Effect of the sodium-glucose cotransporter 2 inhibitor luseogliflozin on pancreatic beta cell mass in db/db mice of different ages

Scientific Reports

Volumn 8, Issue 1, 2018, Pages

  Takahashi, Kiyohiko ^a   Nakamura, Akinobu ^a   Miyoshi, Hideaki ^a   Nomoto, Hiroshi ^a   Kitao, Naoyuki ^a   Omori, Kazuno ^a   Yamamoto, Kohei ^a   Cho, Kyu Yong ^a   Terauchi, Yasuo ^b   Atsumi, Tatsuya ^a  

^a HOKKAIDO UNIVERSITY   (Japan)

^b YOKOHAMA CITY UNIVERSITY   (Japan)

Author keywords

[No Author keywords available]

Indexed keywords

1,5-ANHYDRO-1-(5-(4-ETHOXYBENZYL)-2-METHOXY-4-METHYLPHENYL)-1-THIOGLUCITOL; CCND2 PROTEIN, MOUSE; CYCLIN D2; HOMEODOMAIN PROTEIN; KI 67 ANTIGEN; MAFA PROTEIN, MOUSE; PANCREATIC AND DUODENAL HOMEOBOX 1 PROTEIN; SLC5A2 PROTEIN, MOUSE; SODIUM GLUCOSE COTRANSPORTER 2; SORBITOL; TRANSACTIVATOR PROTEIN; TRANSCRIPTION FACTOR MAF; TRANSCRIPTOME;

AGE; ANIMAL; CYTOLOGY; DISEASE MODEL; DRUG EFFECT; GENETICS; MALE; METABOLISM; MOUSE; MOUSE MUTANT; NON INSULIN DEPENDENT DIABETES MELLITUS; PANCREAS ISLET BETA CELL; PHARMACOLOGY;

AGE FACTORS; ANIMALS; CYCLIN D2; DIABETES MELLITUS, TYPE 2; DISEASE MODELS, ANIMAL; HOMEODOMAIN PROTEINS; INSULIN-SECRETING CELLS; KI-67 ANTIGEN; MAF TRANSCRIPTION FACTORS, LARGE; MALE; MICE; MICE, OBESE; SODIUM-GLUCOSE TRANSPORTER 2; SODIUM-GLUCOSE TRANSPORTER 2 INHIBITORS; SORBITOL; TRANS-ACTIVATORS; TRANSCRIPTOME;

EID: 85046347213     PISSN: None     EISSN: 20452322     Source Type: Journal    
DOI: 10.1038/s41598-018-25126-z     Document Type: Article

References (32)

