The endocrine regulation of growth during early life: a nutritional perspective

1992 ◽  
Vol 15 ◽  
pp. 47-62
Author(s):  
J. M. Bassett
Keyword(s):  
Growth Rate ◽  
Enteral Nutrition ◽  
Cellular Differentiation ◽  
Molecular Mechanisms ◽  
Plasma Concentrations ◽  
Postnatal Growth ◽  
Tissue Growth ◽  
Endocrine Regulation ◽  
Peripheral Tissues ◽  
The Status

AbstractRecent advances in molecular biology have begun to identify many of the molecular mechanisms involved in the control of cellular differentiation and subsequent growth. However, while this information may ultimately permit manipulation of animal growth it is important to remember that the most essential factor for growth remains adequate nutrition. The high correlation of growth rate with milk intake in neonates reminds us that growth is highly dependent on the rapid establishment of enteral nutrition after birth. The endocrine changes consequent on this, as well as the supply of nutrients to support metabolic homeostasis, play important rôles in determining survival.Birth is associated with dramatic changes in the secretion and plasma concentrations of many hormones (including insulin, glucagon, growth hormone (GH), triiodothyronine (T3), adrenaline and cortisol among others). However, while changes in secretion at this time may be of great significance for survival and adaptation during the perinatal period, after this it is only changes in the secretion of insulin and GH which appear closely related to neonatal growth. Sixty percent or more of variation in live-weight gain among lambs during the 1st month of life is positively associated with variation in plasma insulin levels, while associations with GH are strongly negative, despite the evidence for essentiality of GH as a promoter of insulin-like growth factor-1 (IGF-1) production. Observations on other species are consistent with those in lambs.Investigations in foetal lambs have established that insulin's crucial rôle as a primary regulator of anabolic metabolism and growth begins well before birth. However, while birth does not alter this important rôle, the establishment of enteral nutrition changes the way in which its secretion is modulated and increases its rôle as the principal endocrine regulator of glucose homeostasis. Secretion of gastrointestinal hormones in response to the first food plays an important rôle in this, modulating the secretion of insulin and promoting gut development through trophic actions on the mucosa. Insulin itself, also appears to have trophic effects on the liver and is probably an important determinant of nutritionally mediated alterations in hepatic IGF-1 production. Plasma IGF-1 concentrations, like those of insulin, are highly correlated with the rate of postnatal growth, but unlike insulin, the status of plasma IGF-1 as a direct regulator of cellular growth remains controversial. IGF-1 and the large molecular weight proteins to which it is bound in plasma are synthesized by many peripheral tissues as well as the liver and it seems likely that IGF-1, in association with other specific growth factors, acts principally in the extravascular compartment, as a local paracrine/autocrine regulator of cellular differentiation and growth. Whatever the status of the plasma IGF-1 pool its concentration appears to act as a useful index of the rate of tissue growth. While GH is essential for normal postnatal growth and the production of IGF-1, it does not appear rate-limiting in relation to nutritionally determined variations in growth rate. This contrasts strikingly with its rôle in growth manipulation.

scholarly journals Individual variation and the endocrine regulation of behaviour and physiology in birds: a cellular/molecular perspective

2007 ◽  
Vol 363 (1497) ◽  
pp. 1699-1710 ◽  
Author(s):  
Gregory F Ball ◽  
Jacques Balthazart
Keyword(s):  
Individual Variation ◽  
Molecular Mechanisms ◽  
Steroid Hormone ◽  
Molecular Genetic ◽  
Plasma Concentrations ◽  
Individual Variability ◽  
Receptor Expression ◽  
Endocrine Regulation ◽  
Metabolizing Enzyme ◽  
Hormone Receptor Expression

Investigations of the cellular and molecular mechanisms of physiology and behaviour have generally avoided attempts to explain individual differences. The goal has rather been to discover general processes. However, understanding the causes of individual variation in many phenomena of interest to avian eco-physiologists will require a consideration of such mechanisms. For example, in birds, changes in plasma concentrations of steroid hormones are important in the activation of social behaviours related to reproduction and aggression. Attempts to explain individual variation in these behaviours as a function of variation in plasma hormone concentrations have generally failed. Cellular variables related to the effectiveness of steroid hormone have been useful in some cases. Steroid hormone target sensitivity can be affected by variables such as metabolizing enzyme activity, hormone receptor expression as well as receptor cofactor expression. At present, no general theory has emerged that might provide a clear guidance when trying to explain individual variability in birds or in any other group of vertebrates. One strategy is to learn from studies of large units of intraspecific variation such as population or sex differences to provide ideas about variables that might be important in explaining individual variation. This approach along with the use of newly developed molecular genetic tools represents a promising avenue for avian eco-physiologists to pursue.

