Changes of urinary bladder contractility in high-fat diet-fed mice: The role of tumor necrosis factor-α

Eric Wen Chou Fan, Li Jen Chen, Juei Tang Cheng, Yat Ching Tong

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Objectives: To study the role of tumor necrosis factor-α in bladder dysfunction associated with obesity. Methods: Male 8-week-old C57BL/6J mice were divided into three groups: (i) control mice; (ii) vehicle-treated high-fat diet-fed mice; and (iii) etanercept-treated high-fat diet-fed mice. High-fat diet feeding lasted for 12 weeks, vehicle or etanercept (0.8mg/kg/day, a tumor necrosis factor-α antagonist) treatment was given during the last 4 weeks. At the end of the treatment period, serum tumor necrosis factor-α, total cholesterol, triglyceride and blood glucose were measured. Bladder strip contractile responses to 1μmol/L acetylcholine or 50mmol/L KCl were studied in an organ bath. Bladder protein kinase Cζ, nuclear factor-κB and intercellular adhesion molecule-1 expressions were analyzed using western blots. Results: Serum levels of tumor necrosis factor-α total cholesterol, triglyceride and glucose were significantly elevated in high-fat diet-fed mice; and the levels were not ameliorated by etanercept treatment. High-fat diet-fed mouse bladder showed reduced contractile responses to acetylcholine and KCl stimulation accompanied by high expression levels of phospho-protein kinaseCζ, nuclear nuclear factor-κB and intercellular adhesion molecule-1. Etanercept restored normal bladder contractile responses, as well as protein kinaseCζ nuclear factor-κB and intercellular adhesion molecule-1 expressions. Conclusions: A high-fat diet induces bodyweight gain, hyperlipidemia and hyperglycemia in mice. Elevated serum tumor necrosis factor-α level associated with increased protein kinase Cζ phosphorylation, nuclear factor-κB nuclear migration, intercellular adhesion molecule-1 expression and impaired muscle contractility are shown in the high-fat diet-fed mouse bladder. Tumor necrosis factor-α antagonist treatment restores normal bladder contractility, and protein kinaseCζ nuclear factor-κB and intercellular adhesion molecule-1 levels.

Original languageEnglish
Pages (from-to)831-835
Number of pages5
JournalInternational Journal of Urology
Volume21
Issue number8
DOIs
Publication statusPublished - 2014 Aug

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High Fat Diet
Urinary Bladder
Tumor Necrosis Factor-alpha
Intercellular Adhesion Molecule-1
Nuclear Proteins
Protein Kinase C
Acetylcholine
Triglycerides
Serum
Cholesterol
Therapeutics
Hyperlipidemias
Baths
Inbred C57BL Mouse
Hyperglycemia
Blood Glucose
Obesity
Western Blotting
Phosphorylation
Glucose

All Science Journal Classification (ASJC) codes

  • Urology

Cite this

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title = "Changes of urinary bladder contractility in high-fat diet-fed mice: The role of tumor necrosis factor-α",
abstract = "Objectives: To study the role of tumor necrosis factor-α in bladder dysfunction associated with obesity. Methods: Male 8-week-old C57BL/6J mice were divided into three groups: (i) control mice; (ii) vehicle-treated high-fat diet-fed mice; and (iii) etanercept-treated high-fat diet-fed mice. High-fat diet feeding lasted for 12 weeks, vehicle or etanercept (0.8mg/kg/day, a tumor necrosis factor-α antagonist) treatment was given during the last 4 weeks. At the end of the treatment period, serum tumor necrosis factor-α, total cholesterol, triglyceride and blood glucose were measured. Bladder strip contractile responses to 1μmol/L acetylcholine or 50mmol/L KCl were studied in an organ bath. Bladder protein kinase Cζ, nuclear factor-κB and intercellular adhesion molecule-1 expressions were analyzed using western blots. Results: Serum levels of tumor necrosis factor-α total cholesterol, triglyceride and glucose were significantly elevated in high-fat diet-fed mice; and the levels were not ameliorated by etanercept treatment. High-fat diet-fed mouse bladder showed reduced contractile responses to acetylcholine and KCl stimulation accompanied by high expression levels of phospho-protein kinaseCζ, nuclear nuclear factor-κB and intercellular adhesion molecule-1. Etanercept restored normal bladder contractile responses, as well as protein kinaseCζ nuclear factor-κB and intercellular adhesion molecule-1 expressions. Conclusions: A high-fat diet induces bodyweight gain, hyperlipidemia and hyperglycemia in mice. Elevated serum tumor necrosis factor-α level associated with increased protein kinase Cζ phosphorylation, nuclear factor-κB nuclear migration, intercellular adhesion molecule-1 expression and impaired muscle contractility are shown in the high-fat diet-fed mouse bladder. Tumor necrosis factor-α antagonist treatment restores normal bladder contractility, and protein kinaseCζ nuclear factor-κB and intercellular adhesion molecule-1 levels.",
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Changes of urinary bladder contractility in high-fat diet-fed mice : The role of tumor necrosis factor-α. / Fan, Eric Wen Chou; Chen, Li Jen; Cheng, Juei Tang; Tong, Yat Ching.

