Changes of gastrointestinal myoelectric activity and bile acid pool during cholesterol gallstone formation in guinea pigs

Abstract

Abstract: Objective To investigate the changes of gastrointestinal migrating myoelectric complex (MMC) and bile acid pool size during cholesterol gallstone formation in guinea pigs. Methods Seventy-five guinea pigs were randomized into 5 equal groups and given normal diet for 8 weeks, 1% cholesterol diet for 2, 4, and 8 weeks, and cholesterol diet with Vitamin C for 8 weeks, respectively. At the end of the feeding period, the gallbladder motility was assessed by deploying 4 bipolar silver electrodes on the antrum, duodenum, jejunum and ileum. Seven days later, MMC was recorded and the total bile acid pool size measured according to the isotope dilution method. Results After cholesterol feeding, the gallbladder motility declined in 4- and 8-week groups, which showed a reduction of bile acid pool size by 42.75% (P<0.05) and 57.24% (P<0.05), respectively. Compared to the control group, MMCs started mostly in the duodenum. MMC cycle duration was prolonged in the duodenum by 1.32 times in 4-week group (P<0.05) and 1.44 times in 8 week group (P<0.05) whereas MMC amplitude was lowered in the duodenum by 40.91% in 4-week group (P<0.05) and 60.17% in 8 week group (P<0.05). Supplementation of vitamin C caused changes in MMC similar to those observed in the guinea pigs of 2-week group. Conclusions High-cholesterol diet inhibits MMC activity and reduces bile acid pool size in guinea pigs, which, along with impairment of the gallbladder motility, contributes to the formation of cholesterol stone, whereas vitamin C supplement in the diet may help prevent cholelithiasis.

CLC Number:

R364.25

ZHANG Xue-mei, DONG Lei, LIU Li-na. Changes of gastrointestinal myoelectric activity and bile acid pool during cholesterol gallstone formation in guinea pigs[J]. Journal of Southern Medical University, 2005, 25(10): 1251-1255,1260.

