Developmental changes in chicken and turkey insulin-like growth factor-I (IGF-I) studied with a homologous radioimmunoassay for chicken IGF-I

McMurtry, John P.; Francis, G L; Upton, F Z; Rosselot, Gastón; Brocht, Donna M.

doi:10.1677/joe.0.1420225

Cited by 61 publications

(22 citation statements)

References 25 publications

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“…Plasma thyroxine (T 4 ) and tri-iodothyronine (T 3 ) were measured as previously described (Vasilatos-Younken et al 1997). Plasma insulin, IGF-I and IGF-II were measured as described by McMurtry et al (1983McMurtry et al ( , 1994McMurtry et al ( , 1998, and tissue IGF-I was measured as described by Rosselot et al (1995). McMurtry et al (1994) demonstrated that chicken IGF-binding proteins (IGFBPs) are acid-labile, so that interference of IGF-I detection by IGFBPs is not a problem using the indicated method of acid/ethanol extraction.…”

Section: Plasma Hormones and Metabolitesmentioning

confidence: 99%

Altered chicken thyroid hormone metabolism with chronic GH enhancement in vivo: consequences for skeletal muscle growth

Vasilatos‐Younken¹,

Zhou²,

Wang³

et al. 2000

Journal of Endocrinology

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In contrast to most vertebrates, GH reportedly has no effect upon somatic growth of the chicken. However, previous studies employed only one to two dosages of the hormone, and limited evidence exists of a hyperthyroid response that may confound its anabolic potential. This study evaluated the effects of 0, 10, 50, 100 and 200 µg/kg body weight per day chicken GH (cGH) (0-200 GH) infused i.v. for 7 days in a pulsatile pattern to immature, growing broiler chickens (9-10 birds/dosage). Comprehensive profiles of thyroid hormone metabolism and measures of somatic growth were obtained.Overall (average) body weight gain was reduced 25% by GH, with a curvilinear, dose-dependent decrease in skeletal (breast) muscle mass that was maximal (12%) at 100 GH. This profile mirrored GH dose-dependent decreases in hepatic type III deiodinase (DIII) activity and increases in plasma tri-iodothyronine (T 3 ), with both also maximal (74 and 108% respectively) at 100 GH. No effect on type I deiodinase was observed. At the maximally effective dosage, hepatic DIII gene expression was reduced 44% versus controls. Despite dose-dependent, fold-increases in hepatic IGF-I protein content, circulating IGF-I was not altered with GH infusion, suggesting impairment of hepatic IGF-I release. Significant, GH dose-dependent increases in plasma non-esterified fatty acid and glucose, and overall decreases in triacylglycerides were also observed. At 200 GH, feed intake was significantly reduced (19%; P<0·05) versus controls; however, additional control birds pair-fed to this level did not exhibit any responses observed for GH-treated birds.The results of this study support a pathway by which GH impacts on thyroid hormone metabolism beginning at a pretranslational level, with reduced hepatic DIII gene expression, translating to reduced protein (enzyme) expression, and reflected in a reduced level of peripheral T 3 -degrading activity. This contributes to decreased conversion of T 3 to its inactive form, thereby elevating circulating T 3 levels. The hyper-T 3 state leads to reduced net skeletal muscle deposition, and may impair release of GH-enhanced, hepatic IGF-I.In conclusion, GH has significant biological effects in the chicken, but profound metabolic actions predominate that may confound positive, IGF-I-mediated skeletal muscle growth.

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Section: Plasma Hormones and Metabolitesmentioning

confidence: 99%

Altered chicken thyroid hormone metabolism with chronic GH enhancement in vivo: consequences for skeletal muscle growth

Vasilatos‐Younken¹,

Zhou²,

Wang³

et al. 2000

Journal of Endocrinology

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“…Antisera to cIGF-II were prepared in female guinea pigs utilizing a modification of a procedure previously reported (McMurtry et al 1994). Recombinantly derived cIGF-II was conjugated to keyhole limpet haemocyanin using conjugation kits supplied by Pierce Chemical Co., Rockford, IL, USA.…”

Section: Production Of Antiseramentioning

confidence: 99%

“…Antiserum from one guinea pig (40A) was selected for further validation and characterization based on its antibody titre and high affinity for cIGF-II. Anti-guinea pig -globulin serum (secondary antibody) was prepared as previously described (McMurtry et al 1994). The validation and characterization of the RIA were carried out based on the guidelines for hormone immunoassays suggested by Hafs et al (1977).…”

Section: Production Of Antiseramentioning

confidence: 99%

“…Whether these sequence differences are significant for biological function, including metabolism, is not known. Previously, we reported the development of a homologous RIA for cIGF-I and its application to further the understanding of the role of cIGF-I in growth and metabolism in chickens and turkeys (McMurtry et al 1994(McMurtry et al , 1996a. IGF-II is a key regulator of fetal development in mammals (Stewart & Rotwein 1996).…”

Section: Introductionmentioning

confidence: 99%

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Assessment of developmental changes in chicken and turkey insulin-like growth factor-II by homologous radioimmunoassay

