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Islet composition and architecture in streptozotocin-induced diabetic rat following pancreatic duct ligation

Thesis (MScMedSc)--Stellenbosch University, 2015.

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Main Author: Kotze, Patricia Clara
Other Authors: Tchokonte-Nana, Venant
Format: Thesis
Language:en_ZA
Published: Stellenbosch : Stellenbosch University 2015
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access_status_str Open Access
author Kotze, Patricia Clara
author2 Tchokonte-Nana, Venant
author_browse Kotze, Patricia Clara
Tchokonte-Nana, Venant
author_facet Tchokonte-Nana, Venant
Kotze, Patricia Clara
author_sort Kotze, Patricia Clara
collection Thesis
dc_rights_str_mv Stellenbosch University
description Thesis (MScMedSc)--Stellenbosch University, 2015.
format Thesis
id oai:scholar.sun.ac.za:10019.1/98045
institution Stellenbosch University (South Africa)
language en_ZA
last_indexed 2026-06-10T12:42:07.859Z
license_str Other — see source repository
provenance_str_mv Harvested via OAI-PMH from SUNScholar — Stellenbosch University Repository
publishDate 2015
publishDateRange 2015
publishDateSort 2015
publisher Stellenbosch : Stellenbosch University
publisherStr Stellenbosch : Stellenbosch University
record_format dspace
source_str SUNScholar — Stellenbosch University Repository
spelling oai:scholar.sun.ac.za:10019.1/98045 Islet composition and architecture in streptozotocin-induced diabetic rat following pancreatic duct ligation Kotze, Patricia Clara Tchokonte-Nana, Venant Stellenbosch University. Faculty of Medicine and Health Sciences. Dept. of Biomedical Sciences: Anatomy and Histology. Pancreatic duct ligation Diabetes mellitus Islets Islet composition Islet architecture Streptozotocin Rats as laboratory animals UCTD Thesis (MScMedSc)--Stellenbosch University, 2015. ENGLISH ABSTRACT: Diabetes Mellitus is a metabolic disease characterized by the loss of beta cells from the islets, thereby disrupting islet composition and architecture which are important components that influence islet function. The experimental technique of pancreatic duct ligation (PDL), which is thought to induce the regeneration of beta cells within the adult pancreas, was investigated as a novel treatment strategy for diabetes. This study aimed at investigating the possibility that the PDL model may have the capacity to restore normal islet composition and architecture in diabetic animals, which could make it an effective approach to reverse diabetes. Male Wistar rats (n=55) were divided into three study groups: the normal control (NC) group, the diabetic control (DC) group consisting of five subgroups (day 0, 3, 5, 10 and 30) and the experimental (EX) group consisting of four subgroups (day 3, 5, 10 and 30). The experimental group was exposed to PDL. All pancreata were divided into a P1 portion (proximal to the point of ligature) and P2 portion (distal to the point of ligature) for histological assessment. Animals’ non-fasting blood glucose levels (BGLs) and body weights were monitored. The general morphology of the tissue was studied, while an immunohistochemical (IHC) study was performed to determine insulin, pancreatic polypeptide, glucagon and somatostatin protein expression in the P1 and P2 portions of the pancreas. From the IHC slides hormone fractions, staining intensity and distribution were determined as indication of islet composition and architecture. Despite apparent morphological recovery in the islet 30 days post-PDL, islet composition and architecture remained disrupted. Compared to diabetic animals, the proximal portion of the pancreas in experimental animals had a decreased beta cell fraction and increased delta cell fraction thirty days following PDL. These observed changes in islet composition in the part of the pancreas proximal to the ligature are novel findings. There was no change in the diabetic islet composition in the portion of the pancreas distal to the ligature thirty days following PDL. Furthermore, pancreatic duct ligation did not restore body weight or normoglycemia. We conclude that STZ disrupts islet composition and architecture and this could not be restored using PDL; we therefore suggest