scholarly journals IRS2 integrates insulin/IGF1 signalling with metabolism, neurodegeneration and longevity

2014 ◽  
Vol 16 (S1) ◽  
pp. 4-15 ◽  
Author(s):  
M. F. White
Keyword(s):  
Igf1 Signalling

Intestinal insulin/IGF1 signalling through FoxO1 regulates epithelial integrity and susceptibility to colon cancer

2019 ◽  
Vol 1 (3) ◽  
pp. 371-389 ◽  
Author(s):  
A. L. Ostermann ◽  
C. M. Wunderlich ◽  
L. Schneiders ◽  
M. C. Vogt ◽  
M. A. Woeste ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Epithelial Integrity ◽  
Igf1 Signalling

scholarly journals Androgens, diabetes and prostate cancer

2012 ◽  
Vol 19 (5) ◽  
pp. F47-F62 ◽  
Author(s):  
Mathis Grossmann ◽  
Gary Wittert
Keyword(s):  
Prostate Cancer ◽  
Acid Metabolism ◽  
Experimental Studies ◽  
Population Based ◽  
Apparent Paradox ◽  
Prostate Carcinogenesis ◽  
The Metabolic Syndrome ◽  
Metabolic Conditions ◽  
The Individual ◽  
Igf1 Signalling

Metabolic disorders such as diabetes, obesity and the metabolic syndrome have been shown to modulate prostate cancer (PCa) risk and aggressiveness in population-based and experimental studies. While associations between these conditions are modest and complex, two consistent findings have emerged. First, there is observational evidence that obesity and associated insulin excess are linked to increased PCa aggressiveness and worse outcomes. Secondly and somewhat paradoxically, long-standing diabetes may be protective against PCa development. This apparent paradox may be due to the fact that long-standing diabetes is associated with insulin depletion and decreased IGF1 signalling. Men with obesity or diabetes have moderate reductions in their androgen levels. The interconnectedness of metabolic and androgen status complicates the dissection of the individual roles of these factors in PCa development and progression. Metabolic factors and androgens may promote prostate carcinogenesis via multiple mechanisms including inflammation, adipokine action, fatty acid metabolism and IGF signalling. Moreover, androgen deprivation, given to men with PCa, has adverse metabolic consequences that need to be taken into account when estimating the risk benefit ratio of this therapy. In this review, we will discuss the current epidemiological and mechanistic evidence regarding the interactions between metabolic conditions, sex steroids and PCa risk and management.

scholarly journals Effects of androgen and oestrogen on IGF pathways controlling phallus growth

Reproduction ◽  
2019 ◽  
pp. 1-12 ◽  
Author(s):  
Yu Chen ◽  
Hongshi Yu ◽  
Andrew J Pask ◽  
Asao Fujiyama ◽  
Yutaka Suzuki ◽  
...  
Keyword(s):  
Sex Steroids ◽  
Post Partum ◽  
Hormone Treatment ◽  
Tammar Wallaby ◽  
Oestrogen Treatment ◽  
Androgen Treatment ◽  
Reverse Pattern ◽  
Urethral Closure ◽  
First Time ◽  
Igf1 Signalling

The development of the mammalian phallus involves hormone-dependent mesenchymal–epithelial signalling mechanisms that contribute to urethral closure and regulation of phallus elongation and growth. In marsupials, most differentiation and growth of the phallus occurs post-natally, making them amenable to direct hormone treatment. Expression of IGFs, FGFs, EFNB2, MAFB, DLX5 and AP-1 mRNAs in the phallus at day 50 post-partum (pp) were altered after treatment of tammar wallaby young from day 20 to 40 pp with androgen, oestrogen or after castration at day 25 pp. However, the most interesting changes occurred in the IGF pathway genes. Androgen treatment upregulated IGF1 in female phalluses and oestrogen treatment upregulated IGF1 in male phalluses, but it was downregulated by castration. IGFBP3 was higher in female phalluses and downregulated by androgen. IGF1 expression was higher in all untreated male than in female phalluses from day 50 to 150 pp, but IGFBP3 had the reverse pattern. At day 90 pp, when urethral closure in males is progressing and male phallus growth is accelerating. IGF1 and PCNA protein were only detected in the male urorectal septum, suggesting for the first time that closure and elongation may involve IGF1 activation of cell proliferation specifically in male phalluses. These effects of sex steroids on gene expression and on the IGF1 signalling pathway in particular, suggest that the developing phallus may be especially susceptible to perturbation by exogenous hormones.