scholarly journals Home for a rest: stem cell niche of the postnatal growth plate

2020 ◽  
Vol 246 (1) ◽  
pp. R1-R11 ◽  
Author(s):  
Julian C Lui
Keyword(s):  
Stem Cell ◽  
Growth Plate ◽  
Stem Cell Niche ◽  
Molecular Mechanisms ◽  
Bone Growth ◽  
Postnatal Growth ◽  
Lineage Tracing ◽  
Endocrine Regulation ◽  
Technological Advances ◽  
Cell Niche

The resting zone houses a group of slowly proliferating ‘reserve’ chondrocytes and has long been speculated to serve as the stem cell niche of the postnatal growth plate. But are these resting chondrocytes bona fide stem cells? Recent technological advances in lineage tracing and next-generation sequencing have finally allowed researchers to answer this question. Several recent studies have also shed light into the signaling pathways and molecular mechanisms involved in the maintenance of resting chondrocytes, thus providing us with important new insights into the role of the resting zone in the paracrine and endocrine regulation of childhood bone growth.

scholarly journals Maternal Uniparental Disomy of Chromosome 20 (UPD(20)mat) as Differential Diagnosis of Silver Russell Syndrome: Identification of Three New Cases

Genes ◽  
2021 ◽  
Vol 12 (4) ◽  
pp. 588
Author(s):  
Pierpaola Tannorella ◽  
Daniele Minervino ◽  
Sara Guzzetti ◽  
Alessandro Vimercati ◽  
Luciano Calzari ◽  
...  
Keyword(s):  
Growth Retardation ◽  
Molecular Mechanisms ◽  
Uniparental Disomy ◽  
Postnatal Growth ◽  
Molecular Diagnostic ◽  
Growth Delay ◽  
Molecular Defect ◽  
Maternal Uniparental Disomy ◽  
Feeding Difficulties ◽  
Silver Russell Syndrome

Silver Russell Syndrome (SRS, MIM #180860) is a rare growth retardation disorder in which clinical diagnosis is based on six features: pre- and postnatal growth failure, relative macrocephaly, prominent forehead, body asymmetry, and feeding difficulties (Netchine–Harbison clinical scoring system (NH-CSS)). The molecular mechanisms consist in (epi)genetic deregulations at multiple loci: the loss of methylation (LOM) at the paternal H19/IGF2:IG-DMR (chr11p15.5) (50%) and the maternal uniparental disomy of chromosome 7 (UPD(7)mat) (10%) are the most frequent causes. Thus far, about 40% of SRS remains undiagnosed, pointing to the need to define the rare mechanisms in such a consistent fraction of unsolved patients. Within a cohort of 176 SRS with an NH-CSS ≥ 3, a molecular diagnosis was disclosed in about 45%. Among the remaining patients, we identified in 3 probands (1.7%) with UPD(20)mat (Mulchandani–Bhoj–Conlin syndrome, OMIM #617352), a molecular mechanism deregulating the GNAS locus and described in 21 cases, characterized by severe feeding difficulties associated with failure to thrive, preterm birth, and intrauterine/postnatal growth retardation. Our patients share prominent forehead, feeding difficulties, postnatal growth delay, and advanced maternal age. Their clinical assessment and molecular diagnostic flowchart contribute to better define the characteristics of this rare imprinting disorder and to rank UPD(20)mat as the fourth most common pathogenic molecular defect causative of SRS.

scholarly journals Understanding Quantitative Circadian Regulations Are Crucial Towards Advancing Chronotherapy

Cells ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 883 ◽  
Author(s):  
Debajyoti Chowdhury ◽  
Chao Wang ◽  
Ai-Ping Lu ◽  
Hai-Long Zhu
Keyword(s):  
Circadian Rhythms ◽  
Molecular Mechanisms ◽  
Temporal Stability ◽  
Biological Rhythms ◽  
Integrative Approach ◽  
Peripheral Tissues ◽  
Innovative Strategies ◽  
Neural Connections ◽  
Core Components ◽  
The Brain

