. Methods of Producing Transgenic Animals.- 3.1. Microinjection into Fertilized Ova.- 3.2. Retroviral Insertion of Genes.- 3.3. Insertion via Pluripotent Cells.- 3.4. Insertion by Transposons.- 4. Production of Transkaryotic Animals.- 5. Transfer of Growth-Related Genes into Livestock.- 5.1. Integration of Growth-Related Genes.- 5.2. Expression of Integrated Genes.- 5.3. Growth Performance of Transgenic Livestock.- 5.4. Germline Transmission of Fusion Genes.- 5.5. Expression in Animals with Transkaryotic Implants.- 6. Conclusions.- References.- 17 Status of Current Strategies for Growth Regulation.- 1. Introduction.- 2. Steroid Hormone and Xenobiotic Regulation of Animal Growth.- 3. Manipulation of Animal Growth with Exogenous Somatotropin.- 4. Use of Growth Hormone-Releasing Factor (GRF) to Alter Animal Growth.- 5. Use of ?-Adrenergic Agonists to Manipulate Animal Growth.- 5.1. Effects of Adrenergic Agonists in Sheep.- 5.2. Effects of Adrenergic Agonists in Cattle.- 5.3. Effects of Adrenergic Agonists in Swine.- 6. Use of Immunization to Manipulate Animal Growth.- 7. Summary and Perspectives.- References.

An Analysis of Satellite Cell Content in the Semimembranosus Muscle of Japanese Quail (Coturnix coturnix japonica) Selected for Rapid Growth

Transverse sections of the semimembranosus muscle of a control (C) line of Japanese quail and of a line (P) selected for high body weight at 4 weeks of age were observed for nuclear content. The two lines were sampled at 4 days posthatching and at 4 weeks of age. The relative number of satellite cells decreased from 4 days to 4 weeks of age. The total number of satellite cells, however, appeared to increase as muscle length increased; this relation was not influenced by line effects. It was concluded that the greater number of nuclei in the longer fibers of P-line quail was principally the consequence of a greater mitotic rate in the satellite cells of this line compared to the C-line quail.

Skeletal Muscle Development in the Fetal Pig after Decapitation in utero

The effect of fetal decapitation on skeletal muscle growth and development in utero was studied in the pig. Pig fetuses were decapitated at 45 days of gestation and the peroneus longus muscle was analyzed at 110 days of gestation. Muscle wet weight, length, minimum fiber diameter, DNA, RNA, protein content, and incidence of muscle fiber nuclei and satellite cell nuclei were determined in the decapitated fetus and in sham-decapitated control fetuses. Decapitation did not significantly influence (p greater than 0.05) any of the traits measured. Muscle and satellite cell ultrastructure was not altered by decapitation. Therefore, an intact brain and hypothalamic-hypophyseal axis are not critical to growth and development of fetal pig skeletal muscle as measured in this study.

Ultrastructural Analysis of Skeletal Muscle Development in the Fetal Pig

Myogenesis was investigated at the ultrastructural level in the fetal pig at 35, 52, 65, 80, 95 and 110 days of gestation. At each stage of gestation, the predominant type II fiber type portion of the peroneus longus and sartorius muscles was examined. The sequence of events for normal myogenesis in the pig was generally similar to that reported for the skeletal muscle of other vertebrate species. In addition, the time interval for sequential development of myogenesis was similar between the two muscles. Centrioles were identified in primary fetal fibers and also in secondary fibers. No morphological evidence of mitotic activity was found in the myonuclei. The organization of myofibers into fasciculi was unrelated both temporally and spatially to capillary and neural development.

Effect of Fetal Decapitation on the Composition and Metabolic Characteristics of Pig Skeletal Muscle

The effect of fetal decapitation on the compositional and metabolic characteristics of the biceps femoris muscle of the pig was studied. Fetuses were decapitated at 45 days of gestation and sampled at 110 days of gestation. Muscle wet weight was greater and total dry matter was lower in decapitated (D) than in control (C) fetuses. Total muscle triglyceride content was not influenced by decapitation, but the triglyceride concentration was lower in D when compared to C fetuses. Muscle cell number (total muscle DNA) was not influenced by decapitation, but protein/DNA was greater in the muscle of D than C fetuses. Aerobic metabolism, as measured by oxidation of pyruvate, isoleucine, and palmitate to CO2, was not influenced by decapitation. The rate of palmitate esterified and the ratio of palmitate oxidized/esterified was normal in decapitated fetuses. While the tricarboxylic acid cycle appeared to function normally, pentose shunt activity was higher in the decapitated fetal muscle than in control muscle. Although the rate of decarboxylation of leucine was lower in the muscle of D than in C fetuses, the net rate of leucine transaminated was similar between C and D fetuses.