McMurtry¹,

Rosebrough²,

Brocht³

et al. 1998

Journal of Endocrinology

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The development of a homologous RIA for chicken insulin-like growth factor-II (cIGF-II) and its application to investigate the developmental changes in IGF-II in the chicken and turkey are described. A double-antibody RIA has been developed using recombinantly derived cIGF-II as antigen, radiolabelled tracer and standard. Serial dilutions of chicken and turkey plasma were parallel to serial dilutions of cIGF-II standard. We have also established that acid/ethanol extraction of chicken and turkey plasma reduced possible interference of insulin-like growth factor-binding proteins in the RIA. Consumption of a low-protein diet by male chickens lowered plasma IGF-I twofold, whereas IGF-II levels were unchanged. Food withdrawal evoked an increase in circulating IGF-II, while IGF-I levels were reduced. Refeeding returned both growth factors to normal circulating concentrations. During chick embryo incubation, plasma IGF-II levels were tenfold higher than those of IGF-I. In the turkey embryo, plasma IGF-II concentrations were higher than those of IGF-I. During the post-hatch period, IGF-II levels declined with age in chickens. In the growing turkey, IGF-II levels were consistently higher than IGF-I levels. The application of the homologous RIA to monitor plasma levels during embryonic development and posthatch growth in avian species will provide more accurate comparisons of results from studies on the role of IGF-II in growth and metabolism of domestic birds.

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“…Maternal and fetal cord blood plasmas were assayed for IGF-II concentration using an ELISA assay developed with components from R & D Systems (Minneapolis, MN). Because IGF binding proteins present in plasma may compete for IGF-II binding in ELISA, an acid/ethanol extraction of the samples was performed (40,41) to separate binding proteins from IGF-II, followed by centrifugation to remove the binding proteins. Five microliters of plasma, 2.5 L of PBS ϩ 1% BSA (fraction V), and 62.5 L of acid/ethanol (0.25 N HCl in 87% ethanol) were mixed and allowed to stand for 30 min.…”

Section: Subjectsmentioning

confidence: 99%

Association Between Paternally Inherited Haplotypes Upstream of the Insulin Gene and Umbilical Cord IGF-II Levels

et al. 2007

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ABSTRACT:The insulin (INS) and IGF 2 (IGF2) genes are in close proximity to each other and undergo maternal imprinting during fetal growth. We investigated the association between maternal and umbilical cord IGF 2 protein (IGF-II) levels and single nucleotide polymorphisms (SNPs) in the INS and IGF2 genes in 207 healthy African-American mother-newborn pairs. No association was found between maternal IGF-II levels and polymorphism in the INS-IGF2 locus. A significant association was found between newborn IGF-II levels and two SNPs (rs3842738 and rs689) at the 5= end of the INS-IGF2 locus. Analyses of haplotypes inferred from these two SNPs demonstrate a significant relationship between paternally transmitted haplotypes and newborn IGF-II levels, but no association with maternally transmitted haplotypes. B eing small for gestational age is correlated with predisposition to various illnesses, although this association remains controversial (1,2). Full-term, low birth weight infants are at least five times more likely to die in the first year and are second only to premature infants in their rates of morbidity and mortality (3,4). As adults, individuals born small for gestational age (SGA) are at elevated risk of pregnancy-induced hypertension (5), gestational diabetes (6), chronic hypertension (7), type 2 diabetes (8,9), and cardiovascular disease (10).The relationship between birth size and adult predisposition to chronic disease has been heavily debated. According to the "fetal origins" (11) hypothesis, an inadequate uterine environment results in long-term alterations in organ structure and function and in hormonal milieu that make the individual more susceptible to disease. The existence of genetic factors common to both reduced fetal growth and disease predisposition is another explanation. This hypothesis is supported by an inverse correlation between paternal mortality and offspring birth size that is only slightly weaker than that between maternal mortality and offspring birth size (12,13), even after adjusting for lifestyle risk factors and socioeconomic status. Imprinted loci, which include several genes with direct roles in pathogenesis (i.e. insulin, insulin-like growth factor 2 gene (IGF2), insulin-like growth factor gene receptor (IGF2R)), may comprise a key part of this connection.Insulin-like growth factor 2 protein (IGF-II) is expressed abundantly in trophoblast and fetal endothelial cells (14). The IGF2 gene resides within a block of genes at 11p15 that undergo the silencing (or imprinting) of the allele inherited from one of the parents during fetal development. In the case of IGF2, the allele inherited from the mother is imprinted (15) before implantation, around the eight-cell stage (16). Several lines of evidence indicate that IGF2 and other genes at 11p15 have significant effects on fetal growth. Loss of imprinting at 11p15, including biallelic expression of IGF2, is associated with the prenatal overgrowth of Beckwith-Wiedemann Syndrome (17) and with some cases of postnatal overgrowth (18,19)...

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Developmental changes in chicken and turkey insulin-like growth factor-I (IGF-I) studied with a homologous radioimmunoassay for chicken IGF-I

Cited by 61 publications

References 25 publications

Altered chicken thyroid hormone metabolism with chronic GH enhancement in vivo: consequences for skeletal muscle growth

Altered chicken thyroid hormone metabolism with chronic GH enhancement in vivo: consequences for skeletal muscle growth

Assessment of developmental changes in chicken and turkey insulin-like growth factor-II by homologous radioimmunoassay

Association Between Paternally Inherited Haplotypes Upstream of the Insulin Gene and Umbilical Cord IGF-II Levels

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