In: International Journal of Urology, Vol. 21, No. 8, 08.2014, p. 831-835.

Research output: Contribution to journalArticle

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AU - Chen, Li Jen

AU - Cheng, Juei Tang

AU - Tong, Yat Ching

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N2 - Objectives: To study the role of tumor necrosis factor-α in bladder dysfunction associated with obesity. Methods: Male 8-week-old C57BL/6J mice were divided into three groups: (i) control mice; (ii) vehicle-treated high-fat diet-fed mice; and (iii) etanercept-treated high-fat diet-fed mice. High-fat diet feeding lasted for 12 weeks, vehicle or etanercept (0.8mg/kg/day, a tumor necrosis factor-α antagonist) treatment was given during the last 4 weeks. At the end of the treatment period, serum tumor necrosis factor-α, total cholesterol, triglyceride and blood glucose were measured. Bladder strip contractile responses to 1μmol/L acetylcholine or 50mmol/L KCl were studied in an organ bath. Bladder protein kinase Cζ, nuclear factor-κB and intercellular adhesion molecule-1 expressions were analyzed using western blots. Results: Serum levels of tumor necrosis factor-α total cholesterol, triglyceride and glucose were significantly elevated in high-fat diet-fed mice; and the levels were not ameliorated by etanercept treatment. High-fat diet-fed mouse bladder showed reduced contractile responses to acetylcholine and KCl stimulation accompanied by high expression levels of phospho-protein kinaseCζ, nuclear nuclear factor-κB and intercellular adhesion molecule-1. Etanercept restored normal bladder contractile responses, as well as protein kinaseCζ nuclear factor-κB and intercellular adhesion molecule-1 expressions. Conclusions: A high-fat diet induces bodyweight gain, hyperlipidemia and hyperglycemia in mice. Elevated serum tumor necrosis factor-α level associated with increased protein kinase Cζ phosphorylation, nuclear factor-κB nuclear migration, intercellular adhesion molecule-1 expression and impaired muscle contractility are shown in the high-fat diet-fed mouse bladder. Tumor necrosis factor-α antagonist treatment restores normal bladder contractility, and protein kinaseCζ nuclear factor-κB and intercellular adhesion molecule-1 levels.

AB - Objectives: To study the role of tumor necrosis factor-α in bladder dysfunction associated with obesity. Methods: Male 8-week-old C57BL/6J mice were divided into three groups: (i) control mice; (ii) vehicle-treated high-fat diet-fed mice; and (iii) etanercept-treated high-fat diet-fed mice. High-fat diet feeding lasted for 12 weeks, vehicle or etanercept (0.8mg/kg/day, a tumor necrosis factor-α antagonist) treatment was given during the last 4 weeks. At the end of the treatment period, serum tumor necrosis factor-α, total cholesterol, triglyceride and blood glucose were measured. Bladder strip contractile responses to 1μmol/L acetylcholine or 50mmol/L KCl were studied in an organ bath. Bladder protein kinase Cζ, nuclear factor-κB and intercellular adhesion molecule-1 expressions were analyzed using western blots. Results: Serum levels of tumor necrosis factor-α total cholesterol, triglyceride and glucose were significantly elevated in high-fat diet-fed mice; and the levels were not ameliorated by etanercept treatment. High-fat diet-fed mouse bladder showed reduced contractile responses to acetylcholine and KCl stimulation accompanied by high expression levels of phospho-protein kinaseCζ, nuclear nuclear factor-κB and intercellular adhesion molecule-1. Etanercept restored normal bladder contractile responses, as well as protein kinaseCζ nuclear factor-κB and intercellular adhesion molecule-1 expressions. Conclusions: A high-fat diet induces bodyweight gain, hyperlipidemia and hyperglycemia in mice. Elevated serum tumor necrosis factor-α level associated with increased protein kinase Cζ phosphorylation, nuclear factor-κB nuclear migration, intercellular adhesion molecule-1 expression and impaired muscle contractility are shown in the high-fat diet-fed mouse bladder. Tumor necrosis factor-α antagonist treatment restores normal bladder contractility, and protein kinaseCζ nuclear factor-κB and intercellular adhesion molecule-1 levels.

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