that a comparative study using a Type 2 diabetic model, where there is limited damage to pre-existing beta cells, may yield different results. AFRIKAANSE OPSOMMING: Diabetes Mellitus is ʼn metaboliese siekte wat deur die verlies van beta selle uit die eilande van Langerhans gekarakteriseer word. Hierdie verlies van beta selle ontwrig eiland komposisie en argitektuur, twee belangrike komponente van eiland funksie. Die eksperimentele tegnieke van pankreatiese buisafbinding (in Engels PDL), wat moontlik beta sel regenerasie in die volwasse pankreas kan induseer, is ondersoek as behandelings-strategie vir diabetes. Hierdie studie het ten doel gehad om die moontlikheid te ondersoek dat die PDL model die kapasiteit het om normale eiland komposisie en argitektuur te herstel in diabetiese diere, wat dit ʼn effektiewe benadering vir die omkeer van diabetes kan maak. Manlike Wistar rotte (n=55) was in 3 studie groepe verdeel: die normale kontrole (NC) groep, die diabetiese kontrole (DC) groep wat uit vyf subgroepe bestaan (dag 0, 3, 5, 10 en 30) en die eksperimentele (EX) groep wat uit vier subgroepe bestaan (dag 3, 5, 10 en 30). Die eksperimentele groep is aan PDL blootgestel. Alle pankreata is verdeel in ʼn P1 porsie (proksimaal tot die afbinding) en ʼn P2 porsie (distaal tot die afbinding) vir histologiese assessering. Die diere se nie-vastende bloed glukose vlakke en liggaamsgewig is gemonitor. Die algemene morfologie van die pankreas weefsel is bestudeer, terwyl ’n immunohistochemiese (IHC) studie gedoen is om insulien, pankreatiese polipeptied, glukagon en somatostatien proteïen uitdrukking in die P1 en P2 porsies van die pankreas te bepaal. Vanaf die IHC snitte is hormoon fraksie, kleur intensiteit en verspreiding bepaal as aanduidings van eiland komposisie en argitektuur. Ten spyte van ooglopende morfologiese herstel in die eilande op dag 30 na PDL, het eiland komposisie en argitektuur versteur gebly. In vergelyking met die diabetiese diere, het die proksimale deel van die pankreas van eksperimentele diere verlaagde beta sel fraksie en verhoogde delta sel fraksie getoon dertig dae na PDL. Die waarneming van veranderde komposisie in die deel van die pankreas proksimaal tot die afbinding is nuut. Daar was geen verandering in diabetiese eiland komposisie in die deel van die pankreas distaal tot die afbinding dertig dae na PDL nie. Verder het PDL nie liggaamsgewig of bloedsuiker genormaliseer nie. Ons gevolgtrekking is dat STZ eiland komposisie en argitektuur ontwrig en dat dit nie met PDL herstel kon word nie; daarom stel ons ʼn vergelykende studie in ʼn tipe 2 diabetes model voor, waar die skade aan reeds bestaande beta selle beperk is, wat ander resultate mag lewer. 2015-12-14T07:43:59Z 2015-12-14T07:43:59Z 2015-12 Thesis http://hdl.handle.net/10019.1/98045 en_ZA Stellenbosch University xvi, 108 pages : colour illustrations application/pdf Stellenbosch : Stellenbosch University
spellingShingle Pancreatic duct ligation
Diabetes mellitus
Islets
Islet composition
Islet architecture
Streptozotocin
Rats as laboratory animals
UCTD
Kotze, Patricia Clara
Islet composition and architecture in streptozotocin-induced diabetic rat following pancreatic duct ligation
title Islet composition and architecture in streptozotocin-induced diabetic rat following pancreatic duct ligation
title_full Islet composition and architecture in streptozotocin-induced diabetic rat following pancreatic duct ligation
title_fullStr Islet composition and architecture in streptozotocin-induced diabetic rat following pancreatic duct ligation
title_full_unstemmed Islet composition and architecture in streptozotocin-induced diabetic rat following pancreatic duct ligation
title_short Islet composition and architecture in streptozotocin-induced diabetic rat following pancreatic duct ligation
title_sort islet composition and architecture in streptozotocin induced diabetic rat following pancreatic duct ligation
topic Pancreatic duct ligation
Diabetes mellitus
Islets
Islet composition
Islet architecture
Streptozotocin
Rats as laboratory animals
UCTD
url http://hdl.handle.net/10019.1/98045
work_keys_str_mv AT kotzepatriciaclara isletcompositionandarchitectureinstreptozotocininduceddiabeticratfollowingpancreaticductligation