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An Experimental Model of Diet-Induced Metabolic Syndrome in Rabbit: Methodological Considerations, Development, and Assessment
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Sphincter of Oddi dysfunction in hypercholesterolemic rabbits.

Xiao-Yong Zhang1, Guang-Bin Cui, Ke-Jun Ma

  • 1Department of Radiology, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, China. zhang-xy@fmmu.edu.cn

European Journal of Gastroenterology & Hepatology
|February 28, 2008
PubMed
Summary

High cholesterol causes sphincter of Oddi dysfunction (SOD), leading to gallbladder issues and gallstones. Abnormal calcium signaling in SO smooth muscle cells is a key factor in SOD development.

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Area of Science:

  • Gastroenterology
  • Biliary Physiology
  • Cellular Mechanisms

Background:

  • Gallbladder evacuation dysfunction is a major risk factor for gallstone formation, but its underlying mechanisms are not fully understood.
  • The sphincter of Oddi (SO) is crucial for regulating gallbladder emptying and biliary tract pressure.
  • Sphincter of Oddi dysfunction (SOD) can lead to cholestasis and gallstone development.

Purpose of the Study:

  • To investigate the impact of hypercholesterolemia on the motility of the sphincter of Oddi (SO).
  • To elucidate the cellular mechanisms responsible for hypercholesterolemia-induced SO dysfunction (SOD).

Main Methods:

  • New Zealand white rabbits were fed a high-cholesterol diet for 8 weeks.
  • Evaluated gallbladder emptying rates, SO pressure (manometry), and in vivo peristaltic movements (ultrasound).
  • Assessed intracellular calcium ([Ca]i) levels and calcium oscillations in primary SO smooth muscle cells using laser scanning confocal fluorescence microscopy.

Main Results:

  • Hypercholesterolemia induced gallbladder cholestasis and impaired CCK-8-stimulated emptying.
  • Increased basal SO pressure and abnormal intracellular calcium ([Ca]i) overload and oscillations were observed in SO cells.
  • Passive SO dilation partially improved cholestasis, but gallbladder emptying remained suboptimal.

Conclusions:

  • Hypercholesterolemia initiates SO dysfunction (SOD), increasing resistance to gallbladder evacuation and causing cholestasis.
  • Abnormalities in intracellular calcium ([Ca]i) handling, including overload and altered oscillations, are implicated in the pathogenesis of SOD.