Diabetes enhances the intrahepatic vascular response to endothelin‐1 in cirrhotic rats: association with the ET<sub>A</sub> receptor and <scp>pERK</scp> up‐regulation

Lee, Jing Yi; Lee, Fa Yauh; Huo, Teh Ia; Wang, Sun Sang; Lin, Han Chieh; Chuang, Chiao Lin; Lee, Shou Dong

doi:10.1111/liv.12527

Cited by 2 publications

(1 citation statement)

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“…The commonly investigated rat models of diabetes have beenWistar and Sprague Dawley rat strains induced by a single injection of streptozotocin (40 -60 mg/kg) [12] [31]. In our previous experience, however, diabetes induction by single higher doses of streptozotocin in these animal models is often associated with the occurrence of complete and irreversible damage of the pancreas.…”

Section: Discussionmentioning

confidence: 99%

Hyperbaric Oxygen Treatment in a Diabetic Rat Model Is Associated with a Decrease in Blood Glucose, Regression of Organ Damage and Improvement in Wound Healing

Prabowo¹,

Nataatmadja²,

Hadi³

et al. 2014

Health

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Diabetes leads to widespread complications including pancreatic β-cell damage, nephropathy and impaired wound healing. Hyperbaric oxygen therapy (HBOT) has been shown to improve wound healing through induction of stem cell recruitment and the potential to inhibit progression of diabetic complications. We aimed to determine the efficacy of HBOT in wound healing and organ preservation in a diabetic rat model. Diabetes was induced in male Wistar rats (n = 10/group) using streptozotocin (20 mg/kg sc) daily for 3 days. A wound was inflicted on the skin over the back and the rats were given HBOT (2.3 ATA for 1 h/day) for 1, 3, 5, 7 or 10 days or were not treated. Blood glucose, pancreatic β-cell damage, diabetic nephropathy and wound healing progression were assessed. Diabetic rats not treated with HBOT had significantly higher blood glucose levels compared to controls (26.7 ± 3.3 mmol/L vs. 5.8 ± 0.4 mmol/L; P ≤ 0.05). This was associated with significant increase in the percentage of β-cell damage (72% ± 9% vs. 10% ± 2%; P ≤ 0.05) and diabetic nephropathy. HBOT for 3 days and longer in diabetic rats reduced hyperglycemia to control levels. Pancreatic β-cell damage was negligible in rats treated with HBOT for 5 days and longer while diabetic nephropathy was diminished in animals treated for 10 days. Similarly HBOT induced wound healing and accelerated epithelial closure from 5 days of HBOT. In summary, our findings show the efficacy of HBOT in this diabetic rat model. There was significant reduction of hyperglycemia and inhibition of diabetic complications in the form of preservation of pancreatic S. Prabowo et al. 1951 and kidney structure and accelerated wound healing.

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Section: Discussionmentioning

confidence: 99%

Hyperbaric Oxygen Treatment in a Diabetic Rat Model Is Associated with a Decrease in Blood Glucose, Regression of Organ Damage and Improvement in Wound Healing

Prabowo¹,

Nataatmadja²,

Hadi³

et al. 2014

Health

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Endothelial dysfunction in cirrhosis: Role of inflammation and oxidative stress

Vairappan

2015

WJH

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This review describes the recent developments in the pathobiology of endothelial dysfunction (ED) in the context of cirrhosis with portal hypertension and defines novel strategies and potential targets for therapy. ED has prognostic implications by predicting unfavourable early hepatic events and mortality in patients with portal hypertension and advanced liver diseases. ED characterised by an impaired bioactivity of nitric oxide (NO) within the hepatic circulation and is mainly due to decreased bioavailability of NO and accelerated degradation of NO with reactive oxygen species. Furthermore, elevated inflammatory markers also inhibit NO synthesis and causes ED in cirrhotic liver. Therefore, improvement of NO availability in the hepatic circulation can be beneficial for the improvement of endothelial dysfunction and associated portal hypertension in patients with cirrhosis. Furthermore, therapeutic agents that are identified in increasing NO bioavailability through improvement of hepatic endothelial nitric oxide synthase (eNOS) activity and reduction in hepatic asymmetric dimethylarginine, an endogenous modulator of eNOS and a key mediator of elevated intrahepatic vascular tone in cirrhosis would be interesting therapeutic approaches in patients with endothelial dysfunction and portal hypertension in advanced liver diseases.

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Diabetes enhances the intrahepatic vascular response to endothelin‐1 in cirrhotic rats: association with the ET_A receptor and pERK up‐regulation

Abstract: Cirrhotic rats with diabetes showed higher intrahepatic ET-1 vasoresponsiveness than normoglycemic cirrhotic rats. This effect is not affected by changes in perfused glucose concentration and may be related, at least in part, to intrahepatic ETA R receptor and pERK over-expression.

Cited by 2 publications

References 41 publications

Hyperbaric Oxygen Treatment in a Diabetic Rat Model Is Associated with a Decrease in Blood Glucose, Regression of Organ Damage and Improvement in Wound Healing

Hyperbaric Oxygen Treatment in a Diabetic Rat Model Is Associated with a Decrease in Blood Glucose, Regression of Organ Damage and Improvement in Wound Healing

Endothelial dysfunction in cirrhosis: Role of inflammation and oxidative stress

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Diabetes enhances the intrahepatic vascular response to endothelin‐1 in cirrhotic rats: association with the ETA receptor and pERK up‐regulation

Abstract: Cirrhotic rats with diabetes showed higher intrahepatic ET-1 vasoresponsiveness than normoglycemic cirrhotic rats. This effect is not affected by changes in perfused glucose concentration and may be related, at least in part, to intrahepatic ETA R receptor and pERK over-expression.

Cited by 2 publications

References 41 publications

Hyperbaric Oxygen Treatment in a Diabetic Rat Model Is Associated with a Decrease in Blood Glucose, Regression of Organ Damage and Improvement in Wound Healing

Hyperbaric Oxygen Treatment in a Diabetic Rat Model Is Associated with a Decrease in Blood Glucose, Regression of Organ Damage and Improvement in Wound Healing

Endothelial dysfunction in cirrhosis: Role of inflammation and oxidative stress

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Diabetes enhances the intrahepatic vascular response to endothelin‐1 in cirrhotic rats: association with the ET_A receptor and pERK up‐regulation