Abstract

The incidence of gallstone is higher in patients with diabetes mellitus than in general popula- tion. It is generally attributed to hypomotility and lowered emptying function of the gallblad- der. In this study, we investigate if chronic hy- perglycemia is correlated with reduced contrac- tile function of the bile ducts in rat. Hypergly- cemic rats were induced by streptozotocin-nic-otinamide treatment. Hyperglycemic rats were sacrificed eight months after induction and bile ducts were removed for the subsequent studies. The bile duct contractility of the normal rats is consistently higher than that of the hypergly- cemic rats. The contractities were measured to be 5.5 ± 0.2 mg vs. 4.2 ± 0.1 mg without CCK stimulation, and 5.5 ± 0.3 mg vs. 7.9 ± 0.4 mg with CCK stimulation, respectively for hypergly-cemic and normal rats. There was no significant difference in plasma CCK concentration in hy- perglycemic rats and normal rats. The expres- sion of CCK-A receptor protein in the bile duct tissue was decreased in hyperglycemic rats compared with that of the normal rats, and it may, at least in part, responsible for a reduced contractility. A reduced bile duct motility may cause bile retention, and may be one of the factors predispose to gallstone formation in type 2 diabetes patients, which is characterized with chronic hyperglycemia.

Highlights

  • IntroductionCholelithiasis is one of the most prevalent gastroentero-logic diseases in humans. It is a complex metabolic disorders, and its exact pathogenic mechanisms have not been fully elucidated

  • Cholelithiasis is one of the most prevalent gastroentero-logic diseases in humans

  • Gallstones represent a serious burden for the health care systems: over 10% of Europeans and Americans carry gallbladder stones [1], and the prevalence of gallstone disease seems to be rising as a result of longer life expectancy [2]

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Summary

Introduction

Cholelithiasis is one of the most prevalent gastroentero-logic diseases in humans. It is a complex metabolic disorders, and its exact pathogenic mechanisms have not been fully elucidated. Cholelithiasis is one of the most prevalent gastroentero-. It is a complex metabolic disorders, and its exact pathogenic mechanisms have not been fully elucidated. But symptoms and severe complications ensure in around 25% of the cases, necessitating surgical removal of the gallbladder [3]. In the US about 3,000 deaths (0.12% of all deaths) per year are attributed to complications of cholelithiasis and gallbladder disease [6]. Nonsurgical approaches, including gallstone dissolution by ursodeoxycholic acid and extracorporeal shockwave lithotripsy, have increasingly lost their impact on therapy and are performed only for uncomplicated symptomatic cholecystolithiasis in a very small number of selected patients

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