Impaired intestinal sugar transport in cirrhotic rats: Correction by low doses of insulin-like growth factor I

Castilla‐Cortázar, Inma; Prieto, Jesús; Urdaneta, Elena; Pascual, María Belén; Núñez, Marina; Zudaire, Enrique; García, María del Carmen Macías; Quiroga, Jorge; Santidrian, Santiago

doi:10.1053/gast.1997.v113.pm9322513

Cited by 66 publications

(79 citation statements)

References 7 publications

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“…Impaired production of IGF-I in advanced liver disease has been suggested to contribute to malnutrition in cirrhotic patients-reviewed in [3]. In support of this notion, we have previously shown that the administration of low doses of IGF-I can correct the impaired intestinal absorption of nutrients in CCl 4 -cirrhotic rats [7][8][9]. Furthermore, systemic administration of IGF-I to rats with chronic liver disease (CCl 4 -induced cirrhosis) resulted in improved liver function and reduced collagen deposition [10].…”

Section: Introductionmentioning

confidence: 79%

“…These alterations are likely to play a role in the metabolic derangements associated with chronic liver disease. In this regard, we have previously shown that treatment with low doses of IGF-I is able to improve the nutritional status, intestinal absorption, osteopenia, hypogonadism and the impaired liver function in rats with CCl 4 -induced cirrhosis [4,[7][8][9][10]. However, the mechanism of action of IGF-I regarding the improvement of liver function is poorly understood.…”

Section: Discussionmentioning

confidence: 99%

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Altered liver gene expression in CCl4-cirrhotic rats is partially normalized by insulin-like growth factor-I

Mirpuri

Garcı́a-Trevijano

Castilla‐Cortázar

et al. 2002

The International Journal of Biochemistry & Cell Biology

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We have previously shown that the administration of low doses of insulin-like growth factor-I (IGF-I) to CCl 4 -cirrhotic rats improves liver function and reduces fibrosis. To better understand the mechanisms behind the hepatoprotective effects of IGF-I, and to identify those genes whose expression is affected in cirrhosis and after IGF-1 treatment, we have performed differential display of mRNA analysis by means of polymerase chain reaction (PCR) in livers from control and CCl 4 -cirrhotic rats treated or not with IGF-I. We have identified 16 genes that were up-or down-regulated in the cirrhotic liver. IGF-I treatment partially normalized the expression of eight of these genes, including serine proteinase inhibitors such as serpin-2 and alpha-1-antichymotripsin, alpha-1-acid glycoprotein, and alpha-2u-globulin. Additionally, we show that IGF-I enhanced the regenerative activity in the cirrhotic liver, as determined by the increased expression of the proliferating cell nuclear antigen (PCNA). Finally, IGF-I treatment partially restored the expression of growth hormone receptor (GHR) and the levels of global genomic DNA methylation, which are reduced in human and experimental cirrhosis. Taken together, our observations confirm the hepatoprotective effects of IGF-I, and suggest that this action can be exerted in part through the normalization of liver gene expression, growth hormone (GH) responsiveness and global genomic DNA methylation.

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Section: Introductionmentioning

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Altered liver gene expression in CCl4-cirrhotic rats is partially normalized by insulin-like growth factor-I

Mirpuri

Garcı́a-Trevijano

Castilla‐Cortázar

et al. 2002

The International Journal of Biochemistry & Cell Biology

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“…In cirrhosis the reduction of receptors for GH in hepatocytes and the diminished ability of the hepatic parenchyma to synthesize cause a progressive decrease in serum IGF-I levels [135]. We have also shown previously that short courses of treatment with low doses of IGF-I in rats with carbon tetrachloride-induced cirrhosis had many systemic beneficial effects, and showed hepatoprotective and antioxidant properties, including mitochondrial protection [2,3,6,41].…”

Section: Aging and Others Conditions Of "Igf-i Deficiency" And Oxidatmentioning

confidence: 74%

“…We propose that IGF-I can exert direct effects on cells and can alter in opposite ways the expression of antioxidant enzymes depending on the ROS levels. This regulation may contribute to the citoprotective effects of treatment with low doses of IGF-I in experimental "IGF-I deficiency" conditions [2,5,6,[40][41][42]. This model is summarized in Fig.…”

Section: Foxo Transcription Factorsmentioning

confidence: 99%

“…Oxidative stress is thought to contribute to the development of a wide range of diseases including neurodegenerative (Alzheimer, Parkinson, Amyotrophic Lateral Sclerosis…), diabetes, cancer, rheumatoid arthritis, cardiovascular and liver diseases several of them are related with low levels of IGFs such as degenerative and aging disorders [1][2][3][4][5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

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Protection Against Oxidative Stress and “IGF-I Deficiency Conditions”

Morón¹,

Castilla‐Cortázar²

2012

Antioxidant Enzyme

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Partial IGF‐1 deficiency induces brain oxidative damage and edema, which are ameliorated by replacement therapy

et al. 2016

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Insulin‐like growth factor 1 (IGF‐1) induces multiple cytoprotective effects on every tissue, including the brain. Since the mechanisms by which IGF‐1 produces neuroprotection are not fully understood, the aim of this work was to delve into the underlying mechanisms. IGF‐1 deficient mice (Hz) were compared with wild type (WT) and Hz mice treated with low doses of IGF‐1 (2 µg/100 g body weight/day) for 10 days (Hz + IGF). Gene expression, quantitative PCR, histology, and magnetic resonance imaging were performed in the three groups. IGF‐1 deficiency induced increased oxidative damage determined by markers of lipid peroxidation and hypoxia, as well as gene expression of heat shock proteins, antioxidant enzymes, and molecules involved in inflammation, apoptosis, and mitochondrial protection. These changes correlated with edema and learning impairment in Hz mice. IGF‐1 therapy improved all these alterations. In conclusion, IGF‐1 deficiency is responsible for increased brain oxidative damage, edema, and impaired learning and memory capabilities which are rescued by IGF‐1 replacement therapy. © 2016 BioFactors, 42(1):60–79, 2016

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Impaired intestinal sugar transport in cirrhotic rats: Correction by low doses of insulin-like growth factor I

Cited by 66 publications

References 7 publications

Altered liver gene expression in CCl4-cirrhotic rats is partially normalized by insulin-like growth factor-I

Altered liver gene expression in CCl4-cirrhotic rats is partially normalized by insulin-like growth factor-I

Protection Against Oxidative Stress and “IGF-I Deficiency Conditions”

Partial IGF‐1 deficiency induces brain oxidative damage and edema, which are ameliorated by replacement therapy

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