Main Article Content

Abstract

Background: Sleep disturbance accelerates type 2 diabetes mellitus by reducing insulin secretion and by the occurrence of difficulty in controlling sleep behaviour in humans so that it is necessary conduct a study by using experimental animals.
Objective: This study aims to determine histophotometric differences of pancreas and differences of glucose tolerance in male albino rats (Rattus norvegicus) after induced by stress paradoxical sleep deprivation (PSD) and total sleep deprivation (TSD).
Methods: This study applied a post-test only with control groups consisting of 30 male albino rats (Wistar strain) divided randomly into 3 groups: control group, PSD group and TSD group. The mean number and diameter of islets of Langerhans were calculated per slide and were averaged for each group at a magnification of 400 X. The percentage of beta cells in one islet of Langerhans was (ß-p) that was a number of normal beta cells (Bn) divided for the total beta cells (Bt) (normal and damaged) x 100%. The glucose level based on the sampling time was made a curve shape, and the area under the 0-to-120-minute curves (AUC0-120) was calculated by using a trapezoidal formula.
Results: The lowest AUC0-120 level of glucose was the control group (14,082 ± 955mg/dL) and the highest was the TSD group (16,293 ± 2,195 mg/dL); the Post-Hoc LSD test showed a significant difference (p<0.05) between the control-PSD group and the TSD-control group. The mean result of pancreatic ß cells mass with the lowest number was in the TSD group (76.3 ± 4.8), and the highest result was in the control group (94.3 ± 2.7); Post-Hoc LSD showed a significant difference (p <0.05) in the control-PSD group and the TSD-control group. The lowest mean in cell diameter of islets of Langerhans was in the TSD group (0.132 ± 0.031 mm), and the highest mean was in the control group (0.213 ± 0.019 mm).
Conclusion: Sleep deprivation could reduce pancreatic ß cell mass and cell diameter of islets of Langerhans and increase glucose tolerance levels.

Article Details

How to Cite
Arjadi, F., Gumilas, N. S. A., Harini, I. M., Samodro, P., & Andromeda, A. (2021). The decrease of histomorphometry and function of pancreas in male albino rats after induced by sleep deprivation. JKKI : Jurnal Kedokteran Dan Kesehatan Indonesia, 12(2), 109–115. https://doi.org/10.20885/JKKI.Vol12.Iss2.art3

References

  1. Rakshit K, Thomas AP, Matveyenko AV. Does disruption of circadian rhythms contribute to beta-cell failure in type 2 diabetes?. Current Diabeteses Reports. 2014;14(4):474–8.
  2. Villafuerte G, Miguel-Puga A, Rodríguez EM, Machado S, Manjarrez E, Arias-Carrión O. Sleep deprivation and oxidative stress in animal models: A systematic review. Oxidative Medicine and Cellular Longevity. 2015;1–15.
  3. Briançon-Marjollet A, Weiszenstein M, Henri M, Thomas A, Godin-Ribuot D, Polak J. The impact of sleep disorders on glucose metabolism: Endocrine and molecular mechanisms. Diabetology and Metabolic Syndrome. 2015;7(1):1–16.
  4. Farid M, Darwin E, Sulastri D. Pengaruh hiperglikemia terhadap gambaran histopatologis pulau langerhans mencit. Jurnal Kesehatan Andalas. 2014;3(3):420–8.
  5. Keane KN, Cruzat VF, Carlessi R, De Bittencourt PIH, Newsholme P. Molecular events linking oxidative stress and inflammation to insulin resistance and ß-cell dysfunction. Oxidative Medicine and Cellular Longevity.. 2015;2015:181643.
  6. Kilimnik G, Jo J, Periwal V, Zielinski MC, Hara M. Quantification of islet size and architecture. Islets. 2012;4(2):167–72.
  7. Kim NH, Lee SK, Eun CR, Seo JA, Kim SG, Choi KM, et al. Short sleep duration combined with obstructive sleep apnea is associated with visceral obesity in Korean adults. Sleep. 2013;36(5):723–9.
  8. Barf RP, Meerlo P, Scheurink AJW. Chronic sleep disturbance impairs glucose homeostasis in rats. International Journal of Endocrinology. 2010;2010:819414.
  9. Arjadi F, Partadireja G, Maurits LS, Pangestu M. Paradoxical sleep deprivation changes testicular malondialdehyde and caspase-3 expression in male rats. Universa Medicina. 2015;34(2):87.
  10. Spiers JG, Chen HC, Sernia C, Lavidis NA. Activation of the hypothalamic-pituitary-adrenal stress axis induces cellular oxidative stress. Frontiers in Neuroscience. 2015;8:1–6.
  11. Hurrle S, Hsu WH. The etiology of oxidative stress in insulin resistance. Biomedical Journal. 2017;40(5):257–62.
  12. Gerber PA, Rutter GA. The role of oxidative stress and hypoxia in pancreatic beta-cell dysfunction in diabetes mellitus. Antioxidants Redox Signal. 2017;26(10):501–18.
  13. Gale JE, Cox HI, Qian J, Block GD, Colwell CS, Matveyenko A. Disruption of circadian rhythms accelerates development of diabetes through pancreatic ß-cell loss and dysfunction. Journal of Biological Rhythms. 2012;26(5):423–33.
  14. Knutson KL. Impact of sleep and sleep loss on glucose homeostasis and appetite regulation regulation. Sleep Medicine Clinics. 2008;2(2):187–97.
  15. Abunasef SK, Amin HA, Abdel-Hamid GA. A histological and immunohistochemical study of beta cells in streptozotocin diabetic rats treated with caffeine. Folia Histochemica and Cytobiologica. 2014;52(1):42–50.
  16. Kei F and Polonsy KS. Pdx1 and other factors that regulate pancreatic ß-cell survival. Diabetes Obesity and Metabolism. 2010;11(Suppl 4):30–7.
  17. El Khattabi I SA. Preventing p38 MAPK-mediated MafA degradation ameliorates ß-cell dysfunction under oxidative stress. Molecular Endocrinology. 2013;27(7):1078–90.
  18. Robertson RP, Harmon JS. Pancreatic islet ß-cell and oxidative stress: The importance of glutathione peroxidase. FEBS Letters. 2007;581(19):3743–8.