5-Aminolevulinic acid combined with ferrous iron enhances the expression of heme oxygenase-1

2014 ◽  
Vol 19 (2) ◽  
pp. 300-307 ◽  
Author(s):  
Yoshiaki Nishio ◽  
Masayuki Fujino ◽  
Mingyi Zhao ◽  
Takuya Ishii ◽  
Masahiro Ishizuka ◽  
...  
Keyword(s):  
Heme Oxygenase ◽  
Ferrous Iron ◽  
Aminolevulinic Acid ◽  
Heme Oxygenase 1

Hemin Through the Heme Oxygenase 1/Ferrous Iron, Carbon Monoxide System Involved in Zinc Tolerance in Oryza Sativa L.

2018 ◽  
Vol 37 (3) ◽  
pp. 947-957 ◽  
Author(s):  
Qin Chen ◽  
Chunyan Gong ◽  
Xin Ju ◽  
Zhengbo Zhu ◽  
Wenbiao Shen ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Oryza Sativa ◽  
Heme Oxygenase ◽  
Ferrous Iron ◽  
Oryza Sativa L ◽  
Heme Oxygenase 1 ◽  
Zinc Tolerance

scholarly journals Heme Oxygenase-1 Regulates Ferrous Iron and Foxo1 in Control of Hepatic Gluconeogenesis

2021 ◽  
Author(s):  
Ada Admin ◽  
Wang Liao ◽  
Wanbao Yang ◽  
Zheng Shen ◽  
Weiqi Ai ◽  
...  
Keyword(s):  
Iron Overload ◽  
Heme Oxygenase ◽  
Ferrous Iron ◽  
Iron Status ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Iron Chelator ◽  
Heme Oxygenase 1 ◽  
Dependent Manner

The liver is a key player for maintaining glucose homeostasis. Excessive hepatic glucose production is considered to be a key for the onset of type 2 diabetes mellitus. The primary function of heme oxygenase-1 (HO1) is to catalyze the degradation of heme into biliverdin, ferrous iron, and carbon monoxide. Previous studies have demonstrated that the degradation of heme by HO1 in the liver results in mitochondrial dysfunction and drives insulin resistance. In this study, by overexpressing HO1 in hepatocytes and mice, we showed that HO1 promotes gluconeogenesis in a Foxo1-dependent manner. Importantly, HO1 overexpression increased the generation of ferrous iron in the liver, which further activates NF-<a>κB</a> and phosphorylates Foxo1 at Ser273 to enhance gluconeogenesis. We further assessed the role of HO1 in insulin-resistant L-DKO (liver-specific knockout of IRS1 and IRS2 genes) mice, which exhibit upregulation of HO1 in the liver and hepatic ferrous iron overload. HO1 knockdown by shRNA or treatment of iron chelator rescued the aberrant gluconeogenesis in L-DKO mice. In addition, we found that systemic iron overload promotes gluconeogenesis by activating hepatic PKA→Foxo1 axis. Thus, our results demonstrate the role of HO1 in regulating hepatic iron status and Foxo1 to control gluconeogenesis and blood glucose.

Paraquat-generated Oxidative Stress in Rat Liver Induces Heme Oxygenase-1 and Aminolevulinic Acid Synthase

2002 ◽  
Vol 36 (6) ◽  
pp. 633-639 ◽  
Author(s):  
Guillermo O. Noriega ◽  
Soledad Gonzales ◽  
María L. Tomaro ◽  
Alcira M. del C. Batlle
Keyword(s):  
Oxidative Stress ◽  
Heme Oxygenase ◽  
Rat Liver ◽  
Aminolevulinic Acid ◽  
Heme Oxygenase 1

scholarly journals P09235-AMINOLEVULINIC ACID PREVENTS LIPID-INDUCED ER STRESS AND APOPTOSIS BY INDUCING HEME OXYGENASE-1

