Effect of canagliflozin on renal threshold for glucose, glycemia, and body weight in normal and diabetic animal models - PubMed (original) (raw)
doi: 10.1371/journal.pone.0030555. Epub 2012 Feb 15.
Kenji Arakawa, Kiichiro Ueta, Yasuaki Matsushita, Chiaki Kuriyama, Tonya Martin, Fuyong Du, Yi Liu, June Xu, Bruce Conway, Jamie Conway, David Polidori, Kirk Ways, Keith Demarest
Affiliations
- PMID: 22355316
- PMCID: PMC3280264
- DOI: 10.1371/journal.pone.0030555
Effect of canagliflozin on renal threshold for glucose, glycemia, and body weight in normal and diabetic animal models
Yin Liang et al. PLoS One. 2012.
Abstract
Background: Canagliflozin is a sodium glucose co-transporter (SGLT) 2 inhibitor in clinical development for the treatment of type 2 diabetes mellitus (T2DM).
Methods: (14)C-alpha-methylglucoside uptake in Chinese hamster ovary-K cells expressing human, rat, or mouse SGLT2 or SGLT1; (3)H-2-deoxy-d-glucose uptake in L6 myoblasts; and 2-electrode voltage clamp recording of oocytes expressing human SGLT3 were analyzed. Graded glucose infusions were performed to determine rate of urinary glucose excretion (UGE) at different blood glucose (BG) concentrations and the renal threshold for glucose excretion (RT(G)) in vehicle or canagliflozin-treated Zucker diabetic fatty (ZDF) rats. This study aimed to characterize the pharmacodynamic effects of canagliflozin in vitro and in preclinical models of T2DM and obesity.
Results: Treatment with canagliflozin 1 mg/kg lowered RT(G) from 415±12 mg/dl to 94±10 mg/dl in ZDF rats while maintaining a threshold relationship between BG and UGE with virtually no UGE observed when BG was below RT(G). Canagliflozin dose-dependently decreased BG concentrations in db/db mice treated acutely. In ZDF rats treated for 4 weeks, canagliflozin decreased glycated hemoglobin (HbA1c) and improved measures of insulin secretion. In obese animal models, canagliflozin increased UGE and decreased BG, body weight gain, epididymal fat, liver weight, and the respiratory exchange ratio.
Conclusions: Canagliflozin lowered RT(G) and increased UGE, improved glycemic control and beta-cell function in rodent models of T2DM, and reduced body weight gain in rodent models of obesity.
Conflict of interest statement
Competing Interests: The authors have read the journal's policy and have the following conflicts: Drs. Liang, Martin, Du, Conway, Polidori, and Demarest are employees of Johnson & Johnson Pharmaceutical Research & Development, LLC. Drs. Arakawa, Ueta, Matsushita, and Kuriyama are employees of Mitsubishi Tanabe Pharma Corporation, Japan. Canagliflozin (JNJ-28431754/TA-7284) is being developed by Johnson & Johnson Pharmaceutical Research & Development, LLC. in collaboration with Mitsubishi Tanabe Pharma Corporation. This does not alter the authors' adherence to all the PLoS ONE policies on sharing data and materials.
Figures
Figure 1. Inhibitory effects of canagliflozin on human SGLT1 and human SGLT2.
The inhibitory effect of canagliflozin on 14C-AMG uptake in CHOK-hSGLT1 and CHOK-hSGLT2 has been measured in 5 experiments. A typical inhibitory effect on CHOK-hSGLT1 (Panel A) and CHOK-hSGLT2 (Panel B) from a single experiment is presented here.
Figure 2. BG and UGE in untreated and CANA-treated ZDF rats during two GGI studies.
In the first study (GGI only), a GGI was given to untreated ZDF rats (n = 8) to raise BG from 212±24 mg/dl to ∼475 mg/dl over 90 minutes. In the second study (Insulin+GGI), ZDF rats (n = 6/group) were treated with either vehicle or canagliflozin (1 mg/kg), then given insulin to lower BG to 25±1 mg/dl, and finally given the GGI to slowly raise BG. BG and UGE were measured every 5 minutes. Results shown are mean ± S.E. GGI, graded glucose infusion; BG, blood glucose; UGE, urinary glucose excretion; ZDF, Zucker diabetic fatty rats; GG1, graded glucose infusion.
Similar articles
- Analysis of the effect of canagliflozin on renal glucose reabsorption and progression of hyperglycemia in zucker diabetic Fatty rats.