Circadian rhythms have a deep impact on most aspects of physiology. In most organisms, especially mammals, the biological rhythms are maintained by the indigenous circadian clockwork around geophysical time (~24-h). These rhythms originate inside cells. Several core components are interconnected through transcriptional/translational feedback loops to generate molecular oscillations. They are tightly controlled over time. Also, they exert temporal controls over many fundamental physiological activities. This helps in coordinating the body’s internal time with the external environments. The mammalian circadian clockwork is composed of a hierarchy of oscillators, which play roles at molecular, cellular, and higher levels. The master oscillation has been found to be developed at the hypothalamic suprachiasmatic nucleus in the brain. It acts as the core pacemaker and drives the transmission of the oscillation signals. These signals are distributed across different peripheral tissues through humoral and neural connections. The synchronization among the master oscillator and tissue-specific oscillators offer overall temporal stability to mammals. Recent technological advancements help us to study the circadian rhythms at dynamic scale and systems level. Here, we outline the current understanding of circadian clockwork in terms of molecular mechanisms and interdisciplinary concepts. We have also focused on the importance of the integrative approach to decode several crucial intricacies. This review indicates the emergence of such a comprehensive approach. It will essentially accelerate the circadian research with more innovative strategies, such as developing evidence-based chronotherapeutics to restore de-synchronized circadian rhythms.

scholarly journals Desethylamiodarone antagonizes the effect of thyroid hormone at the molecular level

2001 ◽  
pp. 59-64 ◽  
Author(s):  
F Bogazzi ◽  
L Bartalena ◽  
S Brogioni ◽  
A Burelli ◽  
F Raggi ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Molecular Mechanisms ◽  
Thyroid Hormone Receptor ◽  
Molecular Level ◽  
Inhibitory Effect ◽  
Mobility Shift ◽  
Down Regulation ◽  
Nih3t3 Cells ◽  
Peripheral Tissues

OBJECTIVE: To evaluate the molecular mechanisms of the inhibitory effects of amiodarone and its active metabolite, desethylamiodarone (DEA) on thyroid hormone action. MATERIALS AND METHODS: The reporter construct ME-TRE-TK-CAT or TSHbeta-TRE-TK-CAT, containing the nucleotide sequence of the thyroid hormone response element (TRE) of either malic enzyme (ME) or TSHbeta genes, thymidine kinase (TK) and chloramphenicol acetyltransferase (CAT) was transiently transfected with RSV-TRbeta into NIH3T3 cells. Gel mobility shift assay (EMSA) was performed using labelled synthetic oligonucleotides containing the ME-TRE and in vitro translated thyroid hormone receptor (TR)beta. RESULTS: Addition of 1 micromol/l T4 or T3 to the culture medium increased the basal level of ME-TRE-TK-CAT by 4.5- and 12.5-fold respectively. Amiodarone or DEA (1 micromol/l) increased CAT activity by 1.4- and 3.4-fold respectively. Combination of DEA with T4 or T3 increased CAT activity by 9.4- and 18.9-fold respectively. These data suggested that DEA, but not amiodarone, had a synergistic effect with thyroid hormone on ME-TRE, rather than the postulated inhibitory action; we supposed that this was due to overexpression of the transfected TR into the cells. When the amount of RSV-TRbeta was reduced until it was present in a limited amount, allowing competition between thyroid hormone and the drug, addition of 1 micromol/l DEA decreased the T3-dependent expression of the reporter gene by 50%. The inhibitory effect of DEA was partially due to a reduced binding of TR to ME-TRE, as assessed by EMSA. DEA activated the TR-dependent down-regulation by the negative TSH-TRE, although at low level (35% of the down-regulation produced by T3), whereas amiodarone was ineffective. Addition of 1 micromol/l DEA to T3-containing medium reduced the T3-TR-mediated down-regulation of TSH-TRE to 55%. CONCLUSIONS: Our results demonstrate that DEA, but not amiodarone, exerts a direct, although weak, effect on genes that are regulated by thyroid hormone. High concentrations of DEA antagonize the action of T3 at the molecular level, interacting with TR and reducing its binding to TREs. This effect may contribute to the hypothyroid-like effect observed in peripheral tissues of patients receiving amiodarone treatment.

