Journals / Anatomy / 2017 / Cilt: 11 - Sayı: 2

Effect of streptozotocin-induced diabetes on the autonomic ganglia of albino rats

Journal
Anatomy
Pages
51–60
Publication Date
2022-10-11
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusion:The association of the long-standing hyperglycemia with increased neuronal death, altered proportion of neurons and deposition of collagen fibers in autonomic ganglia appear to be important contributing factors likely to be responsible for diabetic autonomic neuropathy

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objectives:One of the common clinical observations regarding long-standing hyperglycemia is autonomic neuropathy,probably due to its unfavorable destructive effects on the neurons of the autonomic ganglia.
📊
Key Findings & Data:Methods: Thirty-six albino rats were divided into six groups (n=6, each) and were designated as control, two weeks, onemonth, two months, four months and six months groups.
💡
Conclusion & Impact:Conclusion:The association of the long-standing hyperglycemia with increased neuronal death, altered proportion of neurons and deposition of collagen fibers in autonomic ganglia appear to be important contributing factors likely to be responsible for diabetic autonomic neuropathy
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Objectives:One of the common clinical observations regarding long-standing hyperglycemia is autonomic neuropathy,probably due to its unfavorable destructive effects on the neurons of the autonomic ganglia. Accordingly, the current studywas aimed to analyze the effect of experimental hyperglycemia on parasympathetic pterygopalatine ganglion (PtG) and sympathetic coeliac ganglion (ClG) of albino rats. Methods: Thirty-six albino rats were divided into six groups (n=6, each) and were designated as control, two weeks, onemonth, two months, four months and six months groups. Diabetes was induced with a single dose of streptozotocin (STZ,60 mg/kg, i.p.). Body weight and blood sugar were monitored at biweekly intervals. At the end of each experimental period, animals were euthanized by deep ether anesthesia and blood samples were collected by direct puncture of heart for biochemical analysis. Animals were perfused with Karnovsky fixative. After 48 hours, tissue samples were collected andprocessed for light microscopy. Results: Biochemical analysis of serum revealed increased serum creatinine and reduced serum total protein. Histopathologyand histomorphometry of ganglia revealed that the progressively increasing duration of hyperglycemia was associated withdecreased proportion of small-sized neurons, increased proportion of large-sized neurons, dark and dead neurons, and thickening of capsular and endoneurial collagen. Conclusion:The association of the long-standing hyperglycemia with increased neuronal death, altered proportion of neurons and deposition of collagen fibers in autonomic ganglia appear to be important contributing factors likely to be responsible for diabetic autonomic neuropathy

🔖

Cite This Article

FAİZAL, M., KHAN, A. A. (2022). Effect of streptozotocin-induced diabetes on the autonomic ganglia of albino rats. Anatomy, Cilt: 11 - Sayı: 2, 51–60. https://ajindex.com/articles/439516

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (15)

  1. Maritim AC, Sanders RA, Watkins JB. Diabetes, oxidative stress, and antioxidants: a review. J Biochem Mol Toxicol 2003;17:24–38.
  2. Phillips M, Cataneo RN, Cheema T, Greenberg J. Increased breath biomarker of oxidative stress in diabetes mellitus. Clin Chim Acta 2004;344:189–94.
  3. Tomlinson DR, Gardiner NJ. Glucose neurotoxicity. Nat Rev Neurosci 2008;9:36–45.
  4. Guven A, Yavuz O, Cam M, Comunoglu C, Sevinc O. Central nervous system complications of diabetes in streptozotocin-induced diabetic rats: a histopathological and immunohistochemical examination. Int J Neurosci 2009;119:1155–69.
  5. Rudchenko A, Akude E, Cooper E. Synapses on sympathetic neurons and parasympathetic neurons differ in their vulnerability to diabetes. J Neurosci 2014;34:8865–74.
  6. Srinivasan S, Stevens M, Wiley JW. Diabetic peripheral neuropathyevidence for apoptosis and associated mitochondrial dysfunction. Diabetes 2000;49:1932–8.
  7. Fernyhough A, Chowdhury SKR, Schmidt RE. Mitochondrial stress and the pathogenesis of diabetic neuropathy. Expert Rev Endocrinol Metab 2010;5:39–49.
  8. Vinik AI, Maser RE, Mitchell BD, Freeman R. Diabetic autonomic neuropathy. Diabetes Care 2003;26:1553–79.
  9. Siessere S, Vitti M, de Sousa, LG, Semprini M, Iyomasa MM, Regalo SC. Anatomic variation of cranial parasympathetic ganglia. Braz Oral Res 2008;22:101–5.
  10. Sisu AM, Petrescu CI, Cebzan CC, Motoc A, Bolintineanu S, vaida AM, Niculescu MC, Rusu MC. The adult coeliac ganglion: a morphologic study. Rom J Morphol Embryol 2008;49:491–4.
  11. Sasahara TH, De souza RR, Machado MR, Da silva RA, Guidi WL, Ribeiro AA. Macro- and microstructural organization of the rabbit's celiac-mesenteric ganglion complex (Oryctolagus cuniculus). Ann Anat 2003;185:441–8.
  12. Schmidt RE, Dorsey DA, Beaudet LN, Frederick KE, Parvin CA, Plurad SB, Levisetti MG. Non-obese diabetic mice rapidly develop dramatic sympathetic neuritic dystrophy a new experimental model of diabetic autonomic neuropathy. Am J Pathol 2003;163: 2077–91.
  13. Olsson Y, Sourander P. Changes in the sympathetic nervous system in diabetes mellitus. J Neurovisc Relat 1968;81:86–95.
  14. Faizal PAM, Khan AA, Elsy B. Effect of experimental hyperglycemia on the trigeminal ganglia of albino rats. Int J Health Sci Res 2017;7: 191–8.
  15. Young B, O’Dowd G, Woodford P. Wheater’s functional histology: a text and colour atlas. 6th edition. Philadelphia (PA): Churchill Livingstone, 2016. 139 p. Ernst MC, Sinal CJ. Chemerin at the crossroads of inflammation and obesity. Trends Endocrinol Metab 2010;21:660–7. King