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Yukari Mae ◽  
Yui Kobayashi ◽  
Tomoaki Takata ◽  
Kohshiro Hosokawa ◽  
Takaaki Sugihara ◽  
...  
Keyword(s):  
Palmitic Acid ◽  
Er Stress ◽  
Therapeutic Effect ◽  
Heme Oxygenase ◽  
Renal Tubule ◽  
Aminolevulinic Acid ◽  
Protoporphyrin Ix ◽  
Kidney Injury ◽  
Heme Oxygenase 1 ◽  
Related Factor

Abstract Background and Aims A growing number of evidence indicates the association with dyslipidemia and the progression of chronic kidney disease. Endoplasmic reticulum (ER) stress and apoptosis in renal tubule are suggested to be linked to the pathophysiology of toxic lipid-induced kidney injury. 5-aminolevulinic acid (ALA) is a precursor of heme oxygenase (HO)-1, which plays an important role in protecting cells from various stresses. In the present study, we aimed to investigate the therapeutic effect of ALA, on toxic lipid-induced ER stress and apoptosis in the renal tubule. Method Renal proximal tubular epithelial cells (RPTECs) were treated with palmitic acid to induce ER stress and apoptosis. ALA was also added with palmitic acid (PA). The gene and protein expressions of NF E2-related factor 2, HO-1, glucose-regulated protein (GRP)78, and C/EBP-homologous protein (CHOP) were quantified. Apoptotic cells were evaluated by caspase-3/7 assay. An HO-1 inhibitor, Zn-protoporphyrin IX, was added to investigate the involvement of HO-1 in ALA-mediated therapeutic effect on the ER stress and apoptosis. Results The expressions of GRP78 and CHOP increased in cells treated with PA. Apoptotic signals also increased with PA treatment. ALA induced a significant increase in the HO-1 expression and that led to the suppression of ER stress response. Apoptotic signals in PA-treated cells also decreased with ALA and the effect of ALA disappeared when combined with Zn-protoporphyrin IX. Conclusion PA-induced ER stress and apoptosis in RPTECs. ALA has a therapeutic effect by suppressing ER stress, possibly through HO-1 induction.

scholarly journals Heme Oxygenase-1 Regulates Ferrous Iron and Foxo1 in Control of Hepatic Gluconeogenesis

2021 ◽  
Author(s):  
Ada Admin ◽  
Wang Liao ◽  
Wanbao Yang ◽  
Zheng Shen ◽  
Weiqi Ai ◽  
...  
Keyword(s):  
Iron Overload ◽  
Heme Oxygenase ◽  
Ferrous Iron ◽  
Iron Status ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Iron Chelator ◽  
Heme Oxygenase 1 ◽  
Dependent Manner

The liver is a key player for maintaining glucose homeostasis. Excessive hepatic glucose production is considered to be a key for the onset of type 2 diabetes mellitus. The primary function of heme oxygenase-1 (HO1) is to catalyze the degradation of heme into biliverdin, ferrous iron, and carbon monoxide. Previous studies have demonstrated that the degradation of heme by HO1 in the liver results in mitochondrial dysfunction and drives insulin resistance. In this study, by overexpressing HO1 in hepatocytes and mice, we showed that HO1 promotes gluconeogenesis in a Foxo1-dependent manner. Importantly, HO1 overexpression increased the generation of ferrous iron in the liver, which further activates NF-<a>κB</a> and phosphorylates Foxo1 at Ser273 to enhance gluconeogenesis. We further assessed the role of HO1 in insulin-resistant L-DKO (liver-specific knockout of IRS1 and IRS2 genes) mice, which exhibit upregulation of HO1 in the liver and hepatic ferrous iron overload. HO1 knockdown by shRNA or treatment of iron chelator rescued the aberrant gluconeogenesis in L-DKO mice. In addition, we found that systemic iron overload promotes gluconeogenesis by activating hepatic PKA→Foxo1 axis. Thus, our results demonstrate the role of HO1 in regulating hepatic iron status and Foxo1 to control gluconeogenesis and blood glucose.

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