Growth rate and habitat of Nautilus pompilius inferred from radioactive and stable isotope studies

Paleobiology ◽  
1981 ◽  
Vol 7 (4) ◽  
pp. 469-480 ◽  
Author(s):  
J. Kirk Cochran ◽  
Danny M. Rye ◽  
Neil H. Landman
Keyword(s):  
Growth Rate ◽  
Half Life ◽  
Activity Ratio ◽  
Sea Water ◽  
Tissue Growth ◽  
Carbon And Oxygen Isotopes ◽  
Nautilus Pompilius ◽  
Radioactive Disequilibrium ◽  
Horizontal Migration ◽  
Isotope Studies

The growth rate of Nautilus pompilius in its natural environment has been determined from radioactive disequilibrium between 210Pb (half-life 22.3 yr) and its granddaughter 210Po (half-life 138 d) in septa of two juvenile specimens. 210Pb and 210Po data from the most recently formed shell material of both specimens indicate that 210Pb from sea water is incorporated into septa during septal formation and 210Po is excluded. Therefore the 210Po/210Pb activity ratio serves as a chronometer to estimate the age of each septum and the time between formation of septa. In the specimens studied the average time between sucessive points in septal deposition is 75 d for the nine most recent septa of one specimen and 23 d for the six most recent septa of the other specimen. These different growth rates, if representative of the ontogeny of each animal, suggest that the timing of septal deposition probably is dependent on the rate of shell and tissue growth coupled with buoyancy requirements and is not a unique period for all Nautilus. The habitat and ontogeny of Nautilus may be inferred from the pattern of stable isotopes of oxygen and carbon in the septa. Both specimens show a pronounced break in δ18O from nearly uniform light values in the first seven septa to heavier values (∼1%) after the seventh septum. We interpret this break to correspond to the hatching of Nautilus. A temperature (i.e. water depth) interpretation of the δ18O data for septa after the eighth is complicated by a positive correlation between δ18O and δ13C. This may reflect horizontal migration of the animal or a kinetically controlled fractionation of carbon and oxygen isotopes during septal formation.

Muscle histochemical and biochemical properties in relation to meat quality during selection for increased lean tissue growth rate in pigs1

1993 ◽  
Vol 71 (4) ◽  
pp. 930-938 ◽  
Author(s):  
Anders Karlsson ◽  
Ann-Charlotte Enfält ◽  
Birgitta Essén-Gustavsson ◽  
Kerstin Lundström ◽  
Lotta Rydhmer ◽  
...  
Keyword(s):  
Growth Rate ◽  
Meat Quality ◽  
Biochemical Properties ◽  
Tissue Growth ◽  
Lean Tissue ◽  
Selection For

scholarly journals Lateralized and Segmental Overgrowth in Children

Cancers ◽  
2021 ◽  
Vol 13 (24) ◽  
pp. 6166
Author(s):  
Alessandro Mussa ◽  
Diana Carli ◽  
Simona Cardaropoli ◽  
Giovanni Battista Ferrero ◽  
Nicoletta Resta
Keyword(s):  
Molecular Mechanisms ◽  
Management Strategies ◽  
Tissue Growth ◽  
Body Region ◽  
Molecular Defects ◽  
Embryonic Tissues ◽  
Cellular Signaling Pathway ◽  
Segmental Overgrowth ◽  
Generation Sequencing ◽  
Specific Management

Congenital disorders of lateralized or segmental overgrowth (LO) are heterogeneous conditions with increased tissue growth in a body region. LO can affect every region, be localized or extensive, involve one or several embryonic tissues, showing variable severity, from mild forms with minor body asymmetry to severe ones with progressive tissue growth and related relevant complications. Recently, next-generation sequencing approaches have increased the knowledge on the molecular defects in LO, allowing classifying them based on the deranged cellular signaling pathway. LO is caused by either genetic or epigenetic somatic anomalies affecting cell proliferation. Most LOs are classifiable in the Beckwith–Wiedemann spectrum (BWSp), PI3KCA/AKT-related overgrowth spectrum (PROS/AROS), mosaic RASopathies, PTEN Hamartoma Tumor Syndrome, mosaic activating variants in angiogenesis pathways, and isolated LO (ILO). These disorders overlap over common phenotypes, making their appraisal and distinction challenging. The latter is crucial, as specific management strategies are key: some LO is associated with increased cancer risk making imperative tumor screening since childhood. Interestingly, some LO shares molecular mechanisms with cancer: recent advances in tumor biological pathway druggability and growth downregulation offer new avenues for the treatment of the most severe and complicated LO.

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