scholarly journals ΔNp63 promotes IGF1 signalling through IRS1 in squamous cell carcinoma

Aging ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 4224-4240 ◽  
Author(s):  
Valentina Frezza ◽  
Claudia Fierro ◽  
Elena Gatti ◽  
Angelo Peschiaroli ◽  
Anna Maria Lena ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Igf1 Signalling

scholarly journals Insulin/IGF1 signalling mediates the effects of β 2 ‐adrenergic agonist on muscle proteostasis and growth

2019 ◽  
Vol 10 (2) ◽  
pp. 455-475 ◽  
Author(s):  
Dawit A. Gonçalves ◽  
Wilian A. Silveira ◽  
Leandro H. Manfredi ◽  
Flávia A. Graça ◽  
Andrea Armani ◽  
...  
Keyword(s):  
Adrenergic Agonist ◽  
Igf1 Signalling

scholarly journals Insulin and IGF1 signalling pathways in human astrocytes in vitro and in vivo; characterisation, subcellular localisation and modulation of the receptors

2015 ◽  
Vol 8 (1) ◽  
Author(s):  
Claire J. Garwood ◽  
Laura E. Ratcliffe ◽  
Sarah V. Morgan ◽  
Julie E. Simpson ◽  
Helen Owens ◽  
...  
Keyword(s):  
Signalling Pathways ◽  
Subcellular Localisation ◽  
Human Astrocytes ◽  
Igf1 Signalling

scholarly journals Elevated Levels of circRUNX1 in Colorectal Cancer Promote Cell Growth and Metastasis via miR-145-5p/IGF1 Signalling

2020 ◽  
Vol Volume 13 ◽  
pp. 4035-4048
Author(s):  
Zhi-Lei Chen ◽  
Xiang-Nan Li ◽  
Chun-Xiang Ye ◽  
Hong-Yu Chen ◽  
Zhen-Jun Wang
Keyword(s):  
Colorectal Cancer ◽  
Cell Growth ◽  
Igf1 Signalling

scholarly journals Mutations in CUL7, OBSL1 and CCDC8 in 3-M syndrome lead to disordered growth factor signalling

2012 ◽  
Vol 49 (3) ◽  
pp. 267-275 ◽  
Author(s):  
D Hanson ◽  
P G Murray ◽  
T Coulson ◽  
A Sud ◽  
A Omokanye ◽  
...  
Keyword(s):  
Fibroblast Cell ◽  
Gh Treatment ◽  
Igf Binding Proteins ◽  
The Status ◽  
Growth Factor Signalling ◽  
Igf Binding ◽  
Igf Binding Protein ◽  
Serum Gh ◽  
Igf1 Signalling ◽  
Fibroblast Cell Lines

3-M syndrome is a primordial growth disorder caused by mutations in CUL7, OBSL1 or CCDC8. 3-M patients typically have a modest response to GH treatment, but the mechanism is unknown. Our aim was to screen 13 clinically identified 3-M families for mutations, define the status of the GH–IGF axis in 3-M children and using fibroblast cell lines assess signalling responses to GH or IGF1. Eleven CUL7, three OBSL1 and one CCDC8 mutations in nine, three and one families respectively were identified, those with CUL7 mutations being significantly shorter than those with OBSL1 or CCDC8 mutations. The majority of 3-M patients tested had normal peak serum GH and normal/low IGF1. While the generation of IGF binding proteins by 3-M cells was dysregulated, activation of STAT5b and MAPK in response to GH was normal in CUL7−/− cells but reduced in OBSL1−/− and CCDC8−/− cells compared with controls. Activation of AKT to IGF1 was reduced in CUL7−/− and OBSL1−/− cells at 5 min post-stimulation but normal in CCDC8−/− cells. The prevalence of 3-M mutations was 69% CUL7, 23% OBSL1 and 8% CCDC8. The GH–IGF axis evaluation could reflect a degree of GH resistance and/or IGF1 resistance. This is consistent with the signalling data in which the CUL7−/− cells showed impaired IGF1 signalling, CCDC8−/− cells showed impaired GH signalling and the OBSL1−/− cells showed impairment in both pathways. Dysregulation of the GH–IGF–IGF binding protein axis is a feature of 3-M syndrome.

Sign in / Sign up

Export Citation Format

Share Document