Kuriyama C, Xu JZ, Lee SP, Qi J, Kimata H, Kakimoto T, Nakayama K, Watanabe Y, Taniuchi N, Hikida K, Matsushita Y, Arakawa K, Saito A, Ueta K, Shiotani M. Kuriyama C, et al. J Pharmacol Exp Ther. 2014 Nov;351(2):423-31. doi: 10.1124/jpet.114.217992. Epub 2014 Sep 12. J Pharmacol Exp Ther. 2014. PMID: 25216746 - SHR3824, a novel selective inhibitor of renal sodium glucose cotransporter 2, exhibits antidiabetic efficacy in rodent models.
Yan PK, Zhang LN, Feng Y, Qu H, Qin L, Zhang LS, Leng Y. Yan PK, et al. Acta Pharmacol Sin. 2014 May;35(5):613-24. doi: 10.1038/aps.2013.196. Acta Pharmacol Sin. 2014. PMID: 24786232 Free PMC article. - Validation of a novel method for determining the renal threshold for glucose excretion in untreated and canagliflozin-treated subjects with type 2 diabetes mellitus.
Polidori D, Sha S, Ghosh A, Plum-Mörschel L, Heise T, Rothenberg P. Polidori D, et al. J Clin Endocrinol Metab. 2013 May;98(5):E867-71. doi: 10.1210/jc.2012-4205. Epub 2013 Apr 12. J Clin Endocrinol Metab. 2013. PMID: 23585665 Free PMC article. Clinical Trial. - Sodium glucose co-transporter 2 inhibitors and their mechanism for improving glycemia in patients with type 2 diabetes.
Davidson JA, Kuritzky L. Davidson JA, et al. Postgrad Med. 2014 Oct;126(6):33-48. doi: 10.3810/pgm.2014.10.2819. Postgrad Med. 2014. PMID: 25414933 Review. - [SGLT-2 inhibition with canagliflozin: a new option for the treatment of type 2 diabetes].
Seufert J. Seufert J. Dtsch Med Wochenschr. 2014 Feb;139 Suppl 2:S52-8. doi: 10.1055/s-0033-1359991. Epub 2014 Jan 30. Dtsch Med Wochenschr. 2014. PMID: 24481633 Review. German. No abstract available.
Cited by
- Model-based meta-analysis of HbA1c reduction across SGLT2 inhibitors using dose adjusted by urinary glucose excretion.
Sato H, Ishikawa A, Yoshioka H, Jin R, Sano Y, Hisaka A. Sato H, et al. Sci Rep. 2024 Oct 21;14(1):24695. doi: 10.1038/s41598-024-76256-6. Sci Rep. 2024. PMID: 39433865 Free PMC article. - Sympathetic Activation Promotes Sodium Glucose Co-Transporter-1 Protein Expression in Rodent Skeletal Muscle.
Matthews JR, Herat LY, Schlaich MP, Matthews VB. Matthews JR, et al. Biomedicines. 2024 Jul 1;12(7):1456. doi: 10.3390/biomedicines12071456. Biomedicines. 2024. PMID: 39062029 Free PMC article. - The relationship between SGLT2 and systemic blood pressure regulation.
Ahwin P, Martinez D. Ahwin P, et al. Hypertens Res. 2024 Aug;47(8):2094-2103. doi: 10.1038/s41440-024-01723-6. Epub 2024 May 23. Hypertens Res. 2024. PMID: 38783146 Free PMC article. Review. - Preclinical Studies of Canagliflozin, a Sodium-Glucose Co-Transporter 2 Inhibitor, and Donepezil Combined Therapy in Alzheimer's Disease.
Stanciu GD, Ababei DC, Solcan C, Bild V, Ciobica A, Beschea Chiriac SI, Ciobanu LM, Tamba BI. Stanciu GD, et al. Pharmaceuticals (Basel). 2023 Nov 16;16(11):1620. doi: 10.3390/ph16111620. Pharmaceuticals (Basel). 2023. PMID: 38004485 Free PMC article. - mTORC1 and SGLT2 Inhibitors-A Therapeutic Perspective for Diabetic Cardiomyopathy.
Saha S, Fang X, Green CD, Das A. Saha S, et al. Int J Mol Sci. 2023 Oct 11;24(20):15078. doi: 10.3390/ijms242015078. Int J Mol Sci. 2023. PMID: 37894760 Free PMC article. Review.
References
- Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes estimates for the year 2000 and projections for 2030. Diabetes Care. 2004;27:1047–1053. - PubMed
- Hoerger TJ, Segel JE, Gregg EW, Saaddine JB. Is glycemic control improving in U.S. adults? Diabetes Care. 2008;31:81–86. - PubMed
- Wright EM, Hirayama BA, Loo DF. Active sugar transport in health and disease. J Intern Med. 2007;261:32–43. - PubMed
- Wright EM, Turk E. The sodium/glucose cotransport family SLC5. Pflügers Arch - Eur J Physiol. 2004;447:510–518. - PubMed
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
Molecular Biology Databases
Miscellaneous