| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Regular Articles |
From the Department of Pathology, Hirosaki University School of Medicine, Hirosaki, Japan
The Goto-Kakizaki (GK) rat is a spontaneously diabetic animal model of non-insulin-dependent diabetes mellitus, which is characterized by progressive loss of ß cells in the pancreatic islets with fibrosis. In the present study, we examined the effects of sucrose feeding on the islet pathology in this model. Six-week-old GK rats were fed with 30% sucrose for 6 weeks to induce severe hyperglycemia, and their condition was compared with that of nontreated rats. Age-matched normal Wistar rats were also given sucrose for the same periods and used for comparison. The sucrose-treated GK rats showed elevated blood glucose levels on oral glucose tolerance tests at 60 minutes and 120 minutes, representing 123% and 127% of values in untreated GK rats, respectively. At the end of the study, the mean ß-cell volume density in GK rats was 50% less than that in untreated Wistar rats. Sucrose feeding further reduced the volume densities of ß cells to only 50% of the levels of age-matched GK rats. Apoptotic cells were found in islet ß cells only in GK rats fed sucrose (mean 0.067%). There appeared to be more islets that immunohistochemically stained strongly positive with 8-hydroxy-deoxyguanosine as a marker of oxidative damage of DNA in GK rats fed sucrose compared with those not given sucrose. GK rats not fed sucrose showed significantly lower proliferative activity of ß cells measured by 5-bromo-2'-deoxyuridine uptake and intensified expression of Bcl-2 immunoreactivities at 6 weeks of age compared with those in age-matched Wistar rats. These two indices were reduced in both GK and Wistar rats with increasing age and were not affected by sucrose feeding in either group. The present study thus indicated that sucrose feeding promoted the apoptosis of ß cells in GK rats through increased oxidative stress without altering their proliferative activity.
This article has been cited by other articles:
 |
|
 |
|
  S. Hashimoto, K. Yamada, T. Kawata, T. Mochizuki, J. Schnermann, and T. Koike Abnormal autoregulation and tubuloglomerular feedback in prediabetic and diabetic OLETF rats Am J Physiol Renal Physiol, March 1, 2009; 296(3): F598 - F604. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Qian, H. Wang, X. Men, W. Zhang, H. Cai, S. Xu, Y. Xu, L. Ye, C. B Wollheim, and J. Lou TRIB3 is implicated in glucotoxicity- and oestrogen receptor-stress-induced {beta}-cell apoptosis J. Endocrinol., December 1, 2008; 199(3): 407 - 416. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Numazawa, H. Sakaguchi, R. Aoki, T. Taira, and T. Yoshida Regulation of the susceptibility to oxidative stress by cysteine availability in pancreatic {beta}-cells Am J Physiol Cell Physiol, August 1, 2008; 295(2): C468 - C474. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. A. Nugent, D. M. Smith, and H. B. Jones A Review of Islet of Langerhans Degeneration in Rodent Models of Type 2 Diabetes Toxicol Pathol, June 1, 2008; 36(4): 529 - 551. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M.-K. Sim, X.-G. Xu, Y.-C. Wong, S.-Z. Sim, and K.-O. Lee Des-Aspartate-Angiotensin I Exerts Hypoglycemic Action via Glucose Transporter-4 Translocation in Type 2 Diabetic KKAy Mice and GK Rats Endocrinology, December 1, 2007; 148(12): 5925 - 5932. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Q. Huang, S. Bu, Y. Yu, Z. Guo, G. Ghatnekar, M. Bu, L. Yang, B. Lu, Z. Feng, S. Liu, et al. Diazoxide Prevents Diabetes through Inhibiting Pancreatic {beta}-Cells from Apoptosis via Bcl-2/Bax Rate and p38-{beta} Mitogen-Activated Protein Kinase Endocrinology, January 1, 2007; 148(1): 81 - 91. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Dungan and J. B. Buse Glucagon-Like Peptide 1-Based Therapies for Type 2 Diabetes: A Focus on Exenatide Clin. Diabetes, April 1, 2005; 23(2): 56 - 62. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Kohler, S. V. Zaitsev, I. I. Zaitseva, B. Leibiger, I. B. Leibiger, M. Turunen, I. L. Kapelioukh, L. Bakkman, I. B. Appelskog, J. Boutet de Monvel, et al. On-Line Monitoring of Apoptosis in Insulin-Secreting Cells Diabetes, December 1, 2003; 52(12): 2943 - 2950. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S.-J. Janket, J. E. Manson, H. Sesso, J. E. Buring, and S. Liu A Prospective Study of Sugar Intake and Risk of Type 2 Diabetes in Women Diabetes Care, April 1, 2003; 26(4): 1008 - 1015. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Tourrel, D. Bailbe, M. Lacorne, M.-J. Meile, M. Kergoat, and B. Portha Persistent Improvement of Type 2 Diabetes in the Goto-Kakizaki Rat Model by Expansion of the {beta}-Cell Mass During the Prediabetic Period With Glucagon-Like Peptide-1 or Exendin-4 Diabetes, May 1, 2002; 51(5): 1443 - 1452. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Wobser, H. Du{beta}mann, D. Kogel, H. Wang, C. Reimertz, C. B. Wollheim, M. M. Byrne, and J. H. M. Prehn Dominant-negative Suppression of HNF-1alpha Results in Mitochondrial Dysfunction, INS-1 Cell Apoptosis, and Increased Sensitivity to Ceramide-, but Not to High Glucose-induced Cell Death J. Biol. Chem., February 15, 2002; 277(8): 6413 - 6421. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Tourrel, D. Bailbe, M.-J. Meile, M. Kergoat, and B. Portha Glucagon-Like Peptide-1 and Exendin-4 Stimulate {beta}-Cell Neogenesis in Streptozotocin-Treated Newborn Rats Resulting in Persistently Improved Glucose Homeostasis at Adult Age Diabetes, July 1, 2001; 50(7): 1562 - 1570. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Federici, M. Hribal, L. Perego, M. Ranalli, Z. Caradonna, C. Perego, L. Usellini, R. Nano, P. Bonini, F. Bertuzzi, et al. High Glucose Causes Apoptosis in Cultured Human Pancreatic Islets of Langerhans: A Potential Role for Regulation of Specific Bcl Family Genes Toward an Apoptotic Cell Death Program Diabetes, June 1, 2001; 50(6): 1290 - 1301. [Abstract] [Full Text]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
