Reduced bile duct contractile function in rats with chronic hyperglycemia

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.

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Liu, C. , Su, H. , Wang, Y. , Tung, T. , Chou, P. , Chou, Y. , Liu, J. and Chen, J. (2010) Reduced bile duct contractile function in rats with chronic hyperglycemia. Health, 2, 1072-1077. doi: 10.4236/health.2010.29157.

Conflicts of Interest

The authors declare no conflicts of interest.

References

[1] Kratzer, W., Mason, R.A. and K?chele, V. (1999) Preva- lence of gallstones in sonographic surveys worldwide. Journal of Clinical Ultrasound, 27(1), 1-7.
[2] Paigen, B. and Carey, M.C. (2002) Gallstones. In: The genetic basis of common disease. Oxford University Press, London, 298-335.
[3] Ransohoff, D.F., Gracie, W.A., Wolfenson, L.B. and Neu- hauser, D. (1983) Prophylactic cholecystectomy or ex- pectant management for silent gallstones: Adecision analysis to assess survival. Annals of Internal Medicine, 99(2), 199-204.
[4] The Southerm Surgeons Club (1999) A prospective analysis of 1518 laparoscopic cholecystectomies. New England Journal of Traditional Chinese Medicine, 324(16), 1073-1078.
[5] BQS Bundesgesch?ftsstelle Qualit?tssicherung (2004) Qualit?t Sichtbar machen. BQS-Qualit?tsbericht 2003, BQS, D?sseldorf, 31-39.
[6] Liver Disease Subcommittee of the Digestive Disease Interagency Coordinating Committee (2005) Action plan for liver disease research. NIH, Bethesda, 145-150.
[7] Carey, M.C. and LaMont, J.T. (1992) Cholesterol gall- stone formation. 1. Physical chemistry of bile and biliary lipid secretion. Program for Liver Diseases, 10, 136-163.
[8] Paumgartner, G. and Sauerbruch, T. (1991) Gallstones: Patho-genesis. Lancet, 338(8775), 1117-1121.
[9] Lammert, F., Carey, M.C. and Paigen, B. (2001) Chro- mosomal organization of candidate genes involved in cholesterol gallstone formation: A murine gallstone map. Gastroenterology, 120(1), 221-238.
[10] Wittenburg, H., Lyons, M.A., Li, R., Churchill, G.A., Carey, M.C. and Paigen, B.J. (2003) FXR and ABCG5/ ABCG8 as determinants of cholesterol gallstone forma- tion from quantitative trait locus mapping in mice. Gas- troenterology, 125(3), 868-881.
[11] Moschetta, A., Bookout, A.L. and Mangelsdorf, D.J. (2004) Prevention of cholesterol gallstone disease by FXR agonists in a mouse model. Nature Medicine, 10 (12), 1352-1358.
[12] Wang, D.Q., Schmitz, F., Kopin, A.S. and Carey, M.C. (2004) Targeted disruption of the murine cholecystokinin-1 receptor promotes intestinal cholesterol absorption and susceptibility to cholesterol cholelithiasis. Journal of Clinical Investigation, 114(4), 521-528.
[13] Pagliarulo, M., Fornari, F., Fraquelli, M., Zoli, F., Giangregorio, A., Grigolon, M., Peracchi, D. and Conte, D. (2004) Gallstone disease and related risk factors in a large cohort of diabetic patients. Digestive and Liver Disease, 36(2), 130-134.
[14] Fraquelli, M., Pagliarulo, M., Colucci, A., Paggi, S. and Conte, D. (2003) Gallbladder mortility in obesity, dia- betes mellitus and coeliac disease. Digestive and Liver Disease, 35(S3), s12-s16.
[15] Chen, C.Y., Lu, C.L., Lee, P.C., Wang, S.S., Chang, F.Y. and Lee, S.D. (1999) The risk factors for gallstone disease among senior citizens: An Oriental study. Hepatogastroen- terology, 46(27), 1606-1612.