Ultrastructure of muscle satellite cells in hypersomatotropic rats.

Female Wistar-Furth rats were injected at one week of age with cells from either the GH1 or GH3 rat pituitary cell lines. Controls were injected with vehicle. Rats were killed at 11 weeks of age and satellite cells in the soleus and extensor digitorum longus (EDL) muscles were examined using transmission electron microscopy. Satellite cells in both the soleus and EDL muscles of rats with tumours which secreted growth hormone generally appeared to be metabolically more active than those cells seen in the muscles of control rats. The source of pituitary cell line did not appear to influence satellite cell ultrastructure. In rare instances, myofibers of tumor-bearing rats appeared to extend cytoplasmic projections around satellite cells as if to engulf the latter. There was no evidence of a pathological condition. Since only one time frame was observed, the effects of prolonged exposure to elevated blood growth hormone levels on satellite cells are not known.

Effect of prepuberal castration on porcine bulbospongiosus muscle.

SummaryThe histochemical profile and ultrastructural properties of the bulbospongiosus muscle (BSM) fibers from 5–6 month old boars and barrows (castrated at 7 days of age), and intact week old piglets were compared. Based on myosin ATPase, preincubated at pH 4.2, BSM of boars contained predominately intermediately staining fibers, whereas BSM of barrows and piglets had a mixture of staining intensities. Fibers from boar BSM stained intensely for SDH, with subsarcolemmal and diffuse location of reaction product. Staining intensity for SDH was variable in BSM from barrows and piglets, with diffuse location of reaction product. The BSM of boars and barrows contained predominately dark fibers when stained for glycogen and phosphorylase, and the fibers were low in stored lipids. While the fibers were smaller in barrow as compared to boar BSM, ultrastructural differences between boar and barrow BSM were not detectable.

Effect of denervation or castration on ultrastructural and histochemical properties of feline bulbocavernosus muscle.

The histochemical and ultrastructural changes in the mature feline bulbocavernosus muscle (BCM) induced after 10 days of denervation or castration were compared. Control BCM, denervated BCM, and BCM from castrated cats reacted similarly for myosin ATPase (predominantly dark staining) and for succinic dehydrogenase (predominantly high). Staining for phosphorylase was decreased in the denervated BCM and BCM from castrated cats. Intrafiber lipid content was reduced after denervation or castration. The appearance of lysosome-like structures in BCM from both treatment groups was the most obvious ultrastructural alteration. Other ultrastructural changes were focal and infrequent.

Regulation of Growth by Negative Growth Regulators

The concept of growth regulation by endogenous inhibitors was first suggested by studies on wound healing and carcinogenesis (see Wang and Hsu, 1986). This area of research has long suffered from the fact that purification of specific compounds that inhibited cell proliferation (or differentiation) of normal cells proved elusive. Although circumstantial evidence was generated over the last 20 years to indicate their existence, studies involving the inhibition of cell proliferation have been the subject of both criticism and controversy (see Iype and McMahon, 1984: Alison, 1986). With the purification of several inhibitiors of cell proliferation from endogenous sources, a firm experimental basis has now been established and this subject area is coming under more intense investigation. Caution must still be raised with respect to the specific physiological role(s) that any of the inhibitors purified or described to date have in regulating the normal processes of growth and development as this kind of evidence has not been reported.

Effect of Maternal Dietary Fat on Skeletal Muscle Cellularity and Satellite Cell Content of the Porcine Fetus at 110 Days of Gestation

Crossbred gilts and sows were fed isocaloric diets that contained 0, 2.3, 12.8 or 29.7% poultry fat beginning at day 80 of gestation. At day 110 of gestation, fetuses were removed by Caesarean section. Maternal dietary fat did not influence fetal weight, sartorius muscle weight, length, composition, cellularity or satellite cell content. It was concluded that feeding diets high in fat during the last trisemester as exercised in this study did not influence the satellite cell content or cellularity of skeletal muscle.