Liver mitochondrial dysfunction is reverted by insulin-like growth factor II (IGF-II) in aging rats

García-Fernández, María; Sierra, Inma; Puche, Juan Enrique; Guerra, L. García; Castilla‐Cortázar, Inma

doi:10.1186/1479-5876-9-123

Cited by 30 publications

(20 citation statements)

References 34 publications

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“…In a small study of pediatric patients with NAFLD, lower IGFII levels correlated with the degree of fibrosis; and our study corroborates this finding in adults . IGFII was found to protect against the effects of caspases 3 and 9 in the liver, thereby decreasing free radical damage and apoptosis in rats; and this may underlie the association of IGFII with fibrosis . Further studies are warranted.…”

Section: Discussionsupporting

confidence: 85%

Novel plasma biomarkers associated with liver disease severity in adults with nonalcoholic fatty liver disease

et al. 2016

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Despite the high prevalence of nonalcoholic fatty liver disease (NAFLD), therapeutic options and non-invasive markers of disease activity and severity remain limited. We investigated the association between plasma biomarkers and liver histology in order to identify markers of disease activity and severity in patients with biopsy-proven NAFLD. Thirty-two plasma biomarkers chosen a priori as possible discriminators of NAFLD were measured on participants enrolled in the Nonalcoholic Steatohepatitis Clinical Research Network (NASH CRN). Dichotomized histologic outcomes were evaluated using centrally read biopsies. Biomarkers with statistically significant associations with NAFLD histology were evaluated for associations with clinical factors and evaluated in multivariable models adjusted for clinical factors. Of 648 participants (74.4% white, 61.7% female, mean age 47.7 years), 58.0% had definite NASH, 55.5% had mild/no fibrosis (stage 0-1) and 44.4% had significant fibrosis (stage 2-4). Increased activated plasminogen activator inhibitor 1 had a strong association with definite NASH compared to not NASH or borderline NASH in multivariable analysis (Odds Ratio [OR] = 1.20, 95% confidence interval (CI): 1.08 – 1.34, p<0.001). Biomarkers associated with significant fibrosis (vs. mild/no fibrosis) in multivariable analysis included higher levels of IL-8, monocyte chemoattractant protein-1, resistin, soluble IL-1 receptor I, soluble IL-2 receptor α, tumor necrosis factor α and lower levels of insulin-like growth factor II. Conclusions Specific plasma biomarkers are significantly associated with disease activity and severity of fibrosis in NAFLD and are potentially valuable tools for noninvasive stratification of patients with NAFLD and identification of targets for therapeutic intervention.

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Section: Discussionsupporting

confidence: 85%

Novel plasma biomarkers associated with liver disease severity in adults with nonalcoholic fatty liver disease

et al. 2016

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“…15 In addition, increased levels of mitochondria-generated H 2 O 2 , with concomitant increases in lipid peroxidation, reduced total antioxidant capacity and increased mitochondrial dysfunction is observed in liver from aging rats compared to young animals. 17 Interestingly, primary hepatocytes from old rats exhibit greater reductions in ATP levels and mitochondrial membrane potential after H 2 O 2 and tert-butyl hydroperoxide treatment than do hepatocytes from young animals. 25 Aging leads to increased lipid peroxidation and levels of protein carbonylation in liver mitochondria of rats, mice and nonhuman primates.…”

Section: Oxidative Stress and Antioxidant Responses In Liver Agingmentioning

confidence: 98%

“…16 Liver mitochondria from old rats show a reduction in mitochondrial membrane potential and ATP synthesis as well as increased proton leaks. 17 Reductions in the activity of key mitochondrial metabolic enzymes emphasize the role of mitochondrial dysfunction in liver aging. Recent studies show that age-associated metabolomic perturbations in the mitochondrial electron transport chain and glucose and phospholipid metabolism are observed in mouse liver.…”

Section: Evidence For Age-associated Loss Of Mitochondrial Bioenergetmentioning

confidence: 99%

Oxidative Stress, Aging and Mitochondrial Dysfunction in Liver Pathology

Ayala‐Peña

Torres‐Ramos

2014

Aging

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“…It was first reported 20 years ago that systemic IGFs could cross the blood-brain barrier (BBB) [12]. In fact, this work was based on previous data, which had confirmed the presence of IGF-1 receptors in brain capillary endothelial cells (which constitute the BBB), their role being to internalize the IGFs to the central nervous system (CNS) from the circulation [13] and the neuroprotective activities of IGFs therapy in aging animals [1,2,14,15].…”

Section: Introductionmentioning

confidence: 95%

“…Although the exact action mechanisms of IGF-1 in the CNS have not been fully elucidated, there is a collected body of evidence of its neuroprotective activity associated with mitochondrial protection and antioxidant defenses in aging animals [1,2,14,15]. Both of these mechanistic pathways, which may be linked, are currently being studied in more detail.…”

Section: Introductionmentioning

confidence: 99%

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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Liver mitochondrial dysfunction is reverted by insulin-like growth factor II (IGF-II) in aging rats

Cited by 30 publications

References 34 publications

Novel plasma biomarkers associated with liver disease severity in adults with nonalcoholic fatty liver disease

Novel plasma biomarkers associated with liver disease severity in adults with nonalcoholic fatty liver disease

Oxidative Stress, Aging and Mitochondrial Dysfunction in Liver Pathology

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

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