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Pantoprazole may improve beta cell function and diabetes mellitus

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Abstract

Background

Proton pump inhibitors induce hypergastrinemia by suppressing gastric acidity. Gastrin has incretin-like stimulating actions on beta cells. Proton pump inhibitors have been shown to decrease glycosylated hemoglobin.

Aim

We aimed to observe changes in beta cell function in diabetic and non-diabetic subjects given pantoprazole for an acid-related ailment.

Methods

Seventy-nine male patients (38 non-diabetic and 41 type-2 diabetic receiving only metformin therapy) were followed for 12 weeks after pantoprazole 40 mg/day was given. Fasting plasma glucose, HbA1c, fasting insulin, Pancreatic B cell function (HOMA-B), proinsulin and c-peptide levels were measured before and after the treatment.

Results

In non-diabetic patients (n = 38), FPG decreased, whereas c-peptide, log-HOMA-B, increased significantly (p = 0.002, p = 0.03, p = 0.042, respectively) after 12 weeks of pantoprazole administration. In type 2 diabetic patients, FPG, HbA1c and weight decreased, whereas log-HOMA-B, c-peptide and log-proinsulin levels increased significantly after pantoprazole treatment (p = 0.003, p = 0.007, p < 0.001; p < 0.001; p = 0.017, p = 0.05, respectively). After pantoprazole treatment, pancreatic B-cell function was correlated with c-peptide and insulin and inversely with FBG and HbA1c levels in the whole group (r = 0.37, p = 0.001; r = 0.60, p < 0.001, r = −0.29, p = 0.011 and r = −0.28, p = 0.013, respectively). After pantoprazole treatment, HbA1c was correlated with FBG (r = 0.75, p < 0.001) and inversely with only log-HOMA-B level (r = −0.28, p = 0.013).

Conclusions

Pantoprazole administration seems to correlate with increased beta cell function. Pantoprazole administration improves HbA1c, HOMA-B, c-peptide and proinsulin levels. Since beta cell loss plays a significant role in the pathogenesis of type 2 diabetes, PPI-based therapies may be useful in the treatment of diabetes.

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References

  1. Rooman I, Lardon J, Bouwens L (2002) Gastrin stimulates beta-cell neogenesis and increases islet mass from transdifferentiated but not from normal exocrine pancreas tissue. Diabetes 51(3):686–690

    Article  CAS  PubMed  Google Scholar 

  2. Lugari R, Dei Cas A, Ugolotti D, Finardi L, Barilli AL, Ognibene C, Luciani A, Zandomeneghi R, Gnudi A (2002) Evidence for early impairment of glucagon-like peptide 1-induced insulin secretion in human type 2 (non insulin-dependent) diabetes. Horm Metab Res 34(3):150–154

    Article  CAS  PubMed  Google Scholar 

  3. Dammann HG, Burkhardt F (1999) Pantoprazole versus omeprazole: influence on meal-stimulated gastric acid secretion. Eur J Gastroenterol Hepatol 11(11):1277–1282

    Article  CAS  PubMed  Google Scholar 

  4. Rooman I, Bouwens L (2004) Combined gastrin and epidermal growth factor treatment induces islet regeneration and restores normoglycaemia in C57Bl6/J mice treated with alloxan. Diabetologia 47(2):259–265

    Article  CAS  PubMed  Google Scholar 

  5. Mefford IN, Wade EU (2009) Proton pump inhibitors as a treatment method for type II diabetes. Med Hypothesis 73:29–32

    Article  CAS  Google Scholar 

  6. Crouch MA, Mefford IN, Wade EU (2012) Proton pump inhibitor therapy associated with lower glycosylated hemoglobin levels in type 2 diabetes. J Am Board Fam Med 25(1):50–54

    Article  PubMed  Google Scholar 

  7. Mefford IN, Mefford JT, Burris CA (2012) Improved diabetes control and pancreatic function in a type 2 diabetic after omeprazole administration. Case Rep Endocrinol 2012:468609

    CAS  PubMed Central  PubMed  Google Scholar 

  8. Singh PK, Hota D, Dutta P, Sachdeva N, Chakrabarti A, Srinivasan A, Singh I, Bhansali A (2012) Pantoprazole improves glycemic control in type 2 diabetes: a randomized, double-blind, placebo-controlled trial. J Clin Endocrinol Metab 97(11):E2105–E2108

    Article  CAS  PubMed  Google Scholar 

  9. Wallace TM, Levy JC, Matthews DR (2004) Use and abuse of HOMA modeling. Diabetes Care 27(6):1487–1495

    Article  PubMed  Google Scholar 

  10. Tougas G, Earnest DL, Chen Y, Vanderkoy C, Rojavin M (2005) Omeprazole delays gastric emptying in healthy volunteers: an effect prevented by tegaserod. Aliment Pharmacol Ther 22:59–65

