Voluntary running exercise prevents ß-cell failure in susceptible islets of the Zucker diabetic fatty rat.
Am J Physiol Endocrinol Metab
; 302(2): E254-64, 2012 Jan 15.
Article
em En
| MEDLINE
| ID: mdl-22045312
ABSTRACT
Physical activity improves glycemic control in type 2 diabetes (T2D), but its contribution to preserving ß-cell function is uncertain. We evaluated the role of physical activity on ß-cell secretory function and glycerolipid/fatty acid (GL/FA) cycling in male Zucker diabetic fatty (ZDF) rats. Six-week-old ZDF rats engaged in voluntary running for 6 wk (ZDF-A). Inactive Zucker lean and ZDF (ZDF-I) rats served as controls. ZDF-I rats displayed progressive hyperglycemia with ß-cell failure evidenced by falling insulinemia and reduced insulin secretion to oral glucose. Isolated ZDF-I rat islets showed reduced glucose-stimulated insulin secretion expressed per islet and per islet protein. They were also characterized by loss of the glucose regulation of fatty acid oxidation and GL/FA cycling, reduced mRNA expression of key ß-cell genes, and severe reduction of insulin stores. Physical activity prevented diabetes in ZDF rats through sustaining ß-cell compensation to insulin resistance shown in vivo and in vitro. Surprisingly, ZDF-A islets had persistent defects in fatty acid oxidation, GL/FA cycling, and ß-cell gene expression. ZDF-A islets, however, had preserved islet insulin mRNA and insulin stores compared with ZDF-I rats. Physical activity did not prevent hyperphagia, dyslipidemia, or obesity in ZDF rats. In conclusion, islets of ZDF rats have a susceptibility to failure that is possibly due to altered ß-cell fatty acid metabolism. Depletion of pancreatic islet insulin stores is a major contributor to islet failure in this T2D model, preventable by physical activity.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Condicionamento Físico Animal
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Diabetes Mellitus Tipo 2
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Células Secretoras de Insulina
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Dislipidemias
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Ácidos Graxos
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Insulina
Limite:
Animals
Idioma:
En
Revista:
Am J Physiol Endocrinol Metab
Assunto da revista:
ENDOCRINOLOGIA
/
FISIOLOGIA
/
METABOLISMO
Ano de publicação:
2012
Tipo de documento:
Article
País de afiliação:
Canadá