Journal of the Korean Society of Food Science and Nutrition (한국식품영양과학회지)

The Korean Society of Food Science and Nutrition (한국식품영양과학회)
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Effects of Pear Phenolic Compound on the STZ-treated Mice for Induction of Diabetes

배에서 추출한 Phenolic Compound가 Streptozotocin으로 유발된 고혈당 생쥐에 미치는 영향

  • Published : 2002.12.01
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Abstract

This study has been carried out to investigate the effects of the Phenolic compound on the hyperglycemic mice induced with strentozotocin (STZ). The effects of the phenolic compound were assayed by the changes of the blood glucose creatinine and blood urea nitrogen (BUN ) levels, and insulin-immunohistochemical staining and electron microscopical observation for $\beta$ -cells of the Langerhan's islet, under the same experimental conditions. For this purpose male mice were fed with phenolic compound (PA group, IS mg/kg/day; PB group, 90 mg/kg/day)in their diet while the control group received the same commercial diet, for 6 weeks. The blood glucose contents was examined by tail vein blood once a week for 6 weeks. Samples of the pancreas removed after that period were processed for the immunohistochemical identification of $\beta$ -cells as well as for measuring ultrastructural changes of $\beta$-cells. The levels of serum glucose were decreased significantly (p<0.05) on the PB group compared with the control and PA group. The blood BUN and creatinine levels are slightly decreased in the phenolic compound feeding groups compared with control group. The $\beta$-cells on Langerhnan's islet were destructed by administration of STZ, so that a few of insulin-positive cells were observed in the control group. A lot of insulin-positive cells were observed in the PB group compared with the control group. According to the electron microscopical observation $\beta$-cells are recovered from the damage in the PA group. The $\beta$-cell contained a lot of electron dense and pale granules compared with control group. These results suggest that administration of the pear phenolic compound to the mice helped recovery from the damage induced by STZ.

배에서 추출한 phenolic compound가 streptozotocin(STZ)응 투여하고 고혈당을 유발시킨 생쥐에 미치는 영향을 밝히고자, 생쥐의 혈당, 혈중 creatinine, BUN의 변화 및 insulin-면역 조직화학적 검색과 췌장섬 $\beta$-세포의 전자현미경관찰을 통한 미세구조 변화를 관찰하였다. 실험군은 정상적인 동물 사료를 식이토록 한 대조군, 사료에 phenolic compound(PA군, 13 mg/g/kg/day; PB군,90 mg/kg/day)를 혼합하여 6주 동안 섭식하게 한 실험군으로 구분하였다. 대조군의 혈당 농도는 4주부터 높게 나타났으며, PA군의 혈당은 대조군에 비하여 유의성 (p<0.05)있게 감소하였으며, 특히 PB군에서는 4주부터 감소하기 시작하여 6주까지 유의성 (p<0.05)있게 감소하였다. BUN과creatinine의 농도는 대조군에 비하여 실험군에서 다소 감소하였으나 유의성은 없었다. STZ을 투여한 대조군의 췌장섬은 대부분 파괴되어 insulin-면역조직화학적 반응을 보인 세포들이 거의 관찰되지 않았으나, PB군에서는 다수의 췌장섬이 관찰될 뿐만 아니라 인슐린-면역조직화학 반응이 양성으로 관찰되었다. 전자현미경관찰 결과 대조군의 $\beta$-세포에서는 인슐린 함유 과립들이 소수 관찰되었으나 PB군에서는 이들 과립들이 다수 관찰되었다. 이상의 결과로 보아 phenolic compound를 섭식한 실험군 생쥐는 STZ에 의해서 손상된 췌장섬이 회복 또는 재생되어 $\beta$-세포의 인슐린 분비가 복원되 어 가고 있다고 사료되었다.

