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Diabetologia

, Volume 32, Issue 3, pp 160–162 | Cite as

Effect of nicotinamide therapy upon B-cell function in newly diagnosed Type 1 (insulin-dependent) diabetic patients

  • G. Mendola
  • R. Casamitjana
  • R. Gomis
Originals

Summary

This study describes the effects of nicotinamide therapy on B-cell function in Type 1 (insulin-dependent) diabetes. C-peptide secretion was studied in 20 patients newly diagnosed with Type 1 diabetes at basal state and also after an i.v. glucagon stimulus. Patients were randomly allocated according to a single-blind schedule, to one of the following treatments over a 45-day period: Group 1: 10 patients, nicotinamide 1 g/day; Group 2: 10 patients, placebo. The C-peptide secretion tests were performed before treatment and on days 15, 45, 180, 365 of the follow-up. The clinical and metabolic data were similar in the two groups of patients. Basal and stimulated C-peptide levels increased by 45 days in both groups, but the increase in stimulated C-peptide response was greater in the nicotinamide group (p<0.01). However, the B-cell function decreased after the period of nicotinamide administration. No difference in the number of clinical remissions or insulin requirement and HbA1 between the groups was observed. These data suggest that treatment of Type 1 diabetes with nicotinamide at diagnosis is associated with a moderate increase of C-peptide secretion recovery.

Key words

Type 1 (insulin-dependent) diabetes mellitus nicotinamide treatment B cell function 

References

  1. 1.
    Botazzo GF, Pujol-Borrell R, Gale E (1986) Autoimmunity and diabetes: progress, consolidation and controversy. Alberti KGMM, Krall LP (eds) The diabetes annual 2. Elsevier, London, pp 13–29Google Scholar
  2. 2.
    Stiller CR, Dupre J, Gent MR, Jenner PA, Keown PA, Laupacis A, Martell R, Rodger NW, Graffenried B, Wolfe MJ (1984) Effects of cyclosporine immunosuppression in insulin-dependent diabetes mellitus of recent onset. Science 223: 1362–1367Google Scholar
  3. 3.
    Elliot RB, Crossley JR, Berryman CC, James AG (1981) Partial preservation of pancreatic B-Cell function in children with diabetes. Lancet II: 1–4Google Scholar
  4. 4.
    Ludvigsson J, Heding L, Lieden G, Marner B, Lernmark Å (1983) Plasmapheresis in the initial treatment of insulin-dependent diabetes mellitus in children. Br Med J 286: 176–178Google Scholar
  5. 5.
    Yamada K, Nonaka K, Hanafusa T, Miyazaki A, Toyoshima H, Tarui S (1982) Preventive and therapeutic effects of large-dose nicotinamide injections on diabetes associated with insulitis Diabetes 31: 749–753Google Scholar
  6. 6.
    Uchigata Y, Yamamoto H, Nagai H, Okamoto H (1983) Effect of poly-(ADP-ribose) synthetase inhibitor administration to rats before and after injection of alloxan and streptozotocin on islet proinsulin synthesis. Diabetes 32: 316–318Google Scholar
  7. 7.
    Yonemura Y, Takashima T, Miwa K, Miyazadi I, Yamamoto H, Okamoto H (1984) Amelioration of diabetes mellitus in partially depancreatized rats by poly-ADP-ribose synthetase inhibitors: evidence of islet B-cell regeneration. Diabetes 33: 401–404Google Scholar
  8. 8.
    Vague Ph, Vialettes B, Lassman-Vague V, Vallo JJ (1987) Nicotinamide may extend remission phase in insulin dependent diabetes. Lancet I: 619Google Scholar
  9. 9.
    Tarn AC, Smith CP, Spencer KM, Botazzo GF, Gale EAM (1987) Type 1 (insulin dependent) diabetes: a disease of slow clinical onset? Br Med J 294: 342–345Google Scholar
  10. 10.
    National Diabetes Data Group (1979) Classification and diagnosis of diabetes mellitus and other categories of glucose intolerance. Diabetes 28: 1039–1057Google Scholar
  11. 11.
    Kuzuya T, Matsuda A, Saito T, Yoshia S (1976) Human C-peptide immuno-reactivity (CPR) in blood and urine evaluation of radioimmunoassay method and its clinical applications. Diabetologia 12: 511–518Google Scholar
  12. 12.
    Bonifacio E, Dawkins RL, Lernmark Å (1987) Immunology and diabetes workshop: report of the second international workshop on the standardisation of cytoplasmic islet cell antibodies. Diabetologia 30: 273Google Scholar
  13. 13.
    Passey RB, Gillum RL, Fuller JB, Urry FM, Giles ML (1977) Evaluation and comparison of 10 glucose methods and the reference method recommended in the product class standard. Clin Chem 23: 131–135Google Scholar
  14. 14.
    Gomis R, Figuerola D, Micalo T, Millan M, Peig M (1981) Hemoglobina glucosilada como indice de control de la diabetes mellitus. Med Clin (Barcelona) 76: 251–254Google Scholar
  15. 15.
    Yamamoto H, Uchigata Y, Okamoto H (1981) DNA strand breaks in pancreatic islet by “in vivo” administration of alloxan or streptozotocin. Biochem Biophys Res Commun 103: 1014–1020Google Scholar
  16. 16.
    Yamamoto H, Uchigata Y, Okamoto H (1981) Streptozotocin and alloxan induce DNA strand breaks and poly-(ADP-ribose) synthetase in pancreatic islet. Nature 294: 284–286Google Scholar
  17. 17.
    Yamamoto H, Okamoto H (1980) Protection by picolinamide, a novel inhibitor of poly-(ADP-ribose) synthetase, against both streptozotocin-induced depression of proinsulin synthesis and reduction of NAD content in pancreatic islets. Biochem Biophys Res Commun 95: 474–481Google Scholar
  18. 18.
    Okamoto H (1981) Regulation of proinsulin synthesis in pancreatic islets and a new aspect to insulin-dependent diabetes. Mol Cell Biochem 37: 43–61Google Scholar

Copyright information

© Springer-Verlag 1989

Authors and Affiliations

  • G. Mendola
    • 1
  • R. Casamitjana
    • 1
  • R. Gomis
    • 1
  1. 1.Endocrinology and Diabetes UnitHormonal Laboratory, Hospital Clinic, University of Barcelona, School of MedicineBarcelonaSpain

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