References

[1] Apstein MD, Carey MC. Pathogenesis of cholesterol gallstones: a parsimonious hypothesis[J]. Eur J Clin Invest, 1996, 26(5): 343-52.
[2] Holzbach RT. Newer pathogenetic concepts in cholesterol gallstone formation-a unitary hypothesis [J]. Digestion, 1997, 58( 1): 29-32.
[3] Gustafsson U, Sahin S, Einarsson C. Biliary liquid composition in patients with cholesterol and pigment gallstones and gallstone-free subjects: deoxycholic acid does not contribute to formation of cholesterol gallstones [J]. Eur J Clin Invest, 2000, 30 (12):1099-106.
[4] Vlahcevic ZR, Bell CC Jr, Buhac L, et al. Diminished bile acid pool size in patients with gallstones [J]. Gastroenterology, 1970, 59(2):165-73.
[5] Francesco A, Giuseppe M, Costanza M, et al. Sluggish small bowel motility is involved in determining increased biliary deoxycholic acid in cholesterol gallstone patients[J]. Am J Gastroenterol, 1999,94(9): 2453-9.
[6] van Erpecum, van Berge H. Gallstone: an intestinal disease[J] ? Gut,1999, 44(3): 435-8.
[7] Stolk MF, Van Erpecum KJ, Smout AJ, et al. Motor cycles with phase Ⅲ in antrum are associated with high motilin levels and prolonged gallbladder emptying [J]. Am J Physiol, 1993, 264 (27):596-600.
[8] 古赛,唐承薇,钟晓明.B超测定胆囊排空率餐后测定时间的探讨[J].胃肠病学,2002,7(4):218-20.Gu S, Tang CW, Zhong XM. Investigation of postprandial phase of gallbladder emptying measured by ultrasonography [J]. Chin J Gastroenterol, 2002, 7(4):218-20.
[9] Dodds WJ, Groh WJ, Darweesh RM, et al. Sonographic measurement of gallbladder volume[J]. AJR, 1985, 145(5): 1009-11.
[10] William CD, Ronald DA, Lynn JB, et al. Determination of bile acid pool size in man: a simplified method with advantages of increased precision, shortened analysis time, and decreased isotope exposure [J]. J Lipid Res, 1975, 16(2): 155-8.
[11] Hayes KC, Stephan ZF, Pronczuk A, et al. Lactose protects against estrogen-induced pigment gallstones in hamsters fed nutritionally adequate purified diets[J]. J Nutr, 1989, 119(11): 1726-36.
[12] Xu G, Senal G, Batta AK, et al. Glycocholic acid and glycodeoxycholic acid but not glycoursocholic acid inhibit bile acid synthesis in the rabbit[J]. Gastroenterology, 1992, 102(5): 1717-23.
[13] Mok HY, Perry PM, DoMing RH. The control of bile acid pool size:Effect of jejunal resection and phenobarbitone on bile acid metabolism in the rat[J]. Gut, 1974, 15(1): 247-53.
[14] Xu GR, Benjamin LS, Sarah S, et al. Ileal bile acid transport regulates bile acid pool, synthesis, and plasma cholesterol levels differently in cholesterol-fed rats and rabbits [J]. J Lipid Res, 2000,41 (2): 298-304.
[15] Torchia EC, Cheema SK, Agellon LB. Coordinate regulation of bile acid biosynthetic and recovery pathways [J]. Biochem Biophys Res Commun, 1996, 225(1): 128-33.
[16] Al-Ansari N, Xu G, Kollman-Bauerly K, et al. Analysis of the effect of intestinal resection on rat ileal bile acid transporter expression and on bile acid and cholesterol homeostasis [J]. Pediatr Res, 2002,52(2): 286-91.
[17] Luiking YC, van der Reijden AC, van Berge Henegouwen GP, et al.Migrating motor complex cycle duration is determined by gastric or duodenal origin ofphaseⅢ [J]. Am J Physiol, 1998, 275 (1):1246-51.
[18] Marzio L, Pieramico O, Grossi L, et al. Evaluation of the refractory period of the human migrating motor complex through induction of premature phase Ⅲ [J]. J Gastrointest Motil, 1992, 4(1): 99-105.
[19] Xu QW, Scott RB, Tan DT, et al. Alter migrating myoelectrical complex in an animal model of cholesterol gallstone disease: the effect oferythromycin[J]. Gut, 1998, 43(6): 817-22.
[20] Sander KM. A case for interstitial cells of Cajal as pacemakers and mediators of neurotransmission in the gastrointestinal tract [J].Gastroenterology, 1996, 111(2): 492.
[21] Scott RB, Strasberg SM, El Sharkawy TY, et al. Regulation of the fasting enterohepatic circulation of bile acids by the migrating myoelectric complex in dogs[J]. J Clin Invest, 1983, 71(3): 644-54.
[22] Benjamin DR. Cholelithiasis in infants: the role total parenteral nutrition and gastrointestinal dysfunction[J]. J Pediatr Surg, 1982, 17(4): 386.
[23] 褚先秋.小儿胆囊结石、回肠病变与胆囊畸形[J].中国普通外科杂志,1994,3(1):8-9.Chu XQ. Cholelithiasis, ileal disorder and congenital abnormality of gallbladder in children[J]. Chin J Gen Surg, 1994, 3(1): 8-9.
[24] Shaffer EA, Bomzon A, Lax H, et al. The source of calcium for CCK-induced contraction of the guinea pig bladder [J]. Regul Pept,1992, 37(1): 15-26.
[25] 陈凛,顾倬云.胆汁酸池变化在豚鼠实验性胆色素结石形成中的意义[J].中华外科杂志,1992,30(8):496-8.Chen L, Gu ZY. Change of bile acid pool size plays role in chloesterol gallstone formation in guinea pigs [J]. Chin J Surg, 1992, 30(8): 496-8.