1718-P: Heme Oxygenase-1 Promotes Hepatic Glucose Production via Increasing the Intracellular Ferrous Iron

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1718-P ◽  
Author(s):  
WANG LIAO ◽  
WANBAO YANG ◽  
QUAN PAN ◽  
ZHENG SHEN ◽  
WEIQI AI ◽  
...  
Keyword(s):  
Heme Oxygenase ◽  
Ferrous Iron ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Heme Oxygenase 1 ◽  
Hepatic Glucose

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.

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.

FoxO3 regulates hepatic glucose production

2013 ◽  
Vol 51 (01) ◽  
Author(s):  
S Gul ◽  
KH Holzmann ◽  
F Leithäuser ◽  
H Maier ◽  
B Böhm ◽  
...  
Keyword(s):  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Hepatic Glucose

Hyperglycemia per se does not inhibit hepatic glucose production in man

1989 ◽  
Vol 120 (3_Suppl) ◽  
pp. S20
Author(s):  
M.J. MÜLLER ◽  
K.J. ACHESON ◽  
A. G. BURGER ◽  
E. JEQUIER ◽  
A. VON ZUR MÜHLEN
Keyword(s):  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Hepatic Glucose ◽  
Per Se

Regulation of Hepatic Glucose Production by Transforming Growth Factor Beta 1 via Protein Kinase A

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2441-PUB ◽  
Author(s):  
QUAN PAN ◽  
YUNMEI CHEN ◽  
HUI YAN ◽  
WANBAO YANG ◽  
ZHENG SHEN ◽  
...  
Keyword(s):  
Growth Factor ◽  
Protein Kinase ◽  
Protein Kinase A ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Hepatic Glucose ◽  
Growth Factor Beta ◽  
Kinase A

64-LB: Aerobic Exercise Decreases Hepatic Glucose Production via Asprosin Pathway in Diabetic Rats

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 64-LB
Author(s):  
JEONGRIM KO ◽  
TAE NYUN KIM ◽  
DAE YUN SEO ◽  
JIN HAN
Keyword(s):  
Aerobic Exercise ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Diabetic Rats ◽  
Hepatic Glucose

Pancreas transplantation in diabetic humans normalizes hepatic glucose production during hypoglycemia

Diabetes ◽  
1994 ◽  
Vol 43 (5) ◽  
pp. 661-666 ◽  
Author(s):  
Z. Barrou ◽  
E. R. Seaquist ◽  
R. P. Robertson
Keyword(s):  
Pancreas Transplantation ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Hepatic Glucose

The role of autoregulation of the hepatic glucose production in man. Response to a physiologic decrement in plasma glucose

Diabetes ◽  
1986 ◽  
Vol 35 (2) ◽  
pp. 186-191 ◽  
Author(s):  
I. Hansen ◽  
R. Firth ◽  
M. Haymond ◽  
P. Cryer ◽  
R. Rizza
Keyword(s):  
Plasma Glucose ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Hepatic Glucose
Sign in / Sign up

Export Citation Format

Share Document