Keywords

References

  1. Tisch R, McDevitt H. 1966. Insulin-dependent diabetes mellitus. Cell 85: 291-297. https://doi.org/10.1016/S0092-8674(00)81106-X
  2. Pickup JC, Williams G. 1994. Chronic complications of diabetes. Blackwell Scientific Publications, Oxford, United Kingdom. p 313.
  3. Skyler JS 1986. Lessons from studies of insulin pharmacokinetics. Diabetes Care 9: 666-668. https://doi.org/10.2337/diacare.9.6.666
  4. Chien YW, Banga AK. 1989. Potential developments in systemic delivery of insulin. Drug Dev Ind Pharm 15: 1601-1607. https://doi.org/10.3109/03639048909052505
  5. Adjei A, Gupta P. 1994. Pulmonary delivery of therapeutic peptides and proteins. J Control Release 29: 361-369. https://doi.org/10.1016/0168-3659(94)90081-7
  6. Morgan RV, Huntzicker MA. 1996. Delivery of systemic regular insulin via ocular route in dogs. J Ocul Pharmacol Ther 12: 515. https://doi.org/10.1089/jop.1996.12.515
  7. Weir GC, Bonner-Weir S. 1997. Scientific and political impediment to successful islet transplantation. Diabetes 46: 1247-1256. https://doi.org/10.2337/diabetes.46.8.1247
  8. Lewis GF, Zinman B, Groenewoud Y, Vranic M, Giacca A. 1996. Hepatic glucose production is regulated both by direct hepatic effects of insulin in humans. Diabetes 45: 455-462
  9. Roberts RL, Sandra A. 1992. Receptor-mediated endocytosis of insulin by culture endothelial cells. Tissue Cell 24: 603-611. https://doi.org/10.1016/0040-8166(92)90031-2
  10. Swenne I. 1983. Effects of aging on the regenerative capacity of the pancreatic $\beta$-cell of the rat. Diabetes 32: 14-19. https://doi.org/10.2337/diabetes.32.1.14
  11. Booner-Weir S. 2000. Islet growth and development in the adult. J Mol Endocrinol 24: 297-302. https://doi.org/10.1677/jme.0.0240297
  12. Ramiya VK. 2000. Reversal of insulin-dependent diabetes using islets generated in vitro from pancreatic stem cells. Nat Med 6: 278-282. https://doi.org/10.1038/73128
  13. Hellerstrom C, Swenne I. 1991. Functional maturation and proliferationof fetal pancreatic $\beta$-cells. Diabetes 40 (Suppl.2): 89-93. https://doi.org/10.2337/diab.40.2.S89
  14. Rooman I, Schuit F, Biuwens L. 1997. Effects of vascular endothelial grouth factor on growth and differentiation of pancreatic ductal epithelium. Lab Inves 76: 225-232.
  15. Rafaeloff R, Pittenger GL, Barlow SW, Qin XF, Yan B, Rosenberg L, Duguid WP, Vinik AI. 1997. Cloning and seqeencing of thge pancreatic islet neogenesis associated protein (INGAP) gene and its expression in islet neogenesis in hamaster. J Clin Invest 99: 2100-2109. https://doi.org/10.1172/JCI119383
  16. Lefebvre VH, Otonkoski T, Ustinov J, Huotari MA, Pipeleers DG, Bouwens L. 1998. Culture of adult human islet preparations with hepatocyte growth factor and 804G matrix is mitogenic for duct cells but not for $\beta$-cells. Diabetes 47: 134-137. https://doi.org/10.2337/diabetes.47.1.134
  17. Le Roith D. 1997. Insulin-like growth factors. N Engl J Med 336: 633-640. https://doi.org/10.1056/NEJM199702273360907
  18. Mathews LS, Norstedt G, Palmiter RD. 1986. Regulation of insulin-like growth factor I gene expression by growth hormone. Proc Natl Acac Sci USA 83: 9343-9347. https://doi.org/10.1073/pnas.83.24.9343
  19. Smith FE, Rosen KM, Villa-Krmaroff L, Weir GC, Bonner-Weir S. 1991. Enhanced insulin-like growth factor I gene expression in regenerating rat pancreas. Proc Natl Acac Sci USA 88: 6152-6156. https://doi.org/10.1073/pnas.88.14.6152
  20. Hayakawa H, Kawarada Y, Mizumoto R, Hibasami H, Tanaka M, Nakashima K. 1996. Induction and involvement of endogenous IGF-I in pancreas regeneration after partial pancreatectomy in the dog. J Endocrinol 149: 259-267. https://doi.org/10.1677/joe.0.1490259
  21. AOAC. 1980. Official Methods of Analysis. 13th ed. Association of Official Analytical Chemists, Washington, DC.
  22. Murali B, Goyal RK. 2001. Effect of chronic treatment with losartan on streptozotocin induced diabetic nephropathy. Clin Exp Hypertens 23: 513-520. https://doi.org/10.1081/CEH-100106822
  23. Gisela C, Hector DZ, Cesar LA, Gomez D, Juan JG. 2000. Quantitative ultrastructural changes induced by sucrose administration in the pancreatic B cells of normal hamster. Biocell 24: 31-37.
  24. Calbo EL, Bernatchez G, Pelletier G, Iovanna JL, Morisset J. 1997. Down regulation of IGF-I mRA expression during postnatal pancreatic development and overexpression after subtotal pancreatectomy and acute pancreatitis in the rat pancreas. J Mol Endocrinol 18: 233-242. https://doi.org/10.1677/jme.0.0180233
  25. Hugl SR, White MF, Rhodes CJ. 1998. Insulin-like growth factor I (IGF-I)-stimulated pancreatic $\beta$-cell growth is glucose-dependent: synergistic activation of insulin receptor substrate-mediated signal transduction pathway by glucose and IGF-I in Ins-1 cells. J Biol Chem 269: 28783-28789.
  26. George M, Eduard A, Alba C, Cristina C, Jean CD, Bosh F. 2002. $\beta$-cell expression of IGF-I leads to recovery from type 1 diabetes. J Clin Invest 109: 1153-1163. https://doi.org/10.1172/JCI0212969
  27. Bonner-Weir S, Deery D, Leahy JL, Weir GC. 1989. Compensatory growth of pancreatic $\beta$-cells in adult rats after shortterm glucose infusion. Diabetes 38: 49-53. https://doi.org/10.2337/diabetes.38.1.49
  28. Bonner-Weir S, Smith FE. 1994. Islet growth and the growth factors involved. Trends in Endocrinology and metabolism 5: 5137-5140.
  29. Del Zotto H, Gomez Dumm CL, Drago S, Fortion A, Luna GC, Gagliardino JJ. 2002. Mechanism involved in the beta-cell mass increase induced by chronic sucrose feeding to normal rats. J Endocrinol 174: 225-231. https://doi.org/10.1677/joe.0.1740225

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