Low doses of insulin-like growth factor-I improve nitrogen retention and food efficiency in rats with early cirrhosis

Picardi, Antonio; Oliveira, Admar Costa de; Muguerza, Begoña; Tosar, Alicia; Quiroga, Jorge; Castilla‐Cortázar, Inma; Santidrian, Santiago; Prieto, Jesús

doi:10.1016/s0168-8278(97)80026-8

Cited by 55 publications

(64 citation statements)

References 52 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: 78%

“…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: 78%

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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“…Among the endocrine disorders found in CLD, a pivotal role is played by impairment of GH-IGF-1 axis, upon which many metabolic and nutritional abnormalities depend [62][63][64][65][66]. The entire spectrum of GH-IGF-1 axis abnormalities in CLD is referred to as 'acquired GH resistance', and is characterized by low plasma levels of IGF-1, despite normal or elevated serum concentrations of GH.…”

Section: Gh Resistancementioning

confidence: 99%

Diabetes in chronic liver disease: from old concepts to new evidence

Picardi

D’Avola

Gentilucci

et al. 2006

Diabetes Metab. Res. Rev.

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102

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SummaryThe liver is one of the principal organs involved in glucose metabolism together with skeletal muscle and adipose tissue. A link between diabetes and chronic liver disease (CLD) was first observed in the early half of the last century, but to date several questions remain unsolved. Altered glucose tolerance has been well described in alcoholic CLD, non-alcoholic fatty liver disease, chronic hepatitis C and portal hypertension. Moreover, insulin resistance is assuming an ever-growing importance in CLD; chronic hepatitis C has recently been proposed as a metabolic disease and insulin sensitivity as a predictive factor for liver fibrosis.CLD is also complicated by acquired growth hormone (GH) resistance, characterized by low concentrations of insulin-like growth factor-1 (IGF-1) with respect to normal or elevated GH levels. GH resistance in CLD is determined by several factors, including malnutrition, impaired liver function and reduced expression of hepatic GH receptors. We recently described the possible role of tumour necrosis factor-alpha (TNF-α) in blunting the hepatic response to GH in patients with chronic hepatitis C. The role of GH in impaired glucose metabolism is well known, and recent evidence suggests a receptor and/or post-receptor modulation of insulin signalling. Moreover, as in other chronic inflammatory conditions, pro-inflammatory cytokines may directly modulate the signal cascade that follows insulin binding to its receptor in the course of CLD.In this review, the proposed links between impaired glucose tolerance and CLD are analysed, special emphasis being focussed on the most recent findings concerning the interplay of chronic inflammation, GH resistance and insulin resistance.

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“…Serum IGF-I levels have been regarded as a useful index of hepatocellular dysfunction. Serum IGF-I levels are decreased in chronic liver disease (17,18) and it has been observed that administering IGF-1 may improve liver function (19) and decrease oxidative damage and fibrosis (13). Microarray analysis has suggested that the level of IGF-1 is downregulated following exposure to isoflurane anesthesia (20).…”

Section: Introductionmentioning

confidence: 99%

Isoflurane anesthesia induces liver injury by regulating the expression of insulin-like growth factor 1

Zhu

Xiao

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. It has been suggested that isoflurane may cause perioperative liver injury. However, the mechanism of its action remains unknown. The purpose of the present study was to determine this possible mechanism. Sprague-Dawley rats were randomly assigned into one of three groups (all n=12): Control group (exposed to mock anesthesia), isoflurane group (exposed to 2% isoflurane for 90 min), and isoflurane + insulin-like growth factor 1 (IGF-1) group (exposed to 2% isoflurane for 90 min and then treated with IGF-1). Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting were conducted to determine the levels of expression of IGF-1 and its receptor IGF-R. Liver necrosis was assessed by histological examination. TUNEL assay was performed to determine the apoptosis of hepatic cells. In addition, the levels of the proteins caspase-3 and B-cell lymphoma-extra large (Bcl-xL) were measured. Compared with the control group, levels of IGF-1 and IGF-1R mRNA and protein were significantly decreased following exposure to isoflurane (all P<0.05). The necrosis rate and liver apoptosis were significantly increased in the group treated with isoflurane alone compared with the control group (P<0.05), but were significantly decreased compared with the isoflurane group following application of IGF-1 (P<0.05). Additionally, isoflurane exposure significantly increased levels of caspase-3 compared with the control group (P<0.05), but decreased levels of Bcl-xL (P<0.05). By contrast, application of IGF-1 reversed these changes. The present study therefore suggests that isoflurane induces liver injury in part by regulating the expression of IGF-1 and that application of IGF-1 may protect against liver injury induced by isoflurane exposure.

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Low doses of insulin-like growth factor-I improve nitrogen retention and food efficiency in rats with early cirrhosis

Cited by 55 publications

References 52 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

Diabetes in chronic liver disease: from old concepts to new evidence

Isoflurane anesthesia induces liver injury by regulating the expression of insulin-like growth factor 1

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