1. Taylor, S. I. Deconstructing type 2 diabetes. Cell 97, 9-12 (1999).
2. Prentki, M. &Nolan, C. J. Islet beta cell failure in type 2 diabetes. The Journal of clinical investigation 116, 1802-1812, https://doi. org/10.1172/jci29103 (2006).
3. Butler, A. E. et al. Beta-cell deficit and increased beta-cell apoptosis in humans with type 2 diabetes. Diabetes 52, 102-110 (2003).
4. Sakuraba, H. et al. Reduced beta-cell mass and expression of oxidative stress-related DNA damage in the islet of Japanese Type II diabetic patients. Diabetologia 45, 85-96, https://doi.org/10.1007/s001250200009 (2002).
5. U.K. prospective diabetes study 16. Overview of 6 years' therapy of type II diabetes: a progressive disease. U.K. Prospective Diabetes Study Group. Diabetes 44, 1249-1258 (1995).
6. Dalboge, L. S. et al. Characterisation of age-dependent beta cell dynamics in the male db/db mice. PloS one 8, e82813, https://doi. org/10.1371/journal.pone.0082813 (2013).
7. Puff, R. et al. Reduced proliferation and a high apoptotic frequency of pancreatic beta cells contribute to genetically-determined diabetes susceptibility of db/db BKS mice. Hormone and metabolic research 43, 306-311, https://doi.org/10.1055/s-0031-1271817 (2011).
8. Chen, L., Klein, T. &Leung, P. S. Effects of combining linagliptin treatment with BI-38335, a novel SGLT2 inhibitor, on pancreatic islet function and inflammation in db/db mice. Current molecular medicine 12, 995-1004 (2012).
9. Thomas, L. et al. Long-term treatment with empagliflozin, a novel, potent and selective SGLT-2 inhibitor, improves glycaemic control and features of metabolic syndrome in diabetic rats. Diabetes, obesity &metabolism 14, 94-96, https://doi. org/10.1111/j.1463-1326.2011.01518.x (2012).
10. Vallon, V. The mechanisms and therapeutic potential of SGLT2 inhibitors in diabetes mellitus. Annual review of medicine 66, 255-270, https://doi.org/10.1146/annurev-med-051013-110046 (2015).
11. Washburn, W. N. Development of the renal glucose reabsorption inhibitors: a new mechanism for the pharmacotherapy of diabetes mellitus type 2. Journal of medicinal chemistry 52, 1785-1794, https://doi.org/10.1021/jm8013019 (2009).
12. Jurczak, M. J. et al. SGLT2 deletion improves glucose homeostasis and preserves pancreatic beta-cell function. Diabetes 60, 890-898, https://doi.org/10.2337/db10-1328 (2011).
13. Okauchi, S. et al. Protective effects of SGLT2 inhibitor luseogliflozin on pancreatic beta-cells in obese type 2 diabetic db/db mice. Biochemical and biophysical research communications 470, 772-782, https://doi.org/10.1016/j.bbrc.2015.10.109 (2016).
14. Nakamura, A. et al. Control of beta cell function and proliferation in mice stimulated by small-molecule glucokinase activator under various conditions. Diabetologia 55, 1745-1754, https://doi.org/10.1007/s00125-012-2521-5 (2012).
15. Guo, S. et al. Inactivation of specific beta cell transcription factors in type 2 diabetes. The Journal of clinical investigation 123, 3305-3316, https://doi.org/10.1172/jci65390 (2013).
16. Cheng, S. T., Chen, L., Li, S. Y., Mayoux, E. &Leung, P. S. The Effects of Empagliflozin, an SGLT2 Inhibitor, on Pancreatic beta-Cell Mass and Glucose Homeostasis in Type 1 Diabetes. PloS one 11, e0147391, https://doi.org/10.1371/journal.pone.0147391 (2016).
17. Terami, N. et al. Long-term treatment with the sodium glucose cotransporter 2 inhibitor, dapagliflozin, ameliorates glucose homeostasis and diabetic nephropathy in db/db mice. PloS one 9, e100777, https://doi.org/10.1371/journal.pone.0100777 (2014).
18. Robertson, R. P. Chronic oxidative stress as a central mechanism for glucose toxicity in pancreatic islet beta cells in diabetes. The Journal of biological chemistry 279, 42351-42354, https://doi.org/10.1074/jbc.R400019200 (2004).
19. Okamoto, H. et al. Role of the forkhead protein FoxO1 in beta cell compensation to insulin resistance. The Journal of clinical investigation 116, 775-782, https://doi.org/10.1172/jci24967 (2006).
20. Terauchi, Y. et al. Glucokinase and IRS-2 are required for compensatory beta cell hyperplasia in response to high-fat diet-induced insulin resistance. The Journal of clinical investigation 117, 246-257, https://doi.org/10.1172/jci17645 (2007).
21. Hang, Y. et al. The MafA transcription factor becomes essential to islet beta-cells soon after birth. Diabetes 63, 1994-2005, https:// doi.org/10.2337/db13-1001 (2014).
22. Matsuoka, T. A. et al. Preserving Mafa expression in diabetic islet beta-cells improves glycemic control in vivo. The Journal of biological chemistry 290, 7647-7657, https://doi.org/10.1074/jbc.M114.595579 (2015).
23. Matsuoka, T. A. et al. Regulation of MafA expression in pancreatic beta-cells in db/db mice with diabetes. Diabetes 59, 1709-1720, https://doi.org/10.2337/db08-0693 (2010).
24. Harmon, J. S. et al. beta-Cell-specific overexpression of glutathione peroxidase preserves intranuclear MafA and reverses diabetes in db/db mice. Endocrinology 150, 4855-4862, https://doi.org/10.1210/en.2009-0708 (2009).
25. Dor, Y. &Glaser, B. beta-cell dedifferentiation and type 2 diabetes. The New England journal of medicine 368, 572-573, https://doi. org/10.1056/NEJMcibr1214034 (2013).
26. Talchai, C., Xuan, S., Lin, H. V., Sussel, L. &Accili, D. Pancreatic beta cell dedifferentiation as a mechanism of diabetic beta cell failure. Cell 150, 1223-1234, https://doi.org/10.1016/j.cell.2012.07.029 (2012).
27. Wang, Z., York, N. W., Nichols, C. G. &Remedi, M. S. Pancreatic beta cell dedifferentiation in diabetes and redifferentiation following insulin therapy. Cell metabolism 19, 872-882, https://doi.org/10.1016/j.cmet.2014.03.010 (2014).
28. Ishida, E., Kim-Muller, J. Y. &Accili, D. Pair Feeding, but Not Insulin, Phloridzin, or Rosiglitazone Treatment, Curtails Markers of beta-Cell Dedifferentiation in db/db Mice. Diabetes 66, 2092-2101, https://doi.org/10.2337/db16-1213 (2017).
29. Kimura, T. et al. Protective effects of pioglitazone and/or liraglutide on pancreatic beta-cells in db/db mice: Comparison of their effects between in an early and advanced stage of diabetes. Molecular and cellular endocrinology 400, 78-89, https://doi.org/10.1016/j. mce.2014.11.018 (2015).
30. Shao, Y., Yuan, G., Feng, Y., Zhang, J. &Guo, X. Early liraglutide treatment is better in glucose control, beta-cell function improvement and mass preservation in db/db mice. Peptides 52, 134-142, https://doi.org/10.1016/j.peptides.2013.11.011 (2014).
31. Yamamoto, K. et al. TS-071 is a novel, potent and selective renal sodium-glucose cotransporter 2 (SGLT2) inhibitor with antihyperglycaemic activity. British journal of pharmacology 164, 181-191, https://doi.org/10.1111/j.1476-5381.2011.01340.x (2011).
32. Sato, K. et al. Impact of the dipeptidyl peptidase-4 inhibitor vildagliptin on glucose tolerance and beta-cell function and mass in insulin receptor substrate-2-knockout mice fed a high-fat diet. Endocrinology 153, 1093-1102, https://doi.org/10.1210/en.2011-1712 (2012).