    Article  CAS  PubMed  Google Scholar 

  11. Sanaka M, Yamamoto T, Kuyama Y (2010) Effects of proton pump inhibitors on gastric emptying: a systematic review. Dig Dis Sci 55:2431–2440

    Article  CAS  PubMed  Google Scholar 

  12. Meier JJ, Butler AE, Galasso R, Rizza RA, Butler PC (2006) Increased islet beta cell replication adjacent to intrapancreatic gastrinomas in humans. Diabetologia 49(11):2689–2696

    Article  CAS  PubMed  Google Scholar 

  13. Suarez-Pinzon WL, Lakey JR, Brand SJ, Rabinovitch A (2005) Combination therapy with epidermal growth factor and gastrin induces neogenesis of human islet {beta}-cells from pancreatic duct cells and an increase in functional {beta}-cell mass. J Clin Endocrinol Metab 90(6):3401–3409

    Article  CAS  PubMed  Google Scholar 

  14. Bödvarsdóttir TB, Hove KD, Gotfredsen CF, Pridal L, Vaag A, Karlsen AE, Petersen JS (2010) Treatment with a proton pump inhibitor improves glycaemic control in Psammomys obesus, a model of type 2 diabetes. Diabetologia 53(10):2220–2223. doi:10.1007/s00125-010-1825-6

    Article  PubMed Central  PubMed  Google Scholar 

  15. Boj-Carceller D, Bocos-Terraz P, Moreno-Vernis M, Sanz-Paris A, Trincado-Aznar P, Albero-Gamboa R (2011) Are proton pump inhibitors a new antidiabetic drug? A cross sectional study. World J Diabetes 2(12):217–220

    Article  PubMed Central  PubMed  Google Scholar 

  16. Rooman I, Lardon J, Bouwens L (2002) Gastrin stimulates beta-cell neogenesis and increases islet mass from transdifferentiated but not from normal exocrine pancreas tissue. Diabetes 51:686–690

    Article  CAS  PubMed  Google Scholar 

  17. Suarez-Pinzon WL, Yan Y, Power R, Brand SJ, Rabinovitch A (2005) Combination therapy with epidermal growth factor and gastrin increases beta-cell mass and reverses hyperglycemia in diabetic NOD mice. Diabetes 54:2596–2601

    Article  CAS  PubMed  Google Scholar 

  18. Docherty K, Steiner DF (1997) Molecular and cellular biology of the beta cell. In: Porte D Jr, Sherwin RS (eds) Diabetes mellitus. Prentice-Hall, London, pp 29–48

    Google Scholar 

  19. Ward WK, LaCava EC, Paquette TL, Beard JC, Wallum BJ, Porte D Jr (1987) Disproportionate elevation of immunoreactive proinsulin in type 2 (non-insulin-dependent) diabetes mellitus and in experimental insulin resistance. Diabetologia 30:698–702

    Article  CAS  PubMed  Google Scholar 

  20. Drucker DJ (2006) The biology of incretin hormones. Cell Metab 3(3):153–165

    Article  CAS  PubMed  Google Scholar 

  21. Jones CNO, Pei D, Staris P, Polonsky KS, Chen YD-I, Reaven GM (1997) Alterations in the glucose-stimulated insulin secretory dose-response curve and in insulin clearance in nondiabetic insulin-resistant individuals. J Clin Endocrinol Metab 82:1834–1838

    Article  CAS  PubMed  Google Scholar 

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Acknowledgments

This work was not supported by any specific grant.

Conflict of interest

F. Inci, M. Atmaca, M. Ozturk, S. Yildiz, R. Koceroglu, R. Sekeroglu, S. H. Ipekci, L. Kebapcilar declare they have no conflict of interest.

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Authors and Affiliations

  1. Department of Internal Medicine, University of Yuzuncu Yil, Van, Turkey

    F. Inci

  2. Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Yuzuncu Yil, Van, Turkey

    M. Atmaca, M. Ozturk & S. Yildiz

  3. Department of Biochemistry, University of Yuzuncu Yil, Van, Turkey

    R. Koceroglu & R. Sekeroglu

  4. Division of Endocrinology and Metabolism, Department of Internal Medicine, Selcuk University, Konya, Turkey

    S. H. Ipekci & L. Kebapcilar

  5. Department of Endocrinology and Metabolism, Faculty of Medicine, Selcuk University, Konya, Turkey

    L. Kebapcilar

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  1. F. Inci
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  2. M. Atmaca
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  3. M. Ozturk
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  4. S. Yildiz
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  8. L. Kebapcilar
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Correspondence to L. Kebapcilar.

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Inci, F., Atmaca, M., Ozturk, M. et al. Pantoprazole may improve beta cell function and diabetes mellitus. J Endocrinol Invest 37, 449–454 (2014). https://doi.org/10.1007/s40618-013-0040-y

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  • DOI: https://doi.org/10.1007/s40618-013-0040-y

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