[16] Chan, D.C., Chang, T.M., Chen, C.J., Chen, T.W., Yu, J.C. and Liu, Y.C. (2004) Gallbladder contractility and volume characteristics in gallstone dyspepsia. World Journal of Gastroenterology, 10(5), 721-724.
[17] Portincasa, P., Moschetta, A., Berardino, M., Di-Ciaula, A., Vacca, M., Baldassarre, G., Pietrapertosa, A., Camma- rota, R., Tannoia, N. and Palasciano, G. (2004) Impaired gallbladder motility and delayed orocecal transit con- tribute to pigment gallstone and biliary sludge formation in betathalassemia major adults. World Journal of Gas- troenterology, 10(16), 2383-2390.
[18] Mawe, G.M. (1998) Nerves and hormones interact to control gallbladder function. News in Physiological Sci- ences, 13(2), 84-90.
[19] Patankar, R., Ozmen, M.M., Bailiey, I.S. and Johnson, C.D. (1995) Gallbladder motility, gallstones and the sur- geon. Digestive and Liver Disease, 40(11), 2323-2335.
[20] Yu, P., De Prtris, G., Biancani, P., Amaral, J. and Behar, J. (1994) Cholecystokinin-coupled intracellular signaling in human gallbladder muscle. Gastroenterology, 106(3), 763- 770.
[21] Rerup, C.C. (1970) Drugs producing diabetes through damage of the insulin secreting cells. Pharmacological Reviews, 22(2), 485-518.
[22] Masiello, P., Broca, C., Gross, R., Roye, M., Manteghetti, M., Hillaire-Buys, D., Novelli, M. and Ribes, G. (1998) Experimental NIDDM: Development of a new model in adult rats administered streptozotocin and nicotinamide. Diabetes, 47(2), 224-229.
[23] Dieh1, A.K. (1991) Epidemiology and natural history of gallstone disease. Gastroenterology Clinics of North America, 20(1), 1-19.
[24] Mendez-Sanchez, N., Vega, H., Uribe, M., Guevara, L., Ramos, M.H. and Vargas-Vorackova, F. (1998) Risk fac- tors for gallstone disease in Mexicans are similar to those found in Mexican-Americans. Digestive and Liver Dis- ease, 43(5), 935-939.
[25] Ruhl, C.E. and Everhart, J.E. (2000) Association of dia- betes, serum insulin, and C-peptide with gallbladder dis- ease. Hepatology, 31(2), 299-303.
[26] Férézou, J., Combettes-Souverain, M., Souidi, M., Smith, J.L., Boehler, N., Milliat, F., Eckhardt, E., Blanchard, G., Riottot, M., Sérougne, C. and Lutton, C. (2000) Choles- terol, bile acid, and lipoprotein metabolism in two strains of hamster, one resistant, the other sensitive (LPN) to su- crose-induced cholelithiasis. Journal of Lipid Research, 41(12), 2042-2052.
[27] Behar, J., Lee, K.Y., Thompson, W.R. and Biancani, P. (1989) Gallbladder contraction in patients with pigment and cholesterol stones. Gastroenterology, 97, 1479-1484.
[28] Grider, J.R. and Makhlouf, G.M. (1990) Distinct recep- tors for cholecystokinin and gastrin on muscle cells of stomach and gallbladder. The American Journal of Physiology, 259(2), 184-190.
[29] Xiong, D., Chang-You, L., Ying, M., Chang-An, L. and Yu-Jun, S. (2005) Correlation between gene expression of CCK-A receptor and emptying dysfunction of the gall- bladder in patients with gallstones and diabetes mellitus. Hepatobiliary & Pancreatic Diseases International, 4(2), 295-298.
[30] Miyasaka, K., Kanai, S., Ohta, M., Hosoya, H., Sekime, A., Akimoto, S., Takiguchi, S. and Funakoshi, A. (2007) Ageassociated gallstone formation in male and female CCK-1(A) receptor-deficient mice. Journal of Gastroen- terology, 42(6), 493-496.

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