Liver-specific IGF-I gene deficient mice exhibit accelerated diabetes in response to streptozotocin, associated with early onset of insulin resistance

2003 ◽  
Vol 204 (1-2) ◽  
pp. 31-42 ◽  
Author(s):  
R Yu
Keyword(s):  
Insulin Resistance ◽  
Early Onset ◽  
Igf I ◽  
Deficient Mice ◽  
I Gene

Age-dependent onset of liver-specific IGF-I gene deficiency and its persistence in old age: implications for postnatal growth and insulin resistance in LID mice

2005 ◽  
Vol 289 (2) ◽  
pp. E288-E295 ◽  
Author(s):  
Zhengyi Tang ◽  
Rong Yu ◽  
Yarong Lu ◽  
A. F. Parlow ◽  
Jun-Li Liu
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Old Age ◽  
Pancreatic Islet ◽  
Postnatal Growth ◽  
Gene Deficiency ◽  
Igf I ◽  
Age Dependent ◽  
I Gene

To explore the limitations of the liver-specific IGF-I gene-deficient (LID) model and to further evaluate the role of endocrine IGF-I in early postnatal life and old age, we have studied these mice during the prepubertal period (from birth to 3 wk of age) and when they are 2 yr old. During the first 2 wk of life, IGF-I gene deficiency and the resulting reduction in serum IGF-I levels in LID mice did not reach sufficiently low levels when mice experience the most rapid and growth hormone (GH)-independent growth. It suggests that the role of liver-derived IGF-I in prepubertal, GH-independent postnatal growth cannot be established. From our previous studies, liver IGF-I mRNA level was abolished in adult LID mice, which causes elevated GH level, insulin resistance, pancreatic islet enlargement, and hyperinsulinemia. Interestingly in 2-yr-old LID mice, although liver IGF-I mRNA and serum IGF-I levels were still suppressed, serum insulin and GH levels had returned to normal. Compared with same-sex control littermates, aged male LID mice had significantly reduced body weight and fat mass and exhibited normal insulin sensitivity. On the other hand, aged female LID mice exhibited normal weight and marginal resistance to insulin actions. The pancreatic islet percentage (reflecting islet cell mass) was also restored to normal levels in aged LID mice. Thus, although the IGF-I gene deficiency is well maintained into old age, the insulin sensitivity, islet enlargement, and hyperinsulinemia that occurred in young adult mice have been mostly restored to normal levels, further supporting the age-dependent and sexual dimorphic features of the LID mice.

scholarly journals Roles of the Lactogens and Somatogens in Perinatal and Postnatal Metabolism and Growth: Studies of a Novel Mouse Model Combining Lactogen Resistance and Growth Hormone Deficiency

Endocrinology ◽  
2005 ◽  
Vol 146 (1) ◽  
pp. 103-112 ◽  
Author(s):  
Donald Fleenor ◽  
Jon Oden ◽  
Paul A. Kelly ◽  
Subburaman Mohan ◽  
Samira Alliouachene ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Mouse Model ◽  
Double Mutant ◽  
Late Onset ◽  
Growth Failure ◽  
Hormone Deficiency ◽  
Mineral Density ◽  
The Metabolic Syndrome ◽  
Igf I ◽  
Deficient Mice

To delineate the roles of the lactogens and GH in the control of perinatal and postnatal growth, fat deposition, insulin production, and insulin action, we generated a novel mouse model that combines resistance to all lactogenic hormones with a severe deficiency of pituitary GH. The model was created by breeding PRL receptor (PRLR)-deficient (knockout) males with GH-deficient (little) females. In contrast to mice with isolated GH or PRLR deficiencies, double-mutant (lactogen-resistant and GH-deficient) mice on d 7 of life had growth failure and hypoglycemia. These findings suggest that lactogens and GH act in concert to facilitate weight gain and glucose homeostasis during the perinatal period. Plasma insulin and IGF-I and IGF-II concentrations were decreased in both GH-deficient and double-mutant neonates but were normal in PRLR-deficient mice. Body weights of the double mutants were reduced markedly during the first 3–4 months of age, and adults had striking reductions in femur length, plasma IGF-I and IGF binding protein-3 concentrations, and femoral bone mineral density. By age 6–12 months, however, the double-mutant mice developed obesity, hyperleptinemia, fasting hyperglycemia, relative hypoinsulinemia, insulin resistance, and glucose intolerance; males were affected to a greater degree than females. The combination of perinatal growth failure and late-onset obesity and insulin resistance suggests that the lactogen-resistant/GH-deficient mouse may serve as a model for the development of the metabolic syndrome.

