Mechanisms involved in the β-cell mass increase induced by chronic sucrose feeding to normal rats
The aim of the present study was to clarify the mechanisms by which a sucrose-rich diet (SRD) produces an increase in the pancreatic β-cell mass in the rat. Normal Wistar rats were fed for 30 weeks either an SRD (SRD rats; 63% wt/wt), or the same diet but with starch instead of sucrose in the same p...
Autores principales: | , , , , , |
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Formato: | Articulo |
Lenguaje: | Inglés |
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2002
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Acceso en línea: | http://sedici.unlp.edu.ar/handle/10915/84641 |
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I19-R120-10915-84641 |
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institution |
Universidad Nacional de La Plata |
institution_str |
I-19 |
repository_str |
R-120 |
collection |
SEDICI (UNLP) |
language |
Inglés |
topic |
Ciencias Médicas β-cell mass rats sucrose-rich diet |
spellingShingle |
Ciencias Médicas β-cell mass rats sucrose-rich diet Del Zotto, Héctor Herminio Gómez Dumm, César Leandro Alberto Drago, S. Fortino, A. Luna, Georgina Cecilia Gagliardino, Juan José Mechanisms involved in the β-cell mass increase induced by chronic sucrose feeding to normal rats |
topic_facet |
Ciencias Médicas β-cell mass rats sucrose-rich diet |
description |
The aim of the present study was to clarify the mechanisms by which a sucrose-rich diet (SRD) produces an increase in the pancreatic β-cell mass in the rat. Normal Wistar rats were fed for 30 weeks either an SRD (SRD rats; 63% wt/wt), or the same diet but with starch instead of sucrose in the same proportion (CD rats). We studied body weight, serum glucose and triacylglycerol levels, endocrine tissue and β-cell mass, β-cell replication rate (proliferating cell nuclear antigen; PCNA), islet neogenesis (cytokeratin immunostaining) and β-cell apoptosis (propidium iodide). Body weight (g) recorded in the SRD rats was significantly (P<0.05) larger than that of the CD group (556.0 ± 8.3 vs 470.0 ± 13.1). Both serum glucose and triacylglycerol levels (mmol/l) were also significantly higher (P<0.05) in SRD than in CD rats (serum glucose, 8.11 ± 0.14 vs 6.62 ± 0.17; triacyglycerol, 1.57 ± 0.18 vs 0.47 ± 0.04). The number of pancreatic islets per unit area increased significantly (P<0.05) in SRD rats (3.29 ± 0.1 vs 2.01 ± 0.2). A significant increment (2.6 times) in the mass of endocrine tissue was detected in SRD animals, mainly due to an increase in the β-cell mass (P=0.0025). The islet cell replication rate, measured as the percentage of PCNA-labelled β cells increased 6.8 times in SRD rats (P<0.03). The number of apoptotic cells in the endocrine pancreas decreased significantly (three times) in the SRD animals (P=0.03). The cytokeratin-positive area did not show significant differences between CD and SRD rats. The increase of β-cell mass induced by SRD was accomplished by an enhanced replication of β cells together with a decrease in the rate of β-cell apoptosis, without any evident participation of islet neogenesis. This pancreatic reaction was unable to maintain serum glucose levels of these rats at the level measured in CD animals. |
format |
Articulo Articulo |
author |
Del Zotto, Héctor Herminio Gómez Dumm, César Leandro Alberto Drago, S. Fortino, A. Luna, Georgina Cecilia Gagliardino, Juan José |
author_facet |
Del Zotto, Héctor Herminio Gómez Dumm, César Leandro Alberto Drago, S. Fortino, A. Luna, Georgina Cecilia Gagliardino, Juan José |
author_sort |
Del Zotto, Héctor Herminio |
title |
Mechanisms involved in the β-cell mass increase induced by chronic sucrose feeding to normal rats |
title_short |
Mechanisms involved in the β-cell mass increase induced by chronic sucrose feeding to normal rats |
title_full |
Mechanisms involved in the β-cell mass increase induced by chronic sucrose feeding to normal rats |
title_fullStr |
Mechanisms involved in the β-cell mass increase induced by chronic sucrose feeding to normal rats |
title_full_unstemmed |
Mechanisms involved in the β-cell mass increase induced by chronic sucrose feeding to normal rats |
title_sort |
mechanisms involved in the β-cell mass increase induced by chronic sucrose feeding to normal rats |
publishDate |
2002 |
url |
http://sedici.unlp.edu.ar/handle/10915/84641 |
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Repositorios |
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