Genetic associations of residual feed intake with serum insulin-like growth factor-I and leptin concentrations, meat quality, and carcass cross sectional fat area ratios in Duroc pigs

2009 ◽  
Vol 87 (10) ◽  
pp. 3069-3075 ◽  
Author(s):  
M. A. Hoque ◽  
K. Katoh ◽  
K. Suzuki
Keyword(s):  
Growth Factor ◽  
Meat Quality ◽  
Feed Intake ◽  
Serum Insulin ◽  
Residual Feed Intake ◽  
Insulin Like Growth Factor ◽  
Genetic Associations ◽  
Cross Sectional ◽  
Factor I ◽  
Growth Factor I

Effect of feed intake on antimicrobially induced increases in porcine serum insulin-like growth factor I.

1999 ◽  
Vol 77 (12) ◽  
pp. 3208 ◽  
Author(s):  
M R Hathaway ◽  
W R Dayton ◽  
M E White ◽  
T L Henderson ◽  
D A Young ◽  
...  
Keyword(s):  
Growth Factor ◽  
Feed Intake ◽  
Serum Insulin ◽  
Insulin Like Growth Factor ◽  
Porcine Serum ◽  
Factor I ◽  
Growth Factor I

scholarly journals 35 Postnatal Serum Insulin-Like Growth Factor I Deficiency Is Associated with Chronic Lung Disease of Prematurity

2004 ◽  
Vol 56 (3) ◽  
pp. 470-470
Author(s):  
R J Bolt ◽  
M M van Weissenbruch ◽  
H N Lafeber ◽  
H A Delemarre-van de Waal
Keyword(s):  
Growth Factor ◽  
Lung Disease ◽  
Chronic Lung Disease ◽  
Serum Insulin ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Growth Factor I

Early brain amyloidosis in APP/PS1 mice with serum insulin-like growth factor-I deficiency

2012 ◽  
Vol 509 (2) ◽  
pp. 101-104 ◽  
Author(s):  
R. Poirier ◽  
A.M. Fernandez ◽  
I. Torres-Aleman ◽  
F. Metzger
Keyword(s):  
Growth Factor ◽  
Serum Insulin ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Growth Factor I

scholarly journals Three-locus and four-locus QTL interactions influence mouse insulin-like growth factor-I

2006 ◽  
Vol 26 (1) ◽  
pp. 46-54 ◽  
Author(s):  
Philip Hanlon ◽  
William Andrew Lorenz ◽  
Zhihong Shao ◽  
James M. Harper ◽  
Andrzej T. Galecki ◽  
...  
Keyword(s):  
Growth Factor ◽  
Serum Insulin ◽  
Genome Scan ◽  
Chromosome 17 ◽  
Insulin Like Growth Factor ◽  
Mouse Population ◽  
Factor I ◽  
A Genome ◽  
Igf I ◽  
Growth Factor I

A previous analysis of serum insulin-like growth factor I (IGF-I) levels in a mouse population ( n = 961) derived from a cross of (BALB/cJ × C57BL/6J) F1 females and (C3H/HeJ × DBA/2J) F1 males documented quantitative trait loci (QTL) on chromosomes 1, 10, and 17. We employed a newly developed, random walk-based method to search for three- and four-way allelic combinations that might influence IGF-I levels through nonadditive (conditional or epistatic) interactions among 185 genotyped biallelic loci and with significance defined by experiment-wide permutation ( P < 0.05). We documented a three-locus combination in which an epistatic interaction between QTL on paternal-derived chromosomes 5 and 18 had an opposite effect on the phenotype based on the allele inherited at a third locus on maternal-derived chromosome 17. The search also revealed three four-locus combinations that influence IGF-I levels through nonadditive genetic interactions. In two cases, the four-allele combinations were associated with animals having high levels of IGF-I, and, in the third case, a four-allele combination was associated with animals having low IGF-I levels. The multiple-locus genome scan algorithm revealed new IGF-I QTL on chromosomes 2, 4, 5, 7, 8, and 12 that had not been detected in the single-locus genome search and showed that levels of this hormone can be regulated by complex, nonadditive interactions among multiple loci. The analysis method can detect multilocus interactions in a genome scan experiment and may provide new ways to explore the genetic architecture of complex physiological phenotypes.

scholarly journals Neuronal Activity Drives Localized Blood-Brain-Barrier Transport of Serum Insulin-like Growth Factor-I into the CNS

Neuron ◽  
2010 ◽  
Vol 67 (5) ◽  
pp. 834-846 ◽  
Author(s):  
Takeshi Nishijima ◽  
Joaquin Piriz ◽  
Sylvie Duflot ◽  
Ana M. Fernandez ◽  
Gema Gaitan ◽  
...  
Keyword(s):  
Growth Factor ◽  
Blood Brain Barrier ◽  
Neuronal Activity ◽  
Serum Insulin ◽  
Brain Barrier ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Blood Brain ◽  
Growth Factor I

scholarly journals Serum Insulin-Like Growth Factor-I (IGF-I) in Normal Japanese Adults.

1995 ◽  
Vol 42 (6) ◽  
pp. 767-770 ◽  
Author(s):  
MICHIE KITANO ◽  
TAEKO SHIMIZU ◽  
YUKO YAMAZAKI ◽  
YOSHIE UMEZU ◽  
YUKIKO ARAKAWA ◽  
...  
Keyword(s):  
Growth Factor ◽  
Serum Insulin ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Japanese Adults ◽  
Igf I ◽  
Growth Factor I ◽  
Normal Japanese

scholarly journals Role of Nutritional Status in the Regulation of Adrenarche1

1999 ◽  
Vol 84 (11) ◽  
pp. 3936-3944
Author(s):  
Thomas Remer ◽  
Friedrich Manz
Keyword(s):  
Growth Factor ◽  
Nutritional Status ◽  
Healthy Children ◽  
Insulin Like Growth Factor ◽  
Adrenal Androgen ◽  
Cross Sectional ◽  
Factor I ◽  
Growth Factor I ◽  
Excretion Rates

The factors regulating adrenarche are unknown. Recent in vitro studies have demonstrated that insulin and insulin-like growth factor I induce major adrenal steroidogenic enzyme genes and increase the production of adrenal androgens. Literature findings strongly suggest that changes in body mass index (BMI) reflect an integrated nonhormonal index of changes in serum levels and/or bioactivities of insulin and insulin-like growth factor I. We therefore longitudinally investigated individual changes in BMI and urinary 24-h excretion rates of dehydroepiandrosterone sulfate (DHEAS) in a prepuberty (PreC; n = 22, 11 boys and 11 girls) and a puberty (PubC; n = 20, 10 boys and 10 girls) cohort of healthy children. Twenty-four-hour urine samples were collected at yearly intervals during observation periods that lasted at least 4 yr (comprising ≥5 consecutive 24-h urine collections). For 4-yr intervals highly significant tracking coefficients (P &lt; 0.001) of 0.73 (PreC) and 0.93 (PubC) were observed for DHEAS, emphasizing the importance of individual (and genetic) influences on adrenal androgen excretion. In both cohorts almost 3-fold higher median increases in urinary DHEAS excretion rates (P &lt; 0.05) were observed during the 1-yr period of the individually highest rises in BMI compared with the 1-yr period of significantly lower rises in BMI (P &lt; 0.01) in the same children after the factor age was controlled for. However, no consistently significant associations were found between urinary DHEAS output and BMI from simple cross-sectional correlations at defined age points. These findings provide the first in vivo evidence that a change in the nutritional status, measurable in the form of Δ-BMI (but not BMI alone), is an important physiological regulator of adrenarche regardless of individual adrenal androgen excretion level, age, and developmental stage.

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