OP-051 IGF-I GENE POLYMORPHISMS AND LEFT VENTRICULAR FUNCTION IN TURKISH OBESE WOMEN WITH INSULIN RESISTANCE

2010 ◽  
Vol 140 ◽  
pp. S15
Author(s):  
Yalin Tolga Yaylali ◽  
Guzin Fidan Yaylali ◽  
Ibrahim Susam ◽  
Fulya Akin ◽  
Sebahat Turgut
Keyword(s):  
Insulin Resistance ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Gene Polymorphisms ◽  
Left Ventricular ◽  
Obese Women ◽  
Igf I ◽  
I Gene

468: Polymorphic CA Repeats in IGF-I Gene is a Common Genetic Modifier in the Etiology of Prostate Cancer and Benign Prostatic Hyperplasia

2004 ◽  
Vol 171 (4S) ◽  
pp. 125-125
Author(s):  
Lizhong Wang ◽  
Kazunari Sato ◽  
Norihiko Tsuchiya ◽  
Chikara Ohyama ◽  
Shigeru Satoh ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Benign Prostatic Hyperplasia ◽  
Genetic Modifier ◽  
Prostatic Hyperplasia ◽  
Igf I ◽  
I Gene

Reduced bone formation and increased adiposity with insulin resistance in interleukin-11 deficient mice

2014 ◽  
Author(s):  
Bingzi Dong ◽  
Takeshi Kondo ◽  
Yukiyo Ohnishi ◽  
Itsuro Endo ◽  
Masahiro Abe ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Bone Formation ◽  
Interleukin 11 ◽  
Deficient Mice

Regulation of insulin-like growth factor-I gene expression by growth factors in cultured vascular smooth muscle cells

1990 ◽  
Vol 125 (3) ◽  
pp. 381-386 ◽  
Author(s):  
K. E. Bornfeldt ◽  
H. J. Arnqvist ◽  
G. Norstedt
Keyword(s):  
Gene Expression ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Basic Fgf ◽  
Aortic Smooth Muscle ◽  
Factor I ◽  
Igf I ◽  
I Gene

ABSTRACT The aim of this investigation was to study the regulation of insulin-like growth factor-I (IGF-I) gene expression in cultured rat aortic smooth muscle cells. Near-confluent cells were deprived of serum for 24 h and then exposed to IGF-I, insulin, serum, basic fibroblast growth factor (basic FGF), platelet-derived growth factor (PDGF-BB; consisting of B-chain homodimer) or GH for 24 h. Levels of IGF-I mRNA were measured by solution hybridization. The level of IGF-I mRNA was markedly decreased by 10% (v/v) newborn calf serum (78 ± 4 (s.e.m.) % decrease), 1 nmol basic FGF/1 (53 ± 8%), and 1 nmol PDGF-BB/1 (40 ± 3%) when measured after 24 h. The effect of PDGF-BB was significant after 6 h and became more marked after 24 h. GH (1 nmol/l or 0.1 μmol/l or insulin (1 nmol/l had no effect after 24 h, whereas IGF-I (1 nmol/l and insulin (10 μmol/l increased IGF-I mRNA 64 ± 20% and 46±14% respectively. The increase caused by IGF-I was demonstrated after 3 h, and was most marked after 24 h. Using Northern blot analysis of cultured aortic smooth muscle cells, IGF-I transcripts of 7-4, 1.7 and 1.1–0.8 kilobases were observed. Exposure of the cells to 10% serum, 1 nmol basic FGF/1 or 1 nmol PDGF-BB/1 for 48 h increased the cell number by 104 ±7%, 64 ± 3% and 61±22% respectively, while IGF-I, insulin and GH had little effect. In conclusion, IGF-I, and high concentrations of insulin, increased IGF-I mRNA in vascular smooth muscle cells, whereas factors which were stronger mitogens decreased IGF-I gene expression. Journal of Endocrinology (1990) 125, 381–386

scholarly journals Prevention of Cancer Through Lifestyle Changes

2004 ◽  
Vol 1 (3) ◽  
pp. 233-239 ◽  
Author(s):  
R. James Barnard
Keyword(s):  
Insulin Resistance ◽  
Growth Factor ◽  
Serum Insulin ◽  
Lifestyle Changes ◽  
Insulin Like Growth Factor ◽  
Serum Factors ◽  
Igf I ◽  
The Usa ◽  
Prevention Of Cancer ◽  
Major Factors

Cancer is the second leading cause of death in the USA and an abundance of evidence suggests that lifestyle factors including smoking, the typical high-fat, refined-sugar diet and physical inactivity account for the majority of cancer. This review focuses on diet and inactivity as major factors for cancer promotion by inducing insulin resistance and hyperinsulinemia. Elevated levels of serum insulin impact on the liver primarily, increasing the production of insulin-like growth factor I (IGF-I) while reducing the production of insulin-like growth factor binding protein 1 (IGFBP-1) resulting in stimulation of tumor cell growth and inhibition of apoptosis (programmed cell death). Adopting a diet low in fat and high in fiber-rich starch foods, which would also include an abundance of antioxidants, combined with regular aerobic exercise might control insulin resistance, reduce the resulting serum factors and thus reduce the risk for many different cancers